title: Comprehensive transcriptome analysis of the cochleae of 7-month-old Fabp7 (+/+) and Fabp7 (-/-) mice

status: Public on Jun 23 2017

city: Sendai

first: Jun

last: Suzuki

address: 1-1 Seiryo-machi, Aoba-ku

department: Department of Otorhinolaryngology-Head and Neck Surgery

institute: Tohoku University School of Medicine

summary: To discover the molecules and signal pathways that are associated with the anti-aging effects of Fabp7 deficiency, transcriptome analyses were conducted using DNA microarray. The ABR thresholds of Fabp7 (+/+) and Fabp7 (-/-) mice were not significantly different at 7 months of age, but it was speculated that important gene expression changes might arise at approximately this stage. Therefore, 7-month-old Fabp7 (+/+) and Fabp7 (-/-) mice were used for transcriptome analyses.

overall_design: Three samples (total 12 cochleae from 6 mice) per group were collected, and gene expression was measured.


title: Binary polycyclic aromatic hydrocarbon exposure alters the transcriptome inducing inflammation and inhibiting cell communication through p38 MAPK in lung cells

status: Public on Jul 11 2017

city: Aurora

first: Alison

middle: Kendall

last: Bauer

state: CO

address: 12850 E. Montview Blvd.; Rm 3125

department: Environmental and Occupational Health

country: USA

institute: University of Colorado Denver

summary:
Low molecular weight polycyclic aromatic hydrocarbons (LMW PAHs) are generated by the incomplete combustion of organic material and are prevalent and ubiquitous in the environment, presenting a human health concern.  While much is known about the high molecular weight genotoxic species of PAHs, there are insufficient studies for LMW PAHs and their impact on pulmonary health.  Secondhand smoke, or environmental tobacco smoke (ETS), is a mixture of many PAHs, among other constituents.  To study the effect of more than one PAH, we examined single PAH and a binary mixture on the dysregulation of gap junctional intercellular communication (GJIC), activation of mitogen activated protein kinases (MAPK), and induction of inflammation with a focus on the p38 MAPK pathway through transcriptomic analysis.  A mouse non-tumorigenic alveolar type II cell line, C10, along with two normal, non-tumorigenic human bronchial epithelial cell lines, Beas2b and HBE1 cells, for human comparisons.  Our findings in all cell lines indicate that 1-methylanthracene (1-MeA) and fluoranthene (Flthn), can dysregulated GJIC in a dose dependent manner and combining these two compounds lead to a similar effect on GJIC.  MAPKs, particularly P38, are rapidly activated and the inhibition of this MAPK leads to a reversal of PAH dysregulation of GJIC.  A toxicogenomic approach conducted using the C10 cells revealed inflammatory, metabolic, steroid synthesis, and oxidative pathways altered synergistically by a mixture of PAHs (1-MeA and Flthn), followed by qRT-PCR, ELISAs, and immunoblots validation.  Our findings indicated LMW PAHs potential to induce pulmonary inflammation and emphasize the need for mixture exposure research to accurately estimate human exposure risk.
Grant ID: CIA130022
Grant Title: Components of secondhand smoke in COPD.
Funding Source: Flight Attendant Medical Research Institute
Name: Alison,K,Bauer

overall_design: A mouse alveolar type II cell line was used for this study called C10 cells.  Total RNA was extracted from the cells.  There are a total of 18 arrays with an n=3 per treatment group. Five treatment groups were used:  1) DMSO vehicle control at 4h; 2) 45 uM fluoranthene at 4h; 3) 40 uM total PAH mixture  (20 uM 1-methylanthracene: 20 uM fluoranthene) at 4h; 4) 5 uM p38 MAPK inhibitor  (SB203580) + 40 uM total PAH mixture  (20 uM 1-methylanthracene: 20 uM fluoranthene) at 4h; 5) 40 uM total PAH mixture  (20 uM 1-methylanthracene: 20 uM fluoranthene) at 8 h; 6) 5 uM p38 MAPK inhibitor  (SB203580) + 40 uM total PAH mixture  (20 uM 1-methylanthracene: 20 uM fluoranthene) at 8h.

first: Ross

middle: S

last: Osgood

first: Kalpana

last: Velmurugan

first: Pierre

middle: R

last: Bushel

first: Ka-Na

last: Xiong

first: Julie

first: Brad

middle: L

last: Upham

middle: K


title: Salt suppresses IFNγ-inducible chemokines in mouse kidneys with a high-salt condition

status: Public on Jun 12 2017

city: Bunkyo-ku

first: Yohei

last: Arai

state: Tokyo

address: 1-5-45, Yushima

department: Nephrology

country: Japan

institute: Tokyo Dental and Medical University

summary: Transcriptional profiling related cytokines and chemokines of mouse kidneys comparing the kidneys of WNK4 D561A/+ mice fed an 8% high-salt diet with those of WNK4+/+ littermates with a normal diet. Goal was to determine the effects of a high-salt condition on the immune system in kidney.

overall_design: Two-condition experiment: mouse kidneys of WNK4+/+ mice fed a normal diet vs. those of WNK4 D561A/+ mice fed an 8% high-salt diet for 7 days (n = 3).

first: Daiei

last: Takahashi

first: Eisei

last: Sohara


title: Gene expression data from colitis-associated colonic tumors of WT vs. MDR1A KO mice

status: Public on Jun 17 2017

city: Essen

first: Elke

last: Cario

state: NRW

address: Virchowstr. 171

department: Division of Gastroenterology and Hepatology

country: Germany

institute: University of Duisburg-Essen, University Hospital of Essen

summary:
Human Ulcerative colitis (UC) is characterized by chronic colonic inflammation and has been associated with an increased risk of colorectal carcinoma. Gene and protein expression profiles of ABCB1/MDR1 have been shown to be dysregulated in UC and sporadic colorectal cancer. We demonstrated that in a murine model of colitis-associated tumorigenesis, MDR1A KO mice showed reduced tumor load when compared to wildtype (WT) mice. The aim of this study was to identify gene alterations in colitis-associated tumors in the context of MDR1A deficiency.
We used microarrays to assess gene expression profiles of colitis-associated colonic tumors from WT or MDR1A KO mice.

overall_design: We used the azoxymethane (AOM) / dextran sulfate sodium (DSS) – model to study the development of colitis-associated colorectal cancer in WT and MDR1A KO mice. AOM was administered once (10mg/kg body weight) to 6-week-old male mice, followed by treatments with 2.5% DSS (mol wt, 36,000-50,000) for 7 days in drinking water starting on day 0, 21 and 42, respectively. Mice were sacrificed at the experimental endpoint (day 84). At that time the entire colon and rectum were excised, cut longitudinally, and rinsed in ice-cold Hank’s Balanced Salt Solution. During gross examination, tumors were macroscopically visualized by 1% alcian blue staining and excised. Total RNA was extracted from tumor samples. All extracted RNA samples (one tumor per individual mouse; 4 mice per group (WT vs. MDR1A KO); i.e. 4 tumor samples (rep) per group) were analyzed independently. Microarray processing was performed at an Affymetrix Service Provider and Core Facility, “KFB - Center of Excellence for Fluorescent Bioanalytics” (Regensburg, Germany).

first: E

middle: M

last: Hennenberg


title: Expression data from keratinocyte-specific Zfp36-deficient mouse skin treated with imiquimod

status: Public on Jun 14 2017

city: Gosselies

first: Stanislas

last: Goriely

address: 8 rue A. Bolland

department: Institute for Medical Immunology

country: Belgium

institute: Université Libre de Bruxelles

summary: Tristetraprolin (TTP, encoded by Zfp36) regulates the mRNA stability of several important cytokines. Due to the critical role of this RNA-binding protein in the control of inflammation, TTP deficiency leads to the spontaneous development of a complex inflammatory syndrome. So far, this phenotype has been largely attributed to dysregulated production of TNF and IL-23 by myeloid cells such as macrophages or dendritic cells. Here, we generated mice with conditional deletion of TTP in keratinocytes. These mice developed exacerbated inflammation in the imiquimod-induced psoriasis model. Furthermore, these mice progressively developed a spontaneous pathology with systemic inflammation, psoriatic-like skin lesions and dactylitis. Finally, we provide evidence that keratinocyte-derived TNF productin drives the different pathological features. In summary, these findings expand current views on the initiation of psoriasis and related arthritis by revealing the keratinocyte-intrinsic role of TTP.

overall_design: Mice with a specific deletion of Zfp36 in keratinocytes and their littermate control were topically treated or not with imiquimod during 5 consecutive days (5 animals by group). 4h after the last application, skins from abdomen were sampled and prepared for RNA extraction and hybridization on Affymetrix microarrays.


title: Gene expression profile of MDL-860-treated RD cells

status: Public on Jun 28 2017

city: Tokyo

first: Minetaro

last: Arita

state: Japan

address: 4-7-1 Gakuen, Musashimurayama-shi,

department: Department of Virology II

institute: National Institute of Infectious Diseases

summary: To analyze gene expression of RD cells after treatment with an anti-picornavirus compound MDL-860, we have employed whole genome microarray expression profiling as a discovery platform. Human RD cells were treated with mock or MDL-860 (final concentration of 20 uM) for 24 hours. A cluster of genes regulated Nrf2-Keap1 antioxidant pathway were identified by gene ontology analysis.

overall_design: RD cells (human rhabdomyosarcoma cell line) were treated with mock or MDL-860 (final concentration of 20 uM) for 24 hours. Total RNA purified from each treatment was used for microarray analysis.


title: The INO80 chromatin remodeling complex regulates the gene expression under oxidative stress condtion (stress)

first: Masahiko

last: Harata

address: 468-1 Aramaki Aza Aoba, Aoba-ku

department: Graduate School of Agricultural Science

institute: Tohoku University

summary: RNA micro array analyses were performed using Arp5-, Arp8-knockout and Arp8-over expression Nalm-6 cells treated with heme, an oxidative stress inducer. As a result, various genes were up- or down- regulated in both Arp5- and Arp8-knockout cells. Because of these Arps are essential and specific component of the INO80 complex, it was quite possible that the INO80 complex was related to these genes expression under oxidative stress condition.

overall_design: Each cell was treated with heme, an oxidative stress inducer for 12 hour. Total RNAs were extracted and subjected to microarray analysis.

first: Yuichiro

first: Hirokazu

last: Murakami


title: Expression data from kidney in type 2 diabetic db/db mice

status: Public on Jun 10 2017

city: Beijing

first: Haojun

last: Zhang

state: Beijing

address: 2 YingHua Dongjie, Chaoyang District

department: Institute of Clinical Medical Sciences

country: China

institute: China-Japan Friendship Hospital

summary:
Diabetic nephropathy(DN) is a common diabetic microvascular complication, the underlying mechanisms involved in DN remain to be elucidated.
We used microarrays to explore the global profile of gene expression for better understanding the molecular mechanism of diabetic nephropathy in type 2 diabetic db/db mice.

overall_design: Ten-week-old male db/db mice and non-diabetic db/m littermates were housed for 12 weeks and sacrificed at 22 weeks of age, the kidneys were harvested for RNA extraction and hybridization on Affymetrix microarrays.

first: Ping

last: Li


title: The INO80 chromatin remodeling complex regulates the gene expression (no stress)

summary: RNA micro array analyses were performed using Arp5-, Arp8-knockout and Arp8-over expression Nalm-6 cells. As a result, various gene were up- or down-regulated in both Arp5- and Arp8-knockout cells. Because of these Arps are essential and specific component of the INO80 complex, it was quite possible that the INO80 complex was related to these gene expression.

overall_design: The gene locus of Arp5 and Arp8 were disrupted by homologous recombination. In the case of Arp8-knockout cells, Arp8 over expression was caused by tetracycline-regulated (Tet-Off) system incorporation. Total RNAs were extracted and subjected to microarray analysis.


title: Characterization of an astrocyte perivascular endfeet transcriptome

city: Paris

last: de la Grange

address: 29, rue du Faubourg Saint-Jacques

department: Paris Biotech Santé

country: France

institute: GenoSplice technology

summary: We aim to identify mRNAs present in astrocyte endfeet. We performed a microarray study comparing mRNAs extracted from brain vessels purified from 2-month-old C57Bl6 mice, submitted or not to a partial basal lamina  enzymatic digestion,  allowing to remove astrocyte endfeet membranes and their associated astroglial mRNAs from the purified vessels. mRNAs depleted upon basal lamina digestion represent a specific population of astrocyte mRNAs transported in the perivascular endfeet

overall_design: Four independent cDNA libraries were prepared for each condition (digested and undigested 2-month-old C57Bl6 brain vessels) and hybridized on Affymetrix Mouse Gene 2.0 Array

first: Anne-Cécile

last: Boulay

first: Bruno

last: Saubamea

first: Martine

last: Cohen-salmon


title: The INO80 chromatin remodeling complex regulates the gene expression

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: The significance of phosphorylation for FXR

status: Public on May 24 2017

city: RTP

first: NIEHS

last: Microarray Core

state: NC

address: 111 T.W. Alexander Drive

department: DIR

institute: NIEHS

summary:
The serine or threonine between two zinc fingers of the DNA binding domains (DBD) is highly conserved in a majority of nuclear receptors. In the present study, we focused on the serine 154 of farnesoid X receptor (FXR).
To determine the influence of phosphomimetic or non-phosphomimetic mutation for FXR on gene expressions, we employed cDNA microarray analysis using COS-1 cells which ectopically express FXR S154A or FXR S154D with DMSO or CDCA.

overall_design: COS-1 cells were transfected with human FXR S154A mutant or its S154D for 24 hr. The cells were subsequently incubated with 0.1%DMSO or 50 mMCDCA for 24 hr.  Three replicates were used for each treatment group.

last: Negishi

first: Takuyu

last: Hashiguchi


title: Expression data from environmentally enriched mice

status: Public on Jun 01 2017

city: London

first: Fulvio

last: D'Acquisto

address: Charterhouse square

department: William Harvey Research Institute

country: United Kingdom

institute: Queen Mary University of London, Barts and The London School of Medicine and Dentistry

summary:
Environmental enrichment has been shown to induce wholescale alterations to the gene expression profile of experimental animals
we used microarray analysis of whole blood samples taken from mice housed in enriched or standard cage environments to invesigate alterations in imune-modulatory gene expression between these animals

overall_design: RNA was extracted from whole blood taken from animals subject to 2 weeks in an enriched or standard environment, purified and subject to CIP-SEQ microarray analysis

first: Samuel

last: Brod

first: Masahiro

last: Ono

first: Mark

last: Kristiansen


title: Antitumor therapeutic vaccination induces immunosuppressive dendritic cells

city: Pamplona

first: Pablo

last: Sarobe

address: Avda. Pio XII, 55

country: Spain

institute: CIMA

summary:
Vaccination induces immunostimulatory signals which are often accompanied by regulatory mechanisms such as IL-10, which control T-cell activation and inhibit vaccine-dependent antitumor therapeutic effect. Thus, here we characterized IL-10-producing cells treated with therapeutic vaccines. Although several cell subsets produced IL-10 irrespective of treatment, an early vaccine-dependent induction of IL-10 was detected in dendritic cells (DC). IL-10 production defined a DC population characterized by a poorly mature phenotype, lower expression of T-cell stimulating molecules and upregulation of PD-L1. These IL-10+ DC showed impaired in vitro T-cell stimulatory capacity, which was rescued by incubation with IL-10R and PD-L1-inhibiting antibodies.
In vivo IL-10 blockade  during vaccination decreased the proportion of IL-10+ DC and improved their maturation, without modifying PD-L1 expression. Similarly, PD-L1 blockade did not affect IL-10 expression, suggesting independent regulation of these molecules. Interestingly, vaccination combined with simultaneous blockade of IL-10 and PD-L1 induced stronger immune responses, resulting in a higher therapeutic efficacy in tumor-bearing mice. These results show that vaccine-induced immunoregulatory DC with dual expression of IL-10 and PD-L1 impair priming of antitumor immunity, suggesting that therapeutic vaccination protocols may benefit from combined targeting of these molecules.

overall_design: Vert-X mice (n=10) were immunized with OVA + Imiquimod and two day later spleens were harvested an pooled. Splenic IL-10+ and IL-10- DC from pooled material were purified by using anti-CD11c-conjugated magnetic beads  followed by staining with CD11c-APC antibodies and separation with a FACSAria flow cytometer according to their expression of IL-10 (GFP). Gene expression in  IL-10+ and IL-10- DC was compared.


title: Gene expression profile of sendai virus infected primary MEFs.

status: Public on May 31 2017

city: Fukuoka

first: Takumi

last: Koshiba

address: 744 Motooka, Nishi-ku

department: Department of Biology

institute: Faculty of Science, Kyushu University

summary: To investivate the role of mitochondrial-mediate antiviral innate immunity in MEFs, we performed Sendai virus (SeV) infection experiments at the different cultured conditions of the cells.  We analyzed the gene expression profile of MEFs that infected or uninfected with SeV either cultured the cells under glucose or galactose medium, and investigate its differences.  We found that the both cultured conditions of cells showed normal antiviral responses.

overall_design: Primary mouse embryo fibroblasts (pMEFs) were infected with Sendai virus for 6 h and their gene expressions were analyzed.

first: Takuma

last: Yoshizumi


title: Effect of IRE1a and XBP1 knockdown on gene expression in primary mouse keratinocytes expressing an HRas oncogene

city: University Park

first: Adam

middle: B.

last: Glick

state: PA

address: 101 Life Sciences Bld

department: Veterinary and Biomedical Sciences

institute: The Pennsylvania State University

summary: IRE1a is a critical modulator of the unfolded protein response. Its RNAse activity generates the mature transcript for the XBP1 transcription factor and also degrades other ER associated mRNAs in a process termed Regulated IRE1a Dependent mRNA Decay or RIDD. To determine if IRE1a is critical in the response to oncogenic Ras we used ShRNA to knockdown Ire1a or Xbp1 in primary mouse epidermal keratinocytes transduced with a v-HRAS retrovirus.

overall_design: Primary mouse keratinocytes were transduced with a v-Hras retrovirus and either a control ShRNA lentivirus or ShRNA against either Ire1a or Xbp1. RNA isolated from each group at 4 days post lentiviral infection  (n=3 biological replicates per group) was used for microarrays. Primary mouse keratinocytes transduced with control ShRNA lentivirus served as the reference set for gene expression analysis (n=3 biological replicates per group).

first: Nicholas

last: Blazanin

first: Alayna

middle: B

last: Craig-Lucas

first: Christian

last: John

first: Kyle

last: Breech

first: Jeongin

last: Son


title: Atypical chemokine receptor 1 controls haematopoiesis

status: Public on May 22 2017

city: Munich

first: Johan

last: Duchene

state: State...

address: Pettenkorfer Str 8

institute: LMU

summary: Healthy individuals of African ancestry have neutropenia that has been linked with the variant rs2814778(G) of the gene encoding atypical chemokine receptor 1 (ACKR1). This polymorphism selectively abolishes the erythroid cell expression of ACKR1, causing Duffy-negative phenotype. Here we describe an unexpected fundamental role that ACKR1 plays in hematopoiesis and provide the mechanism linking its absence with neutropenia. Nucleated erythroid cells highly expressed ACKR1, which facilitated their direct contacts with the hematopoietic stem cells. The absence of erythroid ACKR1 altered murine hematopoiesis, including stem and progenitor cells, ultimately giving rise to phenotypically distinct neutrophils, which readily left the circulation, causing neutropenia. Duffy-negative individuals developed a distinct profile of neutrophil effector molecules closely reflecting that in the ACKR1-deficient mice. Thus, alternative physiological patterns of hematopoiesis and bone marrow cell outputs depend on the expression of ACKR1 in the erythroid lineage providing major implications for the selection advantages that have resulted in the paramount fixation of the rs2814778(G) polymorphism in Africa.

overall_design: Gene expression in HSPC (LSK and GMP) from WT and ACKR1-deficient mice

first: Igor

last: Novitzky-Basso

first: Antal

last: Rot


title: Expression data of uteri treated with An Agonist for Lysophosphatidic acid receptor3 (LPA3), T13

first: Shizu

last: Aikawa

address: 7-3-1 Hongo

institute: The University of Tokyo

summary: Identification of the genes whose expression levels are regulated by T13 during peri-implantation period

overall_design: 6 different samples (1-6) mixed with uteri from 3 mice, respectively; vehicle-injected pseudopregnant uteri (1,3,5) and lysophosphatidic acid receptor 3 agonist injected pseudopregnant uteri (T13; 2,4,6); 0.5 hr after the injection (1,2), 1 hr after the injection (3,4) and 2 hr after the injection (5,6); A comparison between vehicle vs T13 in each timepoint

first: Kuniyuki

last: Kano

first: Junken

last: Aoki

first: Soken

last: Tsuchiya

first: Yukihiko

last: Sugimoto


title: Expression data from J774A.1 mouse macrophages after neuropeptide-FF (NPFF) treatment

status: Public on Jun 05 2017

city: Ulm

first: Tamás

last: Röszer

address: Albert-Einstein-Allee 11

department: Institute of Neurobiology

institute: University of Ulm

summary:
We treated 80% confluent J774A.1 macrophages with 1 nM neuropeptide-FF (NPFF) for 18 h.
We used microarray as an explorative approach to recognize effects of NPFF on macrophages.

overall_design: J774A.1 cells were cultured in RPMI-1640 with 10% FCS, to reach 80% confluence.


title: Exit from HSC dormancy is controlled via vitamin A/retinoic acid (II)

status: Public on May 15 2017

city: Heidelberg

first: Sandro

last: Altamura

address: Im Neuenheimer Feld 350

department: Dep. Pediatric Hematology, Oncology and Immunology

institute: University of Heidelberg

summary: Identification of the role of retinoic acid on the activation of the dHSCs

overall_design: Mouse HSCs were  cultured in the presence of DMSO (control) or all trans retinoic acid (ATRA)

first: Nina

last: Cabezas-Wallscheid

first: Andreas

last: Trumpp


title: SOXB1 genetic regulation in the developing testes

status: Public on May 21 2017

city: Adelaide

first: Fatwa

last: Adikusuma

state: South Australia

address: MLS building Gate 8 Victoria Drive

department: Molecular & Cellular Biology

country: Australia

institute: University of Adelaide

summary:
Absence of Sox3 in mice only results in subtle phenotype, presumably due to the rescue effects from the family members, SOXB1, which consist of Sox1, Sox2 and Sox3. Obvious defect in Sox3-KO mice is seen only in the testes where Sox1 and Sox2 are not co-expressed. The genetic dysregulation underlying this testis defects is unknown. We also hypothesize that this genetic dysregulation can be rescued by the other SOXB1 members.
We performed microarray analysis to compare Sox3-KO mouse testes with the WT. We also generated Sox3-Sox2KI mice in which the Sox3 ORF is replaced with Sox2 ORF. Microarray was also performed to these knock-in testis samples to find out whether Sox2 can rescue genetic dysregulation resulting from the absence of Sox3.

overall_design: Sox3-KO and Sox3-Sox2KI mice were generated using CRISPR/Cas9 technology. RNAs were extracted from 2 week testes of WT, Sox3-KO and Sox3-Sox2KI mice followed by hybridization to the microarray chip. Three independent Sox3-KO and three Sox3-Sox2KI testes were compared to 6 WT testes in this set of experiment.

first: Paul

last: Thomas


title: Exit from HSC dormancy is controlled via vitamin A/retinoic acid (I)

overall_design: Mouse HSCs were FACS-sorted from mice injected with PBS, all trans retinoic acid (ATRA), polyIC or with ATRA followed by polyIC.


title: Donor T cells in ovarian graft versus host disease

status: Public on May 12 2017

city: Sapporo

first: Daigo

last: Hashimoto

state: Hokkaido

address: N15W7 Kita-ku

department: Department of Hematology

institute: Hokkaido University

summary:
Analysis of donor CD4+ and CD8+ T cells purified from spleens and ovaries after murine syngeneic and allogeneic hematopoietic stem cell transplantation

Infertility associated with ovarian failure is a serious late complication for female survivors of allogeneic hematopoietic stem cell transplantation (SCT). While the role of pretransplant conditioning regimen has been well appreciated, increasing application of reduced-intensity conditioning facilitated us to revisit the other factors possibly affecting ovarian function after allogeneic SCT. We have addressed whether donor T-cell mediated graft-versus-host disease (GVHD) could be causally related to female infertility in mice. To study transcriptomes of donor T cells infiltrating into the ovary, donor T cells were sorted from recipients' ovaries and microarray analysis was performed.

overall_design: Syngeneic splenic CD4+ T cells (n=2), Syngeneic splenic CD8+ T cells (n=3), Allogeneic splenic CD4+ T cells (n=2), Allogeneic splenic CD8+ T cells (n=3),  Allogeneic ovarian CD4+ T cells (n=2),  Allogeneic ovarian CD8+ T cells (n=4)

first: Takanori

last: Teshima

first: Kohta

last: Miyawaki


title: Exit from HSC dormancy is controlled via vitamin A/retinoic acid


title: LOXL2 drives epithelial-mesenchymal transition via activation of IRE1-XBP1 branch of unfolded protein response.

status: Public on May 11 2017

city: Madrid

first: Gema

last: Moreno-Bueno

state: Madrid

address: Arturo Duperier

department: Biochemistry

institute: IIB

summary:
Epithelial-to-Mesenchymal Transition (EMT) is a key process contributing to the aggressiveness of cancer cells. EMT is triggered by activation of different transcription factors collectively known as EMT-TFs. Different cellular cues and cell signalling networks activate EMT at transcriptional and posttranscriptional level in different biological and pathological situations. Among them, overexpression of LOXL2 (lysyl oxidase-like 2) induces EMT independent of its catalytic activity. Remarkably, perinuclear/cytoplasmic accumulation of LOXL2 is a poor prognosis marker of squamous cell carcinomas and is associated to basal breast cancer metastasis by mechanisms no yet fully understood. Here, we report that overexpression of LOXL2 promotes its accumulation in the Endoplasmic Reticulum where it interacts with HSPA5 leading to activation of the IRE1-XBP1-branch of the Unfolded Protein Response (UPR). LOXL2-dependent UPR activation induces the expression of several EMT-TFs: SNAI1, SNAI2, ZEB2 and TCF3 that are direct transcriptional targets of XBP1. Remarkably, inhibition of IRE1 blocks LOXL2-dependent upregulation of EMT-TFs thus hindering EMT induction.
LOXL2 relationship to Endoplasmic Reticulum Stress

overall_design: Microarray experiments were performed using Human Whole Genome V2 4*44K array G4845A (Agilent technologies). Three independent passages from MDCK-II-LOXL2 and MDCK-II-DLOXL2 cells were used, and MDCK-II transfected with empty pcDNA3 vector were used as control. Total RNA was extracted and purified using RNAextraction kit (Qiagen). Microarray labelling and hybridization was performed using the Low RNA Linear Amplification Kit and the In Situ Hybridization Kit Plus (Agilent technologies), respectively, following manufacturer’s protocol. After hybridization and washing, the slides were scanned in an Axon GenePix Scanner (Axon Instruments) and analysed using Feature Extraction Software 10.0 (Agilent technologies). RNA samples from independent MDCK-II-LOXL2 and -DLOXL2-stably transfected cells were labelled with Cy5-dUTP and equal concentrations of RNA from control cells were labelled with Cy3-dUTP. Differentially expressed genes were selected using the False Discovery Rate (FDR) method with an adjusted p-value <0.2.

first: Eva

middle: P

last: Cuevas

first: Pilar

last: Eraso

first: María

middle: J

last: Mazón

first: Vanesa

last: Santos

first: Amparo

last: Cano

first: Francisco

last: Portillo


title: IFI27 is a gene-expression biomarker that identifies influenza-specific immune response in symptomatic patients

city: Braunschweig

first: Robert

last: Geffers

address: Inhoffenstr. 7

department: Dep. Molecular Bacteriology

institute: HCI - Helmholtz Centre for Infection Research

overall_design: identification of biomarkers in influenza infected patients

first: K

last: Schughart

first: R


title: The effect of SPARCL1 overexpression on osteosarcoma MNNG-HOS cell line

status: Public on May 01 2017

city: Nanjing

first: Shujie

last: Zhao

state: Jiangsu

address: 300 Guangzhou Road

institute: The First Affiliated Hospital of Nanjing Medical University

summary: To investigate the altered gene expression levels in SPARCL1 overexpressed cells and vector cells. Each group had a biological repeat (n=3). Results provide insight into the role of SPARCL1 in the progression of osteosarcoma.

overall_design: Three SPARCL1 overexpressed MNNG-HOS cells and three vector MNNG-HOS cells were a comparative group.

first: Dong

last: Zhou

first: Shu-jie


title: Acetytransferase P300 impairs insulin signaling in obesity

status: Public on May 08 2017

city: Baltimore

first: Ling

last: He

state: MD

address: 600 North Wolfe St

department: Department of Pediatrics-Division of Endocrinology

institute: The Johns Hopkins University School of Medicine

type: Expression profiling by high throughput sequencing

summary: Insulin resistance is the hallmark of obese and type 2 diabetes patients. Defective insulin sensitivity in the liver results in increased glucsoe production, which is the major cause of hyperglycemia in diabetic patients. Increased lipopolysaccharide (LPS) leakage from the gut of diet-induced obesity causes insulin resisitance; moreover, activation of deacetylase Sirtuin1 restore insulin sensitivity in obesity. However, the mechanism resulting in insulin resistance by LPS remains poorly understood. Here, we show that Ep300 (P300) harboring an intrinsic acetyltransferase activity was rapidly induced in the liver of animals fed a high-fat diet, and the induction of Ep300 is through LPS-stimulated activation of ER stress. Induced Ep300 impairs insulin signaling by acetylating mediators in insulin signaling. Inhibition of P300 acetyltransferase activity improves insulin signaling. Thus, Ep300 acetyltransferase activity is a therapeutic target.

overall_design: To determine whether P300 plays an important role in the regulation of glucose and lipid metabolism in the liver of obese mouse models, AAV-shRNAs for scrambled control and P300 functional were injected into mice through the jugular. One week after viral injection, mice were fed on a high-fat diet for another week, then, sacrificed after 6h fasting. Liver tissues were collected, snap-frozen in liquid nitrogen, and stored at  80°C until use. There are 8 samples, 4 samples from control group (shSCR), another 4 samples from treated group (shP300).


title: PD-1 regulates KLRG1+ group 2 innate lymphoid cells

status: Public on May 04 2017

city: Bethesda

first: Mingan

last: Sun

state: Maryland

address: Building 6B, 6 Center Drive

department: Eunice Kennedy Shriver National Institute of Child Health and Human Development

institute: National Institute of Health

summary:
Group 2 innate lymphoid cells (ILC-2s) regulate immune responses to pathogens, allergens, tissue remodeling and metabolic homeostasis in response to cytokines. Positive regulation of ILC-2s through ICOS has been recently elucidated but co-receptor mediated negative regulatory axis is yet to be defined.
We demonstrate that PD-1 is an important negative regulator of KLRG1+ILC-2 function in both mice and humans. Increase in KLRG1+ ILC-2 cells numbers were attributed to an intrinsic defect in PD-1 signaling, which resulted in enhanced STAT5 activation. During Nippostrongylus brasiliensis infection, a significant expansion of KLRG1+ ILC-2 subsets occurred in pdcd1-/- mice and on adoptive transfer, pdcd1-/- KLRG1+ ILC-2s significantly reduced worm burden. Furthermore, blocking antibody to PD-1 increased KLRG1+ ILC-2 cell number and reduced disease burden. Therefore PD-1 is an important negative regulator and is vital for maintaining the number and hence function of KLRG1+ ILC-2s.

overall_design: Microarray for wildtype and Pdcd1 knockout mice, each with three replicates

first: Samuel

last: Taylor

first: Yuefeng

last: Huang

first: Grace

last: Mallett

first: Chaido

last: Stathopoulous

first: Tania

middle: C

last: Felizardo

first: Ming-An

first: Evelyn

last: Martin

first: Nathaniel

last: Zhu

first: Emma

last: Woodward

first: Martina

last: Elias

first: Jonathan

last: Scott

first: Nick

last: Reynolds

first: William

middle: E

last: Paul

first: Daniel

middle: H

last: Fowler

first: Shoba

last: Amarnath


title: Expression data of three sets of cells: (1) Schwann cells and macrophages from 1m-old WT DRG, (2) Schwann cells (Nf1-/-) and macrophages (Nf1+/+) from 1m-old neurofibroma, (3) Schwann cells (Nf1-/-) and macrophages (Nf1+/+) from 7m-old neurofibroma

city: Cincinnati

first: Kwangmin

last: Choi

state: Ohio

address: 333 Burnet Avenue

department: Experimental Hematology & Cancer Biology

institute: Cincinnati Children's Hospital Medical Center

summary:
Schwann cells and macrophages were dissociated from normal DRGs and 1- and 7-month-old neurofibroma. Schwann cells from neurofibroma have Nf1-/- phenotypes. All macrophages have Nf1+/+ phenotypes.
We used microarrays (Affymetrix MoGene 2.0 ST GeneChip) to detect transcriptomal changes between 7-month-old neurofibroma Schwann cells (or macrophages)  versus 1-month-old wild-type (or neurofibroma) Schwann cells (or macrophages).

overall_design:
Expression data of three sets of cells: (1)Schwann cells and macrophages from 1-month-old wild-type mouse dorsal root ganglia, (2) Schwann cells (Nf1-/-) and macrophages (Nf1+/+) from  1-month-old  neurofibroma, (3) Schwann cells (Nf1-/-) and macrophages (Nf1+/+) from 7-month-old neurofibroma
We chopped mouse DRG/neurofibromas into 1-3 mm^3 pieces and plated them in dissociation medium containing 20mL L-15 (Mediatech), 0.5 mg/mL collagenase type 1 (Worthington; Lakewood, NJ), and 2.5 mg/mL dispase protease type II (Cambrex; East Rutherford, NJ) at 37°C for 4-6 hours with shaking. The dissociation reaction was stopped by adding DMEM +10%FBS.  Undigested DRG/tumors were excluded by 100µM cell strainer. Cells were collected by centrifugation. For each microarrays (Schwann cell, macrophage), Affymetrix GeneChip Command Console (v4.0.0) was used to create .chp files. All the probe sets on Affymetrix Mouse Gene 2.0 ST array (Mogene-2_0-st-v1.na33.2.mm10) were summarized by Affymetix Expression Console program using robust multi-chip average (RMA) method . After preprocessing steps, data from two batches were combined and their batch effects were corrected using ComBat method

Please note that [1] all MP samples are Nf1+/+ (no mutation on Nf1 gene) and the only difference is their ages (1month, 7month) and [2]  the 'nf1' in sample title reperesents "neurofibroma type1 disease", not "Nf1 gene".

first: Jianqiang

last: Wu

first: Kakajan

last: Komurov

first: Nancy

last: Ratner


title: Lgr5-Expressing Chief Cells Drive Epithelial Regeneration and Cancer in the Oxyntic Stomach

city: Brussels

first: Simon

middle: Lieven Imanuel Johannes

last: Denil

address: Laarbeeklaan 101

department: University Hospital Brussels

institute: VUB/ULB

summary: Adult stem cells residing within tubular glands of the corpus epithelium are believed to fuel daily tissue renewal, but their identity remains controversial. Lgr5, marks both homeostatic stem cells and “reserve” stem cells in multiple tissues. Here, we report Lgr5 expression in a subpopulation of chief cells in mouse and human corpus glands. Using a new, non-variegated Lgr5-2A-CreERT2 mouse model, we show by cell fate mapping that Lgr5-expressing chief cells do not behave as corpus stem cells under homeostatic conditions, but are recruited to function as stem cells to effect epithelial renewal following injury. In vivo ablation of the Lgr5+ cells severely impairs epithelial homeostasis in the corpus, indicating an essential role in maintaining the resident stem cell pool. We additionally define the Lgr5+ chief cells as a major cell of origin of gastric metaplasia. These findings reveal clinically relevant insights into tissue homeostasis, repair and cancer in the corpus.

overall_design: Main treatment was tamoxifen versus controls, applied to three cell populations sorted based on Lgr5GFP signal intenisty (high, low, negative), 3 or 4 technical replicates from individual FACS runs

first: Marc

last: Leushacke

first: Si Hui

last: Tan

first: Angeline

last: Wong

first: Swathi

last: Yada

first: Amin

last: Hajamohideen

first: Liang

middle: T

first: Jasmine

last: Goh

first: Esther

first: Kazuhiro

last: Murakami

last: Barker


title: Suppression of the grainyhead transcription factor 2 gene (GRHL2) inhibits the proliferation, migration, invasion and mediates cell cycle arrest of ovarian cancer cells

status: Public on Apr 21 2017

city: Quebec

first: Dimcho

last: Bachvarov

state: Quebec

address: 9, rue McMahon

country: Canada

institute: CHU-Q, Centre de recherche-HDQ

summary: Previously, we have identified cytosolic form of the grainyhead transcription factor 2 gene (GRHL2) as notably hypomethylated in low-malignant potential (LMP) and high-grade (HG) serous epithelial ovarian tumors, compared to normal ovarian tissues. Here we show that GRHL2 is strongly overexpressed in both LMP and HG serous EOC tumors, thus suggesting that epigenetic mechanisms might be implicated in GRHL2 overexpression in serous epithelial ovarian cancer (EOC). Knockdown of the GRHL2 expression in EOC cells led to sharp decrease of cell proliferation and induced G1-phase cell cycle arrest. Additionally, GRHL2 suppression significantly inhibited EOC cell migration and invasion. Gene expression profiling and consecutive network and pathway analyses confirmed these findings, as numerous genes and pathways known previously to be implicated in ovarian tumorigenesis, including EOC tumor invasion and metastasis, were found to be downregulated upon BCAT1 suppression, while some tumor suppressor genes were induced. Taken together, our data are indicative for a strong oncogenic potential of the GRHL2 gene in advanced EOC and identify this transaminase as a novel EOC biomarker and putative EOC therapeutic target.

overall_design: To better understand the molecular mechanisms of GRHL2 gene action in ovarian cancer cells, we employed the Agilent Whole Human Genome microarrays, containing ~ 44,000 genes to identify global gene expression changes upon GRHL2 suppression in A2780s cells and GRHL2 suppression and overexpression in SKOV3 cells. We compared the gene expression of the previously selected CRISPR/Cas9-mediated GRHL2 knockout A2780s clones KOA1 and KOA1 against the corresponding control (CA) A2780s clone, and the shRNA-mediated GRHL2-knockdown SKOV3 clones sh-S2 and sh-S5 against the corresponding control (CS) SKOV3 clone. Additionally, we compared gene expression of the previously selected GRHL2 overexpressing SKOV3 clones OV1 and OV2 against the corresponding control (CSov) SKOV3 clone. The microarray experiments were performed in duplicates, as four hybridizations were carried out for the GRHL2-suppressing/overexpressing cell clones against the corresponding control, using a fluorescent dye reversal (dye-swap) technique.


title: Gene expression profiling of mouse HSPCs retrovirally transduced with Plzf

status: Public on Apr 26 2017

city: Tsu

first: Tetsuya

last: Nosaka

address: 2-174 Edobashi

department: Department of Microbiology and Molecular Genetics

institute: Mie University Graduate School of Medicine

summary:
We have previously found the immortalization of mouse HSPCs retrovirally transuced with Plzf.
To investigate the moleular mehcanism of the immortalization, we preliminarily performed comprehensive gene expression profiling of Plzf-transduced KSL and myeloid progenitor-enriched (MP) cells using cDNA microarray analysis.

overall_design: For screening of critical target genes involved in the immortalization, KSL and MP cells were retrovirally transduced with Plzf-IRES-EGFP or EGFP.  GFP-positive cells were sorted 48 hours after the transduction, followed by RNA extraction.  The Plzf-transduced cells were compared with the control  GFP-transduced cells.

first: Ryoichi

last: Ono


title: Expression data from mouse brain tissue

status: Public on Apr 19 2017

city: Stanford

first: Joseph

middle: Michael

last: Castellano

state: CA

address: 770 Welch Road

institute: Stanford University

summary: Microarrays were performed to assess changes in gene expression following treatment of aged mice with human plasma from donors of different ages (young=19-24 years; old=61-82 years).

overall_design: Aged mice treated with different groups of human plasma were sacrificed following 6 intravenous injections, and hippocampi were dissected from brain tissue for analysis by whole genome microarray.

first: Tony

last: Wyss-Coray


title: Divalent cations promote the transfer of the IncP-7 plasmid pCAR1 among different Pseudomonas hosts

status: Public on Apr 11 2017

city: Tokyo

first: Hideaki

last: Nojiri

address: 1-1-1 Yayoi, Bunkyo-ku

department: Biotechnology Research Center

type: Expression profiling by genome tiling array

summary: An incompatibility P-7 plasmid pCAR1 can be efficiently transferred among artificial microcosms in the presence of divalent cations Ca2+ and Mg2+. One on one mating assays between Pseudomonas strains with different plasmids showed that the promotion of transfer efficiency by divalent cations was also found in other plasmids including pB10 and NAH7, whereas the impacts were larger in IncP-7 plasmids. The impact on pCAR1 transfer altered by different pairs of donor and recipient strains, and the promotion of transfer efficiency was clearly detected between donors P. resinovorans CA10dm4 and P. fluorescens Pf0-1 to the recipients P. putida KT2440 and CA10dm4. Transcriptome analyses showed that genes on the pCAR1 did not respond to the presence of cations, including the tra/trh genes involved in its transfer. Notably, transcriptions of oprH genes, encoding a putative outer membrane proteins, in both of donor and recipient were commonly upregulated under the cation-limited condition. Transfer frequency of the pCAR1 to the transposon mutant of oprH in KT2440 was not promoted by the cations. This effect was partially recovered by the complementation with oprH gene, suggesting that OprH is involved in the promotion the pCAR1 transfer by divalent cations.

platform_organism:
Pseudomonas
Pseudomonas putida KT2440
Pseudomonas fluorescens Pf0-1

overall_design: Transcriptome analysis was perfoemed using Pseudomonas fluorescens Pf0-1(pCAR1) and Pseudomonas putida KT2440 mating in carbon-free (CF) buffer with/without cations. RNA maps of the donor or the recipient were used as controls. Biologically duplicated data were obtained.

first: Ayako

last: Sakuda

first: Chiho

last: Suzuki-Minakuchi

last: Matsui

first: Yurika

last: Takahashi

first: Kazunori

last: Okada

first: Hisakazu

last: Yamane

first: Masaki

last: Shintani


title: Expression data of GFP-neg and GFP-high cells isolated from mouse SCLC tumors using a GFP reporter for Hes1 expression

first: Julien

last: Sage

address: 265 Campus Drive

department: Pediatrics and Genetics

institute: Stanford

summary:
Small cell lung cancer (SCLC) tumors harbor two subsets of cells that are defined by low (or undetectable) or high expression of Hes1, which is a common downstream target of the Notch signaling pathway.
To better understand the role of the Notch pathway in SCLC tumor heterogeneity, we first isolated cells from these two populations using a GFP-reporter allele for Hes1 expression. We then used microarrays to identify the gene expression differences between these two groups.

overall_design: SCLC tumors were induced by Cre-administration in an Rb/p53/p130 conditional triple knockout mouse model for SCLC that also carried a GFP-reporter allele for Hes1 expression. GFP-negative and GFP-high cells were FACS sorted from pooled tumors 5-6 months after tumor induction. RNA was then extracted and hybridized to Affymetrix GeneChip® Mouse Gene 2.0 ST array.

first: Jing

last: Lim


title: Expression data from Treg cells from Lkb1 or Tgfbr2 knockout mice

status: Public on Apr 15 2017

city: Tianjin

first: Yuechen

last: Luo

address: 288 Nanjing Road, Tianjin, 300020, P.R. China

institute: Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences & Peking Union Medical College

summary: We used microarrays to detail the gene expression of Treg cells from Foxp3Cre/+Lkb1f/f mice versus Foxp3Cre/+ mice, and Foxp3Cre Tgfbr2 f/f mice versus Foxp3Cre mice.

overall_design: CD4+YFP+ Treg cells were sorted from spleen and lymph nodes of mice for RNA extraction with Trizol reagent (Invitrogen). Total RNA was reverse transcribed, amplified, labeled, and hybridized to Mouse Genome 2.0 arrays (Affymetrix).

first: Zhina

last: Sun

first: Xiaolei

first: Di

last: Wu


title: Unique Chemokine Profiles of Lung Tissue Distinguish Post-chemotherapeutic Persistent and Chronic Tuberculosis in a Mouse Model

city: Seoul

first: Soomin

last: Park

address: 50 Yonsei-ro, Seodaemun-gu

department: department of microbiology

country: South Korea

institute: Yonsei university college of medicine

summary: To identify the immunological status of the persistent and chronic stages, we analysed immunological genes in lung tissues from mice infected with M. tuberculosis. Based on the cDNA microarray results, 11 candidate cytokine genes, which were obviously up-regulated during the chronic stage compared with those during the persistent stage, were selected and clustered into three groups: 1) chemokine genes, except those of monocyte chemoattractant proteins (MCPs) (CXCL9, CXCL10, CXCL11, CCL5, CCL19); 2) MCP genes (CCL2, CCL7, CCL8, CCL12); and 3) TNF and IFN-γ genes. Results from the cDNA microarray and quantitative RT-PCR analyses revealed that the mRNA expression of the selected cytokine genes was significantly higher in lung tissues of the chronic stage than of the persistent stage. Three chemokines (CCL5, CCL19 and CXCL9) and three MCPs (CCL7, CCL2 and CCL12) were noticeably increased in the chronic stage compared with the persistent stage.

overall_design: We present a new experimental animal model, in which the reactivation of tuberculosis is induced without administration of immunosuppressive agents, which might disturb immune responses. From lung tissue of chronic or persistent stage of tuberculosis, gene expression was screened using cDNA microarray analysis and confirmed by quantitative RT-PCR.


title: Gene profiling of HAX1-deficient iPSC-derived CD33-positive promyelocytes and their genetically corrected and wid-type counterparts

status: Public on Apr 07 2017

city: Frankfurt

first: Jan-Henning

last: Klusmann

address: Theodor-Stern-Kai 7

department: Pediatric Hematology and Oncology

institute: Goehte University Frankfurt

summary: We investigated iPSC-derived granulopoiesis from Kostmann patients (HAX1-deficient iPSCs) and gene corrected isogenic lines generated by CRISPR-Cas9 gene editing. Utilizing neutrophilic differentiation assay, we have successfully modeled the Kostmann hematologic phenotype that is characterized by perturbed granulocytic differentiation and compensatory overproduction of monocytes. We demonstrate that targeted correction of the HAX1-mutation reestablished a HAX1 and HCLS1-centered transcription network in immature myeloid progenitors, which is involved in the regulation of apoptosis and also myeloid differentiation.

overall_design: HAX1-deficient iPSCs were genetically corrected by CRISPR technology. After neutrophilic in vitro differentiation assay, CD33-positive promyelocytes were purified by flow sorting. HAX1-deficient cells were compared to isogenic and wild-type cells.

first: Erik

last: Pittermann

first: Jan


title: Toxicity of nano- and ionic silver to embryonic stem cells – a comparative toxicogenomic study

city: Laurel

first: Xiugong

last: Gao

address: 8301 Muirkirk Rd

department: HFP/OLOAS/OCT/DT

institute: US FDA

summary:
Transcriptomic changes induced by silver nanoparticles (AgNPs) during spontaneous differentiation of mouse embryonic stem cells (ESCs) were characterized and compared to those induced by Ag+ under otherwise identical conditions.
C57BL/6 mESCs were allowed to differentiate after embryoid body (EB) formation and were exposed to 5.0 µg/ml 20 nm AgNPs or 5.0 µg/ml Ag+ for 24 h.

overall_design: RNA samples were collected at 24 h after exposure. Three replicates were included for each experimental condition.

first: Vanessa

middle: D

last: Topping

first: Zachary

last: Keltner

first: Robert

last: Sprando

first: Jeffrey

last: Yourick


title: Lamin A/C Is Required For ChAT-Dependent Neuroblastoma Differentiation: a microarray gene expression study

status: Public on Apr 18 2017

city: Roma

first: Ivan

last: Arisi

address: viale Regina Elena 295

department: Bioinformatics Facility

country: Italy

institute: European Brain Research Institute

summary: The mouse neuroblastoma N18TG2 clone is unable to differentiate and defective for the enzymes of the biosynthesis of neurotransmitters. The forced expression of choline acetyltransferase (ChAT) in these cells results in the synthesis and release of acetylcholine (Ach) and hence in the expression of neurospecific features and markers. To understand how the expression of ChAT triggered neuronal differentiation, we studied the differences in genome-wide transcription profiles between the N18TG2 parental cells and its ChAT-expressing 2/4 derived clone. The engagement of the 2/4 cells in the neuronal developmental programme was confirmed by the increase of the expression level of several differentiation-related genes and by the reduction of the amount of transcripts of cell-cycle genes. At the same time, we observed a massive reorganisation of cytoskeletal proteins in terms of gene expression, with the accumulation of the nucleoskeletal lamina component Lamin A/C in differentiating cells. The increase of the Lmna transcripts induced by ChAT-espression in 2/4 cells was mimicked treating the parental N18TG2 cells with the acetylcholine-receptor agonist carbachol, thus demonstrating the direct role played by this receptor in neuron nuclei maturation. Conversely, a treatment of 2/4 cells with the muscarinic-receptor antagonist atropine resulted in the reduction of the amount of Lmna RNA. Finally, the hypothesis that Lmna gene product might play a crucial role in the ChAT-dependent molecular differentiation cascade was strongly supported by Lmna knock-down in 2/4 cells leading to the down-regulation of genes involved in differentiation and cytoskeleton formation and to the up-regulation of genes known to regulate self-renewal and stemness.

overall_design: The gene expression profile of the ChAT-expressing 2/4 clone was compared to that of the N18TG2 parental cells, with and without retinoic acid (RA) stimulation using Agilent microarray analysis.

first: Loredana

last: Guglielmi

first: Marta

last: Nardella

first: Carla

last: Musa

first: Mara

last: D'Onofrio

first: Andrea

last: Storti

first: Alessandra

last: Valentini

first: Emanuele

last: Cacci

first: Stefano

last: Biagioni

first: Grabriella

last: Augusti-Tocco

first: Igea

last: D'Agnano

first: Armando

last: Felsani


title: PRDM16 represses the type I Interferon response in adipocytes [expression profiling]

status: Public on Apr 10 2017

first: Hee-Woong

last: Lim

address: 3333 Burnet Ave. MLC 7024

department: Division of Biomedical Informatics

summary: PRDM16 is a strong activator of brown fat-specific genes, while also a repressor of white fat and muscle-specific genes. We asked what other pathways are regulated by PRDM16 in adipocytes that may be critical for brown and/or beige adipogenesis. Using microarray, we found PRDM16 also represses type I Interferon-stimulated genes (ISGs) in adipocytes.

overall_design: We used microarrays to profile changes in gene expression for wildtype and Prdm16 KO adipocytes stimulated with rosiglitazone to induce browning of the adipocytes.

first: Megan

last: Kissig

first: Jeff

last: Ishibashi

first: Matthew

last: Harms

first: Rachel

last: Stine

first: Kyoung-Jae

last: Won

first: Patrick

last: Seale


title: Transcriptomic changes in MYC and PRC2 targets are prominent events in the early pathogenesis of neuroblastoma in TH-MYCN mice

status: Public on Apr 01 2017

city: Nagoya

first: Shoma

last: Tsubota

state: Aichi

address: 65 Tsurumai-cho, Showa-ku

department: Department of Molecular Biology

institute: Nagoya University Graduate School of Medicine

summary: It has been already reported that there are undifferentiated/proliferating neuroblasts in the postnatal sympathetic ganglia in TH-MYCN mice. We established suitable spheroid culture condition that selectively isolates undifferentiated neuroblasts from superior mesenteric ganligon (SMG) of TH-MYCN mice. In the present study, in order to investigate the transcriptomic differences between embryonic day 13.5 (E13.5) WT derived primary spheres and E13.5 TH-MYCN derived passageable spheres, we carried out microarray gene expression analysis. We investigated critical molecular events in MYCN-transformed neuroblastoma cells in TH-MYCN mice.

overall_design: Primary spheres were cultured from E13.5 WT SMG. Passageable spheres were obtained by subculturing spheres from E13.5 TH-MYCN SMG. Four individual biological replicates of E13.5 WT spheres and E13.5 TH-MYCN spheres were subjected to micorarray analyis (two arrays were used for one replicate except for one WT sample).

first: Kenji

last: Kadomatsu


title: MYCN-transformed neuroblasts from TH-MYCN mice are selectively isolated and maintained as spheres in vitro

summary: It has been already reported that there are undifferentiated/proliferating neuroblasts in the postnatal sympathetic ganglia in TH-MYCN mice. We established suitable spheroid culture condition that selectively isolates undifferentiated neuroblasts from superior mesenteric ganligon (SMG) of TH-MYCN mice. In the present study, in order to investigate the transcriptomic differences among 3-week-old WT SMG, TH-MYCN (hemizygote) SMG, and TH-MYCN (hemizygote) spheres, we carried out microarray gene expression analysis. We investigated whether or not undifferentiated cells observed in TH-MYCN SMG were selectively isolated and maintaned as spheres.

overall_design: SMG tissue were dissected from 3-week-old WT and TH-MYCN (hemizygote) mice (biological replicate is eight). Primary spheres were cultured from 3-week-old TH-MYCN (hemizygote) mice (biological replicate is eight). And the primary spheres were  passaged 5 times (biological replicate is four, and array replicate is two for each biological replicate). They were subjected to micorarray analyis.


title: Retinoic acid-free spheroid culture condition is suitable for growth of TH-MYCN neuroblasts

summary: It has been already reported that there are undifferentiated/proliferating neuroblasts in the postnatal sympathetic ganglia in TH-MYCN mice. Given the fact that neuroblastoma is derived from sympathoadrenal progenitors which are originated from neural crest stem cells, we attempted to use the well-established culture condition that has been utilized to maintain derivatives of neural crest stem cells. However, the medium contained retinoic acid (RA) which is known to induce neuroblastoma differentiation and is used in clinical treatment against high-risk patients. In the present study, the medium with RA (RA (+) medium) and without RA (RA (-) medium) were compared. Since undifferentiated neuroblasts are observable at one of the sympathetic ganglia, superior mesenteric ganglion (SMG), in 3-week-old TH-MYCN hemizygote (TH-MYCN+/-) mice with 129+Ter/SvJcl mice background, we dissected and dissociated the SMG to prepare single cells. These cells were cultured in either RA (+) or RA (-) media. Spheres formed in either RA (+) or RA (-) medium were subjected to microarray analysis.

overall_design: Dissociated single cells from a 3-week-old TH-MYCN (hemizygote) SMG were divided into RA (+) and RA (-) medium. Formed primary spheres were subjected to micorarray analyis. RA (+) and RA (-) spheref from four individual biological replicates were analyzed.


title: Emerging role of polycomb repressive complex 2 in the early neuroblastoma tumorigenesis in TH-MYCN transgenic mice and its association with human neuroblastoma

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: MDFIC alters the GR transcriptome in A549 cells

city: RTP

first: NIEHS

last: Microarray Core

address: 111 T.W. Alexander Drive

department: DIR

institute: NIEHS

summary: Glucocorticoids are primary stress hormones that regulate many physiological processes, and synthetic derivatives of these molecules and are widely used in the clinic.  The cellular response to glucocorticoids is remarkably diverse; however, the molecular factors that govern tissue specificity are poorly understood.  The actions of glucocorticoids are mediated by the glucocorticoid receptor (GR).  To discover new proteins that interact with GR and modulate its function, we performed a yeast 2 hybrid assay using as bait the hinge region of GR.  The MyoD family inhibitor domain-containing (MDFIC) protein was identified as a binding partner for GR.  To investigate the function of the GR-MDFIC interaction, we performed a genome-wide microarray in intact and MDFIC deficient A549 cells that were treated with the synthetic glucocorticoid Dexamethasone (Dex).  A large cohort of genes was differentially regulated by GR depending on the presence or absence of MDFIC.  These findings identify a new binding partner for cytoplasmic GR that modulates the receptor transcriptome and contributes to the tissue specific actions of glucocorticoids.

overall_design: A549 cells were transfected with NTC siRNA or MDFIC siRNA. Cells were harvested the day after transfection and re-plated at appropriate tissue culture densities.  Seventy-two hours post-transfection, cells were stimulated with either vehicle (control) or 100nM Dex for 6 hours. Prior to Dex treatment, cells were cultured overnight in medium supplemented with 10% charcoal-stripped FBS.  Total RNA was harvested for microarray analysis using the RNeasy Mini Kit and RNase-Free DNase Kit (Qiagen) from 3 biological replicates of vehicle-treated NTC cells, Dex-treated NTC cells, vehicle-treated MDFIC knockdown cells, and Dex-treated MDFIC knockdown cells.

first: Robert

last: Oakley

first: John

last: Busillo

middle: A

last: Cidlowski


title: The role of dihydropyridines on murine microglial cells

city: Würzburg

first: Claus

middle: Juergen

last: Scholz

address: Josef-Schneider-Str. 2

department: Core Unit SysMed

institute: University Hospital Würzburg

summary: Effects of treatment with Nimodipine on N9 cells

overall_design: Global gene expression profiling in murine N9 cells (cell line)

first: Andrea

last: Schampel

first: Stefanie

last: Kürten


title: Transcriptomic analysis of the the liver of Ppara KO mice

status: Public on Mar 30 2017

city: Lille

first: Jérôme

last: Eeckhoute

address: Bâtiment J&K, Faculté de Médecine de Lille-Pôle Recherche, Boulevard du Professeur Leclerc

institute: CNRS

summary: Livers from wild-type (WT) or Ppara knock-out (Ppara KO) C57Bl6 mice were used to prepare RNA which was then processed for analysis using MoGene-2_0-st Affymetrix microarrays according to standard procedures.

overall_design: Livers from 6 WT or Ppara KO adult female mice (12-14 weeks) were used to prepare RNA which was then processed for analysis using MoGene-2_0-st Affymetrix microarrays according to standard procedures.

first: Jerome

first: Réjane

last: Paumelle


title: Investigating mixotrophic metabolism in the model diatom Phaeodactylum tricornutum.

status: Public on Mar 31 2017

city: Grenoble

first: Valeria

last: Villanova

address: 14 avenue Albert 1er de Belgique

department: LPCV

institute: CEA

summary: Diatoms are prominent marine microalgae, interesting not only from an ecological point of view, but also for their possible use for biotechnology applications. They can be cultivated in phototrophic conditions, using sunlight as the only energy source. Some diatoms, however, can also grow in mixotrophic mode, where both light and external reduced carbon contribute to biomass accumulation. In this study, we investigated the consequences of mixotrophy on the growth and metabolism of the pennate diatom Phaeodactylum tricornutum, using glycerol as a source of reduced carbon. Transcriptomic, metabolomic and physiological data indicate that glycerol affects the central-carbon, carbon-storage and lipid metabolism of the diatom. In particular, glycerol addition mimics some typical responses of nitrogen limitation on lipid metabolism at the level of TAG accumulation and fatty acid composition. However, this compound does not diminish photosynthetic activity and cell growth, at variance with nutrient limitation, revealing essential aspects of the metabolic flexibility of these microalgae and suggesting possible biotechnological applications of mixotrophy.

overall_design: Phaeodactylum tricornutum cultures were growing in 12L/12D cycles in presence and absence of glycerol and harvested after 5 days. Cells grown using only light as source of energy (reference cells) represented the control condition and were compared with cells grown in presence of both light and glycerol (test cells). Three biological replicates were sampled for the two conditions.

first: Giovanni

last: Finazzi

first: Dimitri

last: Petroutsos

first: Antonio

last: Fortunato

first: Angela

last: Falciatore


title: Transcriptomic analysis of GW4064 regulated genes in mouse primary hepatocytes

summary: Mouse primary hepatocytes (MPH) prepared from C57Bl6 male adult mice were challenged with the FXR agonist GW4064 and used to prepare RNA which was then processed for analysis using MoGene-2_0-st Affymetrix microarrays according to standard procedures.

overall_design: 3 independent preparation of mouse primary hepatocytes (MPH) were performed and used to prepare RNA which was then processed for analysis using MoGene-2_0-st Affymetrix microarrays according to standard procedures.

first: Vanessa

last: Dubois


title: Genome-wide expression profiling of wild-type and CCR2-/- CD45RBhigh and CD45RBlow T cells

status: Public on Mar 24 2017

city: Rehovot

first: Idit

last: Shachar

address: Herzel Street

department: Immunology

country: Israel

institute: Weizmann Institute of Science

summary:
Runx1 is expressed in regenerating muscle, specifically in the muscle adult stem cells -- the satellite cells. Its exact role and target genes were yet to be identified.
This experiment aimed at understanding the underlying mechanisms by which C-C chemokine receptor type 2 (CCR2) regulates T cell fate in vivo.

overall_design: We analyzed wt C57BL/6 and CCR2-/- CD45RBhigh and CD45RBlow sorted cells by genome wide expression profiling. The different populations were activated for 2 h at 37C with αCD3/αCD28 antibodies and the different populations were compared.

first: Estzer

last: Bakos


title: Gene expression in Mob1DKO mouse lung

status: Public on Mar 29 2017

city: Fukuoka

first: Kohei

last: Otsubo

address: 3-1-1 Maidashi Higashi-ku

department: Division of Cancer Genetics, Medical Institute of Bioregulation

institute: Kyushu University

summary: Mps One Binder Kinase Activator (MOB)1A/1B are core components of the Hippo pathway. These proteins, which coactivate LArge Tumor Suppressor homolog (LATS) kinases, are also tumor suppressors. To investigate MOB1A/B’s roles in normal physiology and lung cancer, we generated doxycycline (Dox)-inducible, bronchioalveolar epithelium–specific, null mutations of MOB1A/B in mice [SPC-rtTA/(tetO)7-Cre/Mob1aflox/flox/Mob1b-/-; termed luMob1DKO) mice]. Most mutants (70%) receiving Dox in utero [luMob1DKO (E6.5-18.5) mice] died of hypoxia within 1hr post-birth. Their alveolar epithelial cells showed increased proliferation, impaired YAP1/TAZ-dependent differentiation, and decreased surfactant protein production, all features characteristic of human respiratory distress syndrome　(RDS). Intriguingly, mutant mice that received Dox postnatally [luMob1DKO (P21–41) mice] did not develop spontaneous lung adenocarcinomas, and urethane treatment-induced lung tumor formation was decreased (rather than increased). Lungs of luMob1DKO (P21–41) mice exhibited increased detachment of bronchiolar epithelial cells and decreased numbers of the bronchioalveolar stem cells (BASCs) thought to initiate lung adenocarcinomas. YAP1/TAZ-NKX2.1-dependent expression of collagen XVII, a key hemidesmosome component, was also reduced. Thus, a MOB1-YAP1/TAZ-NKX2.1 axis is essential for normal lung homeostasis and expression of the collagen XVII protein necessary for alveolar stem cell maintenance in the lung niche.

overall_design: We isolated lung epithelial cells from Mob1DKO and WT mice and compared their gene expression level.

first: Akira

last: Suzuki


title: MDFIC alteration of the GR transcriptome in COS-1 cells depends on S211 phosphorylation of GR

first: NIEHS

last: Microarray Core

summary: Glucocorticoids are primary stress hormones that regulate many physiological processes, and synthetic derivatives of these molecules and are widely used in the clinic.  The cellular response to glucocorticoids is remarkably diverse; however, the molecular factors that govern tissue specificity are poorly understood.  The actions of glucocorticoids are mediated by the glucocorticoid receptor (GR).  To discover new proteins that interact with GR and modulate its function, we performed a yeast 2 hybrid assay using as bait the hinge region of GR.  The MyoD family inhibitor domain-containing (MDFIC) protein was identified as a binding partner for GR.  Knockdown of MDFIC in A549 cells alters the GR transcriptome.  Overexpression of MDFIC with GR in COS-1 cells also modulates the GR transcriptome by expanding the number of genes regulated in response to glucocorticoid treatment.  Our findings in A549 cells suggest that MDFIC alters the gene regulatory profile of GR by modulating receptor phosphorylation at several residues, including S211.  To further investigate the molecular link between MDFIC-mediated effects on GR phosphorylation at S211 and alterations in the GR transcriptome, we performed a genome-wide microarray in COS-1 cells that were transfected with the GR phosphorylation mutant S211A or S211A and MDFIC.  The transfected cells were treated with vehicle or the synthetic glucocorticoid Dexamethasone (Dex) for 6 hours.  The ability of MDFIC to expand the GR transcriptome was attenuated in cells expressing S211A mutant.

overall_design: COS-1 cells were transfected with the GR phosphorylation mutant S211A or S211A and MDFIC.  The day after transfection, medium was replaced with new medium supplemented with 10% charcoal-stripped FBS.  Forty-eight hours post-transfection, cells were stimulated with either vehicle (control) or 100nM Dex for 6 hours.  Total RNA was harvested for microarray analysis using the RNeasy Mini Kit and RNase-Free DNase Kit (Qiagen) from 3 biological replicates from each group.

first: Robert

last: Oakley

first: John


title: MDFIC alteration of the GR transcriptome in COS-1 cells

summary: Glucocorticoids are primary stress hormones that regulate many physiological processes, and synthetic derivatives of these molecules and are widely used in the clinic.  The cellular response to glucocorticoids is remarkably diverse; however, the molecular factors that govern tissue specificity are poorly understood.  The actions of glucocorticoids are mediated by the glucocorticoid receptor (GR).  To discover new proteins that interact with GR and modulate its function, we performed a yeast 2 hybrid assay using as bait the hinge region of GR.  The MyoD family inhibitor domain-containing (MDFIC) protein was identified as a binding partner for GR.  Knockdown of MDFIC in A549 cells alters the GR transcriptome.  To further investigate the functional effect of MDFIC on the GR transcriptome, we performed a genome-wide microarray in COS-1 cells that were transfected with GR alone or GR and MDFIC.  The transfected cells were treated with vehicle or the synthetic glucocorticoid Dexamethasone (Dex) for 6 hours.  Overexpression of MDFIC was found to expand the GR transcriptome.

overall_design: COS-1 cells were transfected with GR alone or GR and MDFIC.  The day after transfection, medium was replaced with new medium supplemented with 10% charcoal-stripped FBS.  Forty-eight hours post-transfection, cells were stimulated with either vehicle (control) or 100nM Dex for 6 hours.  Total RNA was harvested for microarray analysis using the RNeasy Mini Kit and RNase-Free DNase Kit (Qiagen) from 3 biological replicates from each group.

last: Cidlowski


title: Apoptosis-associated transcriptome changes in peripheral blood leukocytes during EBV antiviral therapy

status: Public on Mar 28 2017

city: Nizhny Novgorod

first: Dmitry

last: Knyazev

address: Malaya Yamskaya, 71

country: Russia

institute: I.N. Blokhina Nizhny Novgorod Research Institute of Epidemiology and Microbiology

summary: refer to the SuperSeries

overall_design: The splicing-sensitive microarray (platform GPL23086) covers 221 genes, each microarray encompasses 4 identical probe-containing areas. Blood samples obtained from 3 EBV patients during acute mononucleosis and after convalescence plus one sample from a patient on acute stage were included in the experiment

first: Nikolay

last: Sakharnov

first: Leonid

last: Solntsev

first: Oleg

last: Utkin


title: The transcriptome of type I murine astrocytes under interferon-gamma exposure and remyelination stimulus

status: Public on Mar 23 2017

city: Moscow

first: Maxim

last: Shkurnikov

address: 2 bld. 85, Ugreshkaya st.

institute: SRC Bioclinicum

summary:
Astrocytes are considered as an important contributor of the central nervous system (CNS) disorders, and particularly multiple sclerosis. Transcriptome of these cells is greatly affected by cytokines released by lymphocytes penetrating the blood-brain barrier, particularly classical pro-inflammatory cytokine interferon-gamma (IFN-gamma).
We report here transcriptomal profiling of astrocytes treated by IFN-gamma and perspective remyelinization agent benztropine. Our findings indicate that expression of genes involved in antigen processing and presentation in astrocytes are significantly upregulated upon IFN-gamma exposure emphasizing critical role of this cytokine in redirecting of immune response towards self-antigens. Data reported herein support previous observations that IFN-gamma-induced JAK-STAT signaling pathway may be regarded as valuable target for the pharmaceutical intervention.

overall_design: Brain of C3H/He mice were used as a source of astrocytes. Cells were treated with IFNγ at a concentration of 250 IU/mL or with benztropine at a concentration of 2.0 μM in culture medium for 48 h before analysis.

first: Anna

last: Kudriaeva

first: Vladimir

middle: V

last: Galatenko

first: Diana

last: Maltseva

first: Nadezhda

last: Khaustova

first: Ekaterina

last: Kuzina

first: Alexander

middle: G

last: Tonevitsky

last: Gabibov

first: Alexey

last: Belogurov


title: Hypertension reduces soluble guanylyl cyclase expression in the mouse aorta via the Notch signaling pathway

status: Public on May 01 2017

city: Lund

first: Catarina

last: Rippe

address: BMC, D12

department: Experimental Sciences

country: Sweden

institute: Lund University

summary: Hypertension is a dominating risk factor for cardiovascular disease. To characterize the genomic response to hypertension, we administered vehicle or angiotensin II to mice and performed gene expression analyses. AngII treatment resulted in a robust increase in blood pressure and altered expression of 235 genes in the aorta, including Gucy1a3 and Gucy1b3 which encode subunits of soluble guanylyl cyclase (sGC). Western blotting and immunohistochemistry confirmed repression of sGC associated with curtailed relaxation via sGC activation. Analysis of transcription factor binding motifs in promoters of differentially expressed genes identified enrichment of motifs for RBPJ, a component of the Notch signaling pathway, and the Notch coactivators FRYL and MAML2 were reduced. Gain and loss of function experiments demonstrated that JAG/NOTCH signaling controls sGC expression together with MAML2 and FRYL. Reduced expression of sGC, correlating with differential expression of MAML2 in stroke prone and spontaneously hypertensive rats was also seen and RNA-Seq data demonstrated correlations between JAG1, NOTCH3, MAML2 and FRYL and the sGC subunits GUCY1A3 and GUCY1B3 in human coronary artery. Notch signaling thus provides a constitutive drive on expression of the major nitric oxide receptor (GUCY1A3/GUCY1B3) in arteries from mice, rats, and humans, and this control mechanism is disturbed in hypertension.

overall_design: 2 months old mice were implanted with miniosmotic pumps containing either angiotensin (1µg/kg/min) (n=8) or saline (n=7). After three weeks aorta was dissected and mRNA was extracted and samples were used for gene expression array.

first: Karl

last: Swärd


title: NRG-1 induces mature ventricular cardiac differentiation from iPS cells contributing to cardiac tissue repair

city: Pamplona

first: Olalla

last: Iglesias-Garcia

address: Pio XII 55

institute: CIMA

summary: Combined treatment with NRG-1 and DMSO led to efficient differentiation of iPS into mature ventricular-like cardiac cells, which were capable of preserving cardiac function and tissue viability when transplanted into a mouse model of myocardial infarction.

overall_design: Gene expression profiles of cardiomyocytes, neonatal or adult, and iPS cells with or without differentiation treatment with DMSO or NRG1 were compared. Gene expression was measured with affymetrix Mouse Gene 2.0 ST Arrays

first: Beatriz

last: Pelacho

first: Juan

middle: R

last: Rodríguez


title: Analysis of Porcupine ablation within the uterine epithelium on gene expression within the uterus

status: Public on Mar 21 2017

city: Montreal

first: Daniel

last: Dufort

address: 1001 Bould. Decaire Room EM0.3211

department: OBGYN

institute: McGill University

summary:
The secretion of mammalian Wnt Ligands within the cell is dependent on the activity of Porcupine, a gene located on the X chromosome that encodes for a membrane bound o-acyl transferase. Porcupine-dependent Wnt signalling was previously shown to be essential for the post-natal maintenance of endometrial glands, structures that are essential for implantation and fertility. Previous data has implicated the multiple members of the Wnt family expressed in the female uterus to be involved in a coordinated crosstalk between the luminal and stromal compartments of the uterus, ensuring the proper development of the uterus and successful fertility. We have generated a conditional mutant of Porcupine in the luminal epithelium (cKOepi) of the uterus, thus eliminating Wnt7a/b and Wnt11, to address the nature of this crosstalk.
Unlike global luminal-stromal mutants, post-natal ablation of Porcupine in the luminal epithelium alone does not affect the maintenance of the endometrial glands in adults. Uterine glands are still visible in the adult cKOepi, albeit in a smaller number than that of control uteri. Despite having uterine glands, cKOepi females remain completely infertile. We have attributed the sterility of these females to be in part due to defects in implantation and decidualization; cKOepi fail to respond to decidual induction by artificial means. Interestingly, progesterone supplementation rescues the observed implantation defects, although observed decidual soon seem to become resorptive. Microarray analysis of cKOepi during implantation has reveals several potential targets for luminal WNT that may be responsible for the observed phenotype including: Lef1, Hoxa10, Wnt4, Wnt16 Notch1, Notch4 and Dll4 .

overall_design: We analyzed gene expression from full uterine samples of 3 floxed control and 3 epithelium-Porcupine Kos.

first: Omar

last: Farah

first: Stephan

last: Bichele

first: Janet

last: Rossant


title: Expression analysis of Wild-type and Ccp2-deficient CHILPs

city: Beijing

first: Benyu

last: Liu

address: 15, Datun Road, Chaoyang district

department: The CAS key Laboratory of Infection and Immunity, Institute of Biophysics

institute: Institute of Biophysics, CAS

summary: Investigation of differentially expressed genes in  Ccp2-deficient CHILPs

overall_design: Gene expression profiling using Lin-CD127+Flt3-CD25- a4b7 + CHILPs from CCP2 deletion mice or WT littermates. Total RNA from each sample was quantified using the NanoDrop ND-1000. The sample preparation and microarray were performed in accordance with the Affymetrix Mouse Gene2.0 analysis protocol (Affymetrix).

first: Buqing

last: Ye

first: Zusen

last: Fan


title: Gene expression in response to fluconazole vs. the combination of  fluconazole and osthole

status: Public on Apr 24 2017

first: Dedong

last: Li

address: Fuxing Road 28

department: department of clinical pharmacology

institute: PLA General Hospital

summary: Transcriptional profiling of Candida albicans comparing fluconazole treated cells with fluconazole and osthole treated cells

overall_design: Clinical fluconazole-resistant strain 0304103 was selected to carry out the expression profile microarray. Two-condition experiment, fluconazole treated vs. fluconazole and osthole treated cells. Biological replicates: 3 control, 3 transfected, independently grown and harvested. One replicate per array.

first: Yan

last: Sun


title: Gene expression in brain tissue from MOG-immunized wild-type or C57BL/6Je/e mice at disease maximum.

city: Duesseldorf

last: Koehrer

address: Universitaetsstr. 1

department: BMFZ

institute: University of Duesseldorf

summary: Neuroprotective effects of NDP-MSH. We have characterized the signaling down-stream of melanocortin-1 receptor ligation to identify pathways mediating neuroprotective effects of NDP-MSH using transcriptional profiling. In this data set we included the expression data obtained from mouse brain tissue (MOG-immunized wild-type or C57BL/6Je/e mice at disease maximum, d14 after immunization). The data were used to obtain differentially regulated genes in wild-type or C57BL/6Je/e mice upon systemic NDP-MSH treatment.

overall_design: In total, 8 samples were analyzed and we generated the following pariwise comparisons: wild-type NDP-MSH vs. PBS, C57BL/6Je/e NDP-MSH vs. PBS

first: K

last: Loser

first: R

last: Deenen


title: Cellular adaptations to eGFP expression

status: Public on Mar 16 2017

first: NIEHS

last: Microarray Core

summary: Fluorescent proteins are an important tool that has become omnipresent in life sciences research. They are frequently used for localization of proteins and monitoring of cells. Green fluorescent protein (GFP) was the first and has been the most used fluorescent protein. Enhanced GFP (eGFP) was optimized from wild-type GFP for increased fluorescence yield and improved expression in mammalian systems. Fluorescent proteins are expressed colorless and immature and, for eGFP, the conversion to the fluorescent form, mature, is known to produce one equivalent of hydrogen peroxide (H2O2) per molecule of chromophore. Even though it has been proposed that this process is non-catalytic and generates nontoxic levels of H2O2, we sought to investigate the role of fluorescent proteins in generating free radicals and inducing oxidative stress in biological systems.

overall_design: Wildtype HeLa cells, HeLa cells stably expressing eGFP and HeLa cells expressing eGFP upon doxycycline exposure (tet system for conditional expression) were used. All expreiments were prepared as three independent cell cultures. The cultures of HeLa.tet and HeLa.tet.eGFP at 70% confluency were exposed to 1 ug/mL doxycycline for 48 h before collection. Confluent cells were collected for RNA isolation by trypsinization, washed with PBS and stored at -80°C.

first: Douglas

last: Ganini

first: Fabian

last: Leinisch

first: Ashutosh

last: Kumar

first: Jinjie

last: Jiang

first: Erik

last: Tokar

first: Christine

last: Malone

first: Robert

middle: M

last: Petrovich

first: Ronald

last: Mason


title: The impact of decitabine treatment in MDS-induced Tet2KD/KDEzh2Δ/Δ  LSK HSPCs

status: Public on Mar 15 2017

city: Chiba

first: Motohiko

last: Oshima

address: 1-8-1 Inohana

institute: Chiba University

summary: To evaluate the impact of DNA demethylating agents on our mouse MDS model, we chose 5-aza-2’-deoxycytidine, decitabine (DAC), one of the DNA demethylating agents, which is incorporated into DNA but not RNA and has 10-fold more potency in DNA demethylation than 5-azacitidine. We transplanted Tet2KD/KDEzh2Δ/Δ MDS cells into lethally irradiated secondary recipients and treated them with DAC (low dose DAC at 0.25mg/kg, 3 times a week, intraperitoneal injection), then purified LSK HSPCs and evaluated the expression profiles.

overall_design: We purified Tet2KD/KDEzh2Δ/Δ -MDS Lineage-Sca-1+c-Kit+ (LSK) HSPCs from secondary recipients 10 weeks post-transplantation and 7 weeks after DAC or PBS treatment and subjected them to microarray analysis.

first: Nagisa

last: Hasegawa

first: Atsushi

last: Iwama


title: Transcriptome profiling of dorsal prostate from four mouse genotypes : wild-type, LXRalpha/beta KO, PTENpc-/- and LXRalpha/beta KO PTENpc-/-

status: Public on Mar 14 2017

city: AUBIERE

first: silvere

last: BARON

address: 10 avenue Blaise Pascal

department: Endocrine, Signaling and Cancer

institute: Université Clermont Auvergne

summary: Advanced prostate cancer (PCa) is a clinical challenge as this state of the disease lacks of curative therapeutic. We exploited human datasets as well as mouse models to decipher mechanisms able to constrain cancer evolution in response to genetic alteration that occurs in PCa. Careful analysis of transcriptomic signature of various PCa datasets reveals activation of the LXR target gene signature. This LXR signature is tightly correlated to PTEN-loss in human. Causal LXR deregulation has been confirmed using prostate mouse carcinomas from Pten-null mutant. Protective role of LXR has been demonstrated by their deletions in a Pten-null context in mouse prostate, thus results in an increase of PCa invasiveness and metastatic dissemination. PTEN deletion governs LXR transcriptional activity through deregulation of cholesterol de novo synthesis that leads to the accumulation of LXR ligands. According to these observations, pharmacological inhibition of cholesterol biosynthesis using statins abolishes LXR target gene expression in response to PTEN-loss. LXR deletion triggers an increased in the epithelial mesenchymal transition process and matrix metalloproteinase accumulations that could explain metastatic spreading. This work highlights LXRs as metabolic sensors that act as gatekeeper able to constrain carcinoma progression.

overall_design: In this study, we used prostatic samples from mice invalidated for PTEN and/or LXRalpha and LXRbeta and corresponding control samples in order to performed a comprehensive transcriptomic analysis of molecular mechanisms involved in mouse prostate carcinogenesis.

first: Silvere


title: Molecular effects of 1-naphthyl-methylcarbamate and solar radiation exposures on human melanocytes

summary: Carbaryl (1-naphthyl-methylcarbamate), a broad-spectrum insecticide, has recently been associated with the development of cutaneous melanoma in an epidemiological cohort study with U.S. farm workers also exposed to ultraviolet radiation, which is known to be the main etiologic factor for skin carcinogenesis. Although comprehensive and well designed, the agricultural epidemiological study was not sufficient to characterize the direct contribution of the insecticide and solar radiation in melanomagenesis. Several studies have explored the synergistic effect of certain chemicals with UV radiation, increasing its deleterious effects on the skin. We hypothesized that carbaryl exposure associated with UV solar radiation may induce melanocyte transformation. This study aimed to characterize human melanocytes after individual or combined exposure to carbaryl (100 μM) and solar radiation (375 mJ/cm2). In a microarray analysis, carbaryl, but not solar radiation, induced an important oxidative stress response, evidenced by the upregulation of antioxidant genes, such as Hemeoxygenase-1 (HMOX1), and downregulation of Microphtalmia-associated Transcription Factor (MITF), the main regulator of melanocytic activity; results were confirmed by qRT-PCR. Carbaryl and solar radiation induced a gene response suggestive of DNA damage and cell cycle alteration. The expression of genes in these categories was notably more intense in the combined treatment group, in a synergistic manner, for CDKN1A, BRCA1/2 and MDM2 genes. Likewise, flow cytometry assays demonstrated S-phase cell cycle arrest, reduced apoptosis levels and faster induction of cyclobutane pyrimidine dimers (CPD) lesions in carbaryl treated groups. Our data suggests that carbaryl is genotoxic to human melanocytes, especially when associated with solar radiation.

overall_design: Twenty-four hours after plating, cells were at 80% confluency and were subjected to the following experimental treatment groups: Group 1: No treatment; Group 2: Irradiation and no treatment; Group 3: Carbaryl treatment; Group 4: Irradiation and carbaryl treatment; Group 5: Vehicle treatment; Group 6: Irradiation and vehicle treatment. Treatment regimen consisted of melanocyte incubation with carbaryl 100 µM (Sigma-Aldrich, St Louis, USA) for 6 hours after single dose exposure to 375mJ/cm2 of solar radiation using a solar simulator (SS2.5kW, Sciencetech Inc., Ontario, Canada) with a global air mass filter (A.M 1.5G, Sciencetech Inc, Ontario, Canada). For the irradiation assays, culture medium was replaced by PBS buffer without Ca2+ or Mg2+ (PBS-A). All experiments were performed in triplicates.

first: Bianca

last: Ferrucio

first: D

last: Fannin

first: Liwen

last: Liu

first: Kevin

last: Gerrish

first: S

middle: S

last: Maria-Engler

last: Paules

first: B

last: Barros


title: Nipple fibroblast gene expression profile

status: Public on Mar 13 2017

city: Irvine

first: Maksim

last: Plikus

state: California

address: 845 Health Sciences Road

department: Developmental and Cell Biology

institute: University of California, Irvine

summary:
The nipple is an example of specialized epidermis.  The unique epidermal stratification and gene expression is induced and maintained by developmental distinct fibroblast populations.
To identify specific signaling modules involved in the maintenance of nipple epidermis we used gene expression profiling of purified fibroblast populations from a murine model of nipple skin formation

overall_design: Gene expression of sorted fibroblasts from the nipple-like skin of the keratin-14 promoter driven parathyroid hormone-related protein mouse with the ventral skin of wild type littermates

first: Hsing-Jung

last: Wu

first: Ji-Won

last: Oh

first: John

last: Foley


title: Expression data from purified medial ganglionic eminence (MGE) interneurons, 3 biological replicates

status: Public on Mar 06 2017

city: Toronto

first: Freda

last: Miller

state: Ontario

address: 686 Bay Street

department: Neurosciences and Mental Health

institute: Hospital for Sick Children

summary:
During development, newborn interneurons migrate throughout the embryonic brain.  Here, we provide evidence that these interneurons act in a paracrine fashion to regulate developmental oligodendrocyte formation.  Specifically, we show that medial ganglionic eminence (MGE) interneurons secrete factors that promote genesis of oligodendrocytes from glially-biased cortical precursors in culture.  Moreover, when MGE interneurons are genetically ablated in vivo prior to their migration, this causes a deficit in cortical oligodendrogenesis.  Modeling of the interneuron-precursor paracrine interaction using transcriptome data identifies the cytokine fractalkine as responsible for the pro-oligodendrocyte effect in culture.  This paracrine interaction is important in vivo, since knockdown of the fractalkine receptor CX3CR1 in embryonic cortical precursors, or constitutive knockout of CX3CR1 causes decreased numbers of oligodendrocyte progenitor cells (OPCs) and oligodendrocytes in the postnatal cortex.  Thus, in addition to their role in regulating neuronal excitability, interneurons act in a paracrine fashion to promote the developmental genesis of oligodendrocytes.
We used microarrays to generate a list of expressed genes in purified medial ganglionic eminence (MGE) interneurons

overall_design: E13 MGE tissue was dissected from CD1 embryos and cultured as described (Tsui et al., 2014). Briefly, embryos were maintained on ice in Hank’s balanced salt solution (HBSS, Gibco) during dissection. Following removal of the cortex and meninges to expose the ventral forebrain, MGE tissue was excised and mechanically triturated in Neurobasal medium (Gibco) containing 40 ng/ml FGF2 (BD Biosciences), 2% B27 supplement (Gibco), and 500 µM L-Glutamine (Gibco). Triturated MGE cells were plated on to four-well chamber slides (Nunc) pre-coated with 2% laminin (BD Biosciences) and 1% poly-D-lysine (Sigma) at a density of 59,000 cells/cm2. On day 5 of culture, 1 μM cytosine β arabinofuranoside C (AraC, Sigma) was added. After 24h of AraC treatment, the medium was changed 3 times at 2h intervals to wash out the AraC and dead cells. Purified MGE neurons were then cultured for 2 additional days.


title: Genome-wide expression data from hippocampus of control and Noonan syndrom (Ptpn11D61Y) mice in response to neuronal stimulation

city: Magdeburg

first: Anna

last: Fejtova

state: Saxony Anhalt

address: Brenneckestrasse, 6

institute: Leibniz Institute for Neurobiology

summary: Microarrays were used to identify the differentially expressed genes in the hippocampus of control and Noonan syndrom mice at basal state and in response to 4AP-Bic stimulation (10 min). Functional analysis was performed to determine the biological significance of the data.

overall_design: Mice heterozygote for a conditional allele Ptpn11floxedD61Y/WT (Chan et al, 2009) and for Emx1IREScre allele (Gorski et al, 2002) were used as model of Noonan syndrom  (NS) in this study. Control mice had same conditional allele but no Emx1IREScre allele.  Acute hippocampal slices were prepared from both control and Ptpn11D61Y mice and treated with DMSO (basal) or 4AP-Bic for 10 min (4AP-2.5 mM and Bicuculline-50 µM in DMSO). After stimulation slices were incubated in ACSF without drugs for other 3 hrs.  Then total RNA was extracted and used for hybridization on arrays. Three biological replicates (independent treatments of slices from 3 control and 3 Ptpn11D61Y mice) were analysed.

first: Santosh

last: Pothula


title: Alveolar macrophage gene expression - PIKfyve knockout

status: Public on Mar 01 2017

city: Ikoma

first: Takumi

last: Kawasaki

state: Nara

address: 8916-5 Takayama

department: Bioscience

institute: Nara Institute of Science and Technology

summary:
comparison of Alveolar macrophge gene expression in wild type and PIKfyve ko
We identifed gene that important for alveolar macrophage development

overall_design: Alveolar macrophage were isolated from wild type or PIKfyve KO adult mice  for RNA extraction and hybridization on Affymetrix microarrays.

first: Taro

last: Kawai


title: Integrated analysis of genetic, behavioral, and biochemical data implicates neural stem cell-induced changes in immunity, neurotransmission and mitochondrial function in Dementia with Lewy Body mice

first: Mathew

last: Blurton-Jones

address: 3014 Gross Hall

department: Department of Neurobiology & Behavior

summary: We previously demonstrated that transplantation of murine neural stem cells (NSCs) can improve motor and cognitive function in a transgenic model of Dementia with Lewy Bodies (DLB).  The underlying neurobiology that mediates such restoration no doubt involves numerous genes acting in concert to modulate signaling within and between host brain cells and transplanted NSCs. In order to identify functionally connected gene networks and additional mechanisms that may contribute to stem cell-induced benefits, we performed weighted gene co-expression network analysis (WGCNA) on striatal tissue isolated from NSC- and vehicle-injected wild-type and DLB mice. WGCNA is proved to be a powerful approach; revealing significant alterations in immune response, neurotransmission, and mitochondria function in response to NSC treatment.

overall_design: Age- and sex-matched transgenic mice over-expressing human wild-type alpha-synuclein (PDGF-β-ASO line D, ASO) and wild-type littermates maintained on a congenic C57B6/J background were examined. Hippocampal/cortical GFP-expressing mouse neural stem cells (NSCs) were microdissected from syngeneic GFP-transgenic mice at postnatal day 1 and transplanted at passage 15. Wild-type (WT) and transgenic littermates (ASO) were randomly divided into groups and received intrastriatal injections of either saline (Veh) or haplotype-matched NSCs. The combination of genotype and treatment resulted in four experimental groups: WT-Veh, WT-NSC, ASO-Veh, ASO-NSC. After one month of treatment, all animals were sacrificed and total RNA extracted from microdissected striatum.Then, RNA was processed and subjected to WGCNA analysis.

first: Anita

last: Lakatos

first: Natalie

last: Goldberg


title: Tlx1 (Hox11) related gene expression profile after intra-splenic islet transplantation in mice

first: Hitomi

last: Nishinakamura

address: 7-45-1 Nanakuma, Jonan-ku

department: Department of Regenerative Medicine and Transplantation

institute: Faculty of Medicine, Fukuoka University

summary: From the past reports, we hypothesized that spleen is an ideal site for inducing regeneration of transplanted islets, and leading to reduce the required number of islets for ameliorating the hyperglycemia of diabetic recipients in mice. In order to confirm this hypothesis, we performed 25 islets transplantation into spleen (SP25); it was not enough number to ameliorate the hyperglycemia of recipient mice, with 100 islets transplantation into beneath the kidney capsule (KC100) to maintain recipients' blood glucose normoglycemic temporary. All recipient mice (n=11) became normoglycemic after receiving SP25 with KC100. On 240 days after transplantation, we performed nephrectomy for removing islet grafts in the kidney. After nephrectomy, 8 of 11 mice remained normoglycemic, and 3 of 11 mice' non-fasting blood glucose levels were maintained around 300 mg/dL. On 290 days after transplantation (50 days after nephrectomy), all recipient mice received splenectomy to remove islet grafts in the spleen. All mice became hyperglycemic after splenectomy, indicating that intra-splenic islet grafts maintained the blood glucose levels of diabetic recipient mice. In order to investigate the gene expression associated with islets engraftment in the spleen, microarray studies were performed in comparison of the Tlx-1 (Hox11) related gene expression profiles of Sample 1, Sample 2 and Sample 3.

overall_design: Twenty-five islets and 100 islets were transplanted into spleen and beneath the kidney capsule of recipient mice, respectively (SP25+KC100). Then, spleen was harvested just after transplantation (Sample 1) or 2 days after transplantation (Sample 2). Furthermore, 100 days after receiving SP25+KC100, nephrectomy was performed for removing islet graft in the kidney, and those nephrectomized mice received splenectomy on 139 days after transplantation for harvesting the spleen sample of the recipient mice (Sample 3). Total RNA was prepared from these spleen.

first: Takeshi

last: Itoh

first: Kenjiro

last: Kumano

first: Shohta

last: Kodama


title: Nutritional targeting of the gut microbiota: a novel approach in the management of endothelial dysfunction

status: Public on Mar 08 2017

city: Brussels

first: Jean-Baptiste

last: Demoulin

address: av Hippocrate 75, B1.74.05

department: de Duve Institute

institute: Université catholique de Louvain

summary: Mice knocked-out or wild type for the apoE gene were recruited for this expression profiling experiment in the cecum. Each group of mice (WT versus cKO) were fed with a n-3 PUFA depleted diet, supplemented or not with prebiotics for the last fifteen days. Then mice were sacrificed and cecal tissues were isolated and processed for RNA extraction. Total RNA of each sample was then pooled with those of the same group and treatment for microarray hybridization.

overall_design: Two groups of mice: (I) WT DEF and KO DEF. Each group was submitted to a diet treatment: (I) without prebiotics and (ii) without prebiotics

first: Emilie

last: Catry

first: Ahmed

last: Essaghir

first: Nathalie

last: Delzenne


title: Transition into inflammatory cancer-associated adipocytes in breast cancer microenvironment requires microRNA regulatory mechanism

status: Public on Mar 09 2017

city: Seoul

first: Hyeong-Gon

last: Moon

address: 101, Daehak-ro Jongno-gu

department: Surgery

institute: Seoul National University Hospital

type:
Expression profiling by array
Non-coding RNA profiling by array

summary: This SuperSeries is composed of the SubSeries listed below.

platform_organism:
Mus musculus
synthetic construct

overall_design: Refer to individual Series