title: Transcriptome regulation by miR-210 in hypoxic glomerular endothelium [RNA-seq]

city: Singapore

first: Chong Yun

last: Pang

address: 60 Nanyang Dr, School of Biological Sciences

country: Singapore

institute: Nanyang Technological University

summary: Hypoxia occurs in both acute and chronic kidney diseases. Despite the central role of tubular injury in acute kidney injury (AKI), a hallmark feature is a reduction in glomerular filtration rate. There is now an increasing interest in the effect of direct injury to the renal vasculature and its potential role in the pathogenesis of AKI. In this study, we profiled glomerular endothelial miRNA and mRNA changes in response to hypoxia in vitro. We identified significant induction of a hypoxia associated miRNA, miR-210-3p, which enhanced cellular glycolytic capacity. Furthermore, integrated transcriptomic analysis identified HIF1A and TFRC as putative miR-210-3p targets. This was corroborated by the strong correlation in glomerular endothelial TfR1 and HIF-1α protein expression in kidney tissue samples. Collectively, our study uncovered a compensatory mechanism in which miR-210-3p supports glomerular endothelial adaptation by modulating bioenergetics, thereby fine-tuning hypoxia responses and limiting cellular injury.

overall_design: Primary glomerular endothelial cells cultured in hypoxic incubator for 4, 12 and 24 hours to mimic renal ischemia. Subsequently, total RNA was extracted for RNA-seq and miRNA seq.

first: Jenny

last: Gilmour

first: Simon

last: Satchell

last: Kirby

first: Neil

last: Sheerin

first: Simi

last: Ali


title: [ac4C-seq] - The RNA helicase domain of NAT10 promotes the biogenesis of hypomodified ribosomes to enhance cancer cell proliferation

status: Public on Jun 30 2026

city: Chicago

first: Daniel

last: Arango

state: IL

address: 303 E Superior St, Office 7-119

country: USA

institute: Northwestern University

summary: N-acetyltransferase 10 (NAT10) is a multifunctional enzyme that harbors RNA acetyltransferase and RNA helicase domains and has emerged as a therapeutic vulnerability in solid and hematological malignancies. By coupling Proteolysis Targeting Chimera-mediated degradation of NAT10 with a deep mutational scanning assay, followed by biochemical, cellular, and in vivo validations, we find that the RNA helicase domain of NAT10 enhances cancer cell proliferation and tumor growth. This proliferative function of NAT10 is independent of RNA acetylation but requires its RNA-binding activity. The RNA helicase domain of NAT10 is required for 18S rRNA binding, promoting biogenesis of the 40S ribosomal subunit, while simultaneously interfering with the deposition of the conserved 18S rRNA modification m¹acp³Ψ. Loss of m¹acp³Ψ in 18S rRNA enhances cancer cell proliferation, revealing that NAT10 promotes the biogenesis of hypomodified ribosomes to facilitate tumor growth. These findings uncover a previously unrecognized mechanism by which NAT10 promotes cancer cell proliferation and establish its RNA helicase domain as a potential therapeutic target.

overall_design: Epitranscriptomic mapping of ac4C using chemical treatment with NaCNBH3 and reverse transcription with the unnatural nucleotide 2-aminodATP.

first: Mahmood

last: Dalhat

first: Hannah

last: Serio

first: Sharath

last: Narayan


title: Ear Photosynthesis Outweighs Flag and Top Second Leaf Contributions to Oat Grain Weight and Oil Accumulation

city: Yangling

first: ningxin

last: guo

address: No. 3, Taicheng Road

country: China

institute: Northwest A&F University

type: Expression profiling by high throughput sequencing

summary: Oat endosperm uniquely accumulates oils, differing from other Poaceae crops and oilseed species that primarily store oils in embryos. Different photosynthetic organs' contribution to grain oil accumulation remains unclear. This study investigated the effects of photosynthesis on grain weight and oil accumulation in the ear, flag leaf, and top second leaf of four oat cultivars with varying oil contents, using shading/excision treatments. Studies have shown that ear shading significantly affects grain weight and lipid accumulation in oats. These effects were more pronounced in high-oil cultivars than low-oil cultivars. We further performed transcriptome profiling on the high-oil oat cultivar BY9 at 4 days after ear shading. Transcriptomic analysis indicated that shading altered expression patterns of genes associated with carbohydrate metabolism, fatty acid synthesis, and triacylglycerol assembly. Our findings highlight the critical role of ear photosynthesis in determining both oil production and yield in oats, providing new insights into oil accumulation mechanisms in cereal crops.

overall_design:
RNA-seq data from the high-oil oat cultivar BY9 under ear shading treatment for four days after flowering and the non-shaded control group.

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Raw data not available; only processed FPKM expression data are submitted.
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first: Yun

last: Wang


title: Maternal obesity Reprograms Offspring Intestinal Epithelium via Tuft Cell-Mediated ECM-Integrin Signaling

city: Beijing

first: Huanling

last: Yu

address: No.10, Xi Tou Tiao, You An Men Wai, Fengtai District, Beijing 100069, P. R. China.

institute: Capital Medical University

summary: We established a maternal obesity rat model using a high-fat diet. scRNA-seq was performed on E19.5 fetal colon. CellChat and hdWGCNA were used to analyze intercellular communication and identify functional modules. Inflammatory cytokines were detected by the Luminex Assay.

overall_design: E19.5 fetal colon from obesity during pregnancy and control rats were analysized by scRNA-seq.

first: Yuchen

last: Wei

first: Xiaxia

last: Cai


title: Hepatic FGFR-ERK-HRG axis regulates heparin-induced thrombocytopenia with thrombosis

city: qingdao

first: tianyu

last: wang

address: yushanlu 5#

institute: Ocean University of China

summary: To identify key plasma proteins altered by heparin challenges and determine its regulatory roles in pathogenic immune complexes formation and thrombosis in HIT

overall_design: Comparative gene expression profiling analysis of RNA-seq for the mouse hepatocytes of control and heparin challenge


title: PFOS exposure on the brain transcriptome of aged mice

city: chengdu

first: ZHENGLU

last: WANG

state: sichuan

address: south of renmin road

institute: Sichuan University

summary: Aged mice were exposed to environmental concentrations of PFOS for 7.5 months. The concentrations were divided into low and high groups. Before assessing cognitive function, the transcriptional changes in brain tissues were measured to reveal the underlying mechanism.

overall_design: 24-month-old aged mice, exposed to low concentration of PFOS at 0.5 micrograms per liter and high concentration at 50 micrograms per liter through drinking water for a period of 7.5 months. After the experiment, the mice were euthanized and their brains were perfused for tissue collection. The eukaryotic transcriptome was then determined.

first: Zhenglu


city: Qingdao

first: Shaoyun

last: Zhou

address: No. 5, Yushan Road, Shinan District

overall_design: Comparative gene expression profiling analysis of RNA-seq for the mice liver of control and heparin challenge


title: Reversible epiblast regionalisation determines differentiation potential of human PSCs [EM-seq]

city: Cambridge

first: Steven

middle: William

last: Wingett

state: Cambs

address: Francis Crick Avenue, Cambridge Biomedical Campus

department: Cell Biology

country: United Kingdom

institute: MRC Laboratory of Molecular Biology

type: Methylation profiling by high throughput sequencing

summary: Although the epiblast in the embryo has the capacity to generate all tissues of the body, its in vitro counterparts often exhibit differentiation biases, posing significant challenges for both basic research and translational applications involving pluripotent stem cells (PSCs). The origins of these biases remain incompletely understood. In this study, we identify regional epiblast identity as the hallmark of differentiation competency through fluctuations in repressive and activating histone posttranslational modifications. We present a novel approach to overcome this bias using a chemical chromatin restoration (CHR) treatment. This method restores transcriptional programs, chromatin accessibility, histone modification profiles, and differentiation potential, effectively recapitulating the competent anterior epiblast-like state. Furthermore, we propose that a high bivalency state is a defining feature of the anterior human epiblast and is a characteristic of unbiased PSCs. We suggest that fluctuations in histone modification marks drive epiblast regionalization, ultimately shaping cellular responses to differentiation cues.

overall_design: EM-seq was performed to identify 5mC and 5hmC in human pluripotent stem cells either competent or noncompetent to generate unguided cerebral organoids. Samples were collected from pairs of lines before and after chromatin restoration treatment (CHR) and a naturally competent line H9. Two biological replicates were generated from independent experiments for each condition.

first: Magdalena

last: Sutcliffe

first: Eugenia

last: Wong

first: Charles

last: Morris

first: Harald

last: Stachelscheid

first: Stefan

last: Schoenfelder

first: Madeline

last: Lancaster


title: Altered miRNA Expression Profile in Human Sperm and Seminal Plasma Following Cryopreservation-Thawing: A Small RNA Sequencing Study

first: Longlong

last: Fu

state: --choose--

address: 大慧寺12号，科研楼2楼，精子库

institute: 国家卫生健康委科学技术研究所

type: Non-coding RNA profiling by high throughput sequencing

summary: Cryopreservation of human semen is widely used in assisted reproductive technology (ART) and male fertility preservation, but inevitably induces cryodamage to spermatozoa. Small non-coding RNAs, particularly microRNAs (miRNAs), play critical roles in post-transcriptional gene regulation and may reflect cellular responses to cryopreservation stress. Seminal plasma, the natural fluid environment of spermatozoa, contains abundant miRNAs that may also reflect post-thaw biological responses. However, the impact of freeze-thawing on miRNA expression in both sperm and seminal plasma remains poorly understood. In this study, we performed small RNA sequencing on sperm and seminal plasma samples from healthy normozoospermic donors. For sperm, 5 individual donors provided paired fresh and post-thaw samples (A1-A5: post-thaw; B1-B5: fresh). For seminal plasma, 30 donors were randomly divided into 3 groups (n=10 per group), pooled, and split into fresh control (D3, D4, D5) and cryopreservation-thawing (C3, C4, C5) groups. In sperm, cryopreservation-thawing induced [X] differentially expressed miRNAs ([Y] upregulated, [Z] downregulated). In seminal plasma, we identified 15 differentially expressed miRNAs (9 upregulated, 6 downregulated). GO and KEGG analyses revealed enrichment in fatty acid degradation, Toll-like receptor signaling, and oxidative phosphorylation pathways in both sample types. Our findings provide a comprehensive resource for understanding the molecular mechanisms of sperm cryodamage and developing biomarker-based tools for post-thaw semen quality assessment in ART settings.

overall_design: Small RNA sequencing of human sperm (10 samples: 5 fresh, 5 post-thaw) and seminal plasma (6 samples: 3 fresh pooled, 3 post-thaw pooled). For sperm: 5 individual donors provided paired fresh and post-thaw samples (A1-A5: post-thaw; B1-B5: fresh). For seminal plasma: 30 donors were randomly divided into 3 groups (n=10 per group), pooled, and split into fresh control (D3, D4, D5) and cryopreservation-thawing (C3, C4, C5) groups. All samples were sequenced on the Illumina NovaSeq 6000 platform with single-end 50 bp reads. Differential expression analysis was performed using DESeq2 with a paired design (design = ~ donor + condition).


title: ArchetypeShift: An R Package Integrating KEGG-Informed Pathway Analysis and IPA-Derived Functional Predictions for Validation of Single-Cell Archetypes

city: Oklahoma City

first: Adam

last: Wilson

state: Oklahoma

address: 800 Research Parkway

department: Pediatrics

institute: University of Oklahoma Health Sciences Center

summary: Archetype analysis is important because clustering of cell types is often nuanced and inexact. We developed a new pipeline to identify and annotate single-cell archetypes from preterm infant small intenstine organoids.

overall_design: Single-cell rna-seq was performed on human ileal enteroids (n = 3) treated with hyaluronan 35 kDa for 48 hours.

first: Hala

last: Chaaban

first: Kathryn

last: Burge


title: Reversible epiblast regionalisation determines differentiation potential of human PSCs [ATAC-seq]

type: Genome binding/occupancy profiling by high throughput sequencing

overall_design: ATAC-seq was performed to assess chromatin accessibility in human pluripotent stem cells either competent or noncompetent to generate unguided cerebral organoids. Samples were collected from two pairs of experimental groups: naturally competent vs naturally noncompetent lines, and lines before and after chromatin restoration treatment (CHR) . Two biological replicates were generated from independent experiments for each condition.

middle: W


title: Effects of Hif-1α inhibition under hypoxic conditions on doxorubicin response in B16.F10 murine melanoma cells

city: Cluj-Napoca

first: Bogdan

last: Dume

address: Mihail Kogălniceanu, no. 1

country: Romania

institute: Babes-Bolyai University

summary: Hipoxia inducible factor 1 (HIF-1) is major regulator of cellular adaptations to low oxygen concentrations, responsible for transcriptional programs that promote metabolic reprogramming, cell survival, and drug resistance. RNA sequencing was performed to characterize transcriptomic changes in B16.F10 murine melanoma cells cultured under 1% hypoxia following Hif-1α silencing and doxorubicin treatment. Differential gene expression analysis of the treatment group revealed extensive downregulation of metabolic pathways (glycolysis, oxidative phosphorylation, cholesterol homeostasis, and mTORC1 signaling). In parallel, genes associated with stress and cell death responses, including p38 MAPK signaling, p53 signaling, Notch signaling, and angiogenesis, were upregulated. Taken together, the treatment, promoted cell death and increased sensitivity to doxorubicin, supporting the potential of targeting hypoxia associated mechanisms to enhance therapeutic efficacy in hypoxic tumors.

overall_design: RNA-seq profiling of B16.F10 murine melanoma cells cultured under hypoxic conditions (1% O2). Cells were transfected with Hif-1α or negative control siRNA and, after 24h, treated with doxorubicinand incubated for additional 24h. Experimental groups included control, negative control siRNA, Hif-1α knockdown, doxorubicin, and Hif-1α knockdown + doxorubicin.

first: Manuela

last: Banciu

first: Emilia

last: Licarete


title: Inhibition of GOT1 Potentiates Ferroptosis and Exacerbates Cell Death in Acute Myeloid Leukemia

city: Nanning

first: Huan

last: Peng

address: 59, Xiangzhu street

institute: Maternal and Child Health hospital of Guangxi Zhuang Autonomous Region

summary: Background Drug resistance, poor treatment response, and low long-term survival rates are major obstacles to the successful long-term treatment of acute myeloid leukemia (AML), a heterogeneous hematologic malignancy. A deeper understanding of the molecular mechanisms underlying AML is therefore essential. GOT1, a key metabolic enzyme, has emerged as a potential regulator of AML progression, though its precise role remains unclear. This study aimed to investigate the expression profile, function significance, and mechanistic involvement of GOT1 in AML. Methods The expression levels of GOT1 in AML patient samples and cell lines were quantified by RT-qPCR. Genetic knockdown (shRNA) and pharmacological inhibition (compound 2C) were employed to suppress GOT1 activity. Functional assays, including CCK-8 assay and Annexin V/PI staining, evaluated proliferation and apoptosis of AML cells. Multi-omics analyses (transcriptomics, proteomics, and metabolomics) were performed to delineate the mechanistic landscape of GOT1 inhibition. Reactive oxygen species levels in AML cells treated with compound 2C were measured by flow cytometry. The combined effects of compound 2C and ferroptosis inducers (RSL3/FIN56) were evaluated using the CCK-8 assay. Results The expression of GOT1 was significantly upregulated in AML patients and cell lines compared to controls. Inhibition of GOT1 suppressed AML proliferation and induced cell death via triggering ferroptosis. Multi-omics profiling revealed perturbations in redox homeostasis and iron metabolism pathways upon GOT1 suppression. Notably, GOT1 inhibition (compound 2C) combined with ferroptosis inducers (RSL3/FIN56) synergistically reduced AML cell viability. Conclusion Our findings demonstrate that GOT1 drives AML progression by modulating ferroptosis susceptibility. Targeting GOT1, either alone or in combination with ferroptosis inducers, represents a novel therapeutic strategy to overcome resistance and improve outcomes in AML.

overall_design: RNA-Seq profiling of  shGOT1 and shNC cells in THP1 cells.

first: Fangshu

last: Liu

first: Wenjue

last: Tang

first: Xin

last: Lin

first: Qiongyou

last: Liang

first: Qinle

last: Zhang

first: Huihong

last: Dou

first: Sheng

last: He


title: Programmed Repair of Disease-Causing UGA Premature Termination Codons in Mammalian Brain

city: Coralville

first: Ahmad

last: Al Saneh

state: IA

address: 1708 5th Street Apartment 404

department: Molecular Physiology and Biophysics

institute: University of Iowa

summary: Protein truncating variants caused by stop codons are the most prevalent class of rare variant mutations in neurodevelopmental diseases, with UGA codons being most common. Suppressor transfer RNA (sup-tRNA) have therapeutic potential for premature termination codon (PTC) rescue, but have thus far underperformed by traditional AAV delivery platforms and progress has been hampered by the lack of methods to non-invasively assess in vivo activity in mammalian brain. To fill this material gap, we utilize transcranial in vivo bioluminescence imaging data from a luciferase-UGA mouse model to optimize viral payloads with sup-tRNA genes. These data demonstrate that U6 promoter-driven and single-stranded AAV2/9 constructs show variable and dose-dependent activity, whereas self-complementary AAV2/9 with the tRNA in a minimal 100bp genomic context provides broad and efficacious PTC rescue. Further, payload tRNA multiplexing and use of tRNA introns enable efficacy of low viral titers and sustained rescue. tRNA sequencing of scAAV delivered ArgUGA sup-tRNA in brain demonstrate no effects on endogenous tRNA levels, their acylation or processing, and these features are also maintained in scAAV delivered ArgUGA sup-tRNA. Collectively, this work defines a scalable strategy for precision UGA PTC stop codon suppression, supporting development of durable genetic rescue therapies for neurodevelopmental disorders in the mammalian brain.

overall_design: The tRNA sequencing was performed on brain tissue from the LumA heterozygous reporter mouse model: a transgenic C57BL/6J line carrying a UGA premature termination codon (p.R387X) in a firefly luciferase reporter gene at the Rosa26 locus. Samples were collected at postnatal day 30 from two groups (n = 3 per group): uninjected controls and mice that had received intracerebroventricular (ICV) injection of scAAV-G(I): a self-complementary AAV2/9 vector encoding the ArgUCA suppressor tRNA (tRNA-Arg-TCA-1-1) within its native 100 bp genomic context and including a tRNA intron — at postnatal day 0–1. The primary variables under investigation were the effects of virally delivered suppressor tRNA on the endogenous tRNA landscape, specifically: global and arginine isodecoder-level tRNA abundance, aminoacylation (charging) status, maturation/processing (mature vs. intron-containing species), and nucleotide modification profiles (assessed via reverse-transcriptase misincorporation signatures). A key outcome was the detection and quantification of the exogenously delivered ArgUCA suppressor tRNA itself relative to the endogenous ArgUCU parental tRNA family.

first: Christopher

last: Ahern


title: LncRNA H19 exacerbates hepatic inflammation and oxidative stress in alcohol-related liver disease by sponging miR-22 to derepress SIRT1

city: Hefei

first: Yue

last: Wang

address: 218 Jixi Road

institute: First Affiliated Hospital of Anhui Medical University

summary: LncRNA H19 is upregulated in various liver diseases and promotes steatosis and inflammation, but its role and mechanism in alcohol-related liver disease (ALD) remain unclear. This study aimed to investigate whether H19 exacerbates ALD via the microRNA-22 (miR-22)/Sirtuin1 (SIRT1) axis.

overall_design: The sample size is 8, with no duplicate samples. The C57BL/6 control group is compared with the alcohol-fed group, in a 4:4 ratio.

first: Long

last: Cheng


title: Reversible epiblast regionalisation determines differentiation potential of human PSCs

first: Steven

last: Wingett

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

overall_design: Refer to individual Series


title: HIF-1–Mediated PPME1 Expression Promotes Breast Cancer Progression via AKT Activation and β-Catenin Recruitment

city: Baltimore

first: YAJING

last: LYU

state: MD

address: 733 N Broadway

department: ICE

institute: Johns Hopkins University

summary: HIF-1-driven upregulation of PPME1 leads to enhanced phosphorylation of β-catenin and its nuclear translocation. Nuclear β-catenin cooperates with HIF-1 to activate transcription of numerous HIF target genes, thereby promoting breast cancer stem cell specification and immune evasion.

overall_design: NTC, HIF1A-KD, PPME1-KD, and CTNNB1-KD subclones of SUM159 cells were exposed to 20% or 1% O2 for 24 hours, and three biological replicates for each condition were subjected to RNA-seq

first: Yajing

last: Lyu

first: Gregg

middle: L

last: Semenza


title: ChIP-seq of human developing cerebellum

city: Toronto

first: Shraddha

last: Pai

state: ON

address: 160 College Street, Room 602

country: Canada

institute: University of Toronto

summary: The cerebellar rhombic lip neural progenitor niche of the prenatal hindbrain is an anatomical structure critical for cerebellar glutamatergic neurogenesis.  Humans have elaborated the rhombic lip niche to include a rhombic lip subventricular zone (RL-SVZ) not seen in mice or macaques. Although developmental disruptions of this progenitor zone can cause cerebellar growth abnormalities – from malformations to tumors – the gene regulatory networks underpinning this unique progenitor niche are unknown. Here we provide a predicted gene regulatory network for the human cerebellar rhombic lip, inferred from epigenomic maps of the developing human cerebellum. We generated DNA methylomes of neuroanatomically-dissected mid-gestation human rhombic lip ventricular zone and RL-SVZ (N=9 samples; 15-16 post conception weeks) using low-input Enzymatic MethylSeq.  We also mapped histone modifications marking active promoters and enhancers in the whole mid-gestation human fetal cerebellum (N=6 samples; 14 and 18 post-conception weeks). Integrating these data, we identified 9,855 differentially-methylated regions (DMR) which converge on binding sites of over three hundred transcription factors, including master regulators of rhombic lip neurogenesis, ATOH1, NEUROD1, and NEUROD2. DMRs hypomethylated in the RL-SVZ are enriched in active enhancers and in human accelerated regions, and are depleted in active promoters. We inferred 81,844 transcription factor-enhancer-gene links, covering 41 transcription factors active in the rhombic lip, and 4,610 target genes that include drivers of cerebellar neurogenesis and pediatric hindbrain cancer. Twenty-five DMRs overlap human accelerated regions located near genes associated with intellectual disability, autism spectrum disorders, and neurological deficits. DMRs are also statistically enriched in copy number aberrations in medulloblastoma, a malignant pediatric hindbrain cancer with subtypes hypothesized to originate in the rhombic lip. Close to one-quarter of the DMRs overlap known copy number aberrations in medulloblastoma, nominating potential enhancer and promoter elements impacted by these genomic aberrations. Collectively, our data provide a rich resource to start decoding the functional impact of non-coding variation on gene regulation in the developing cerebellum and on genomic dysregulation in diseases of cerebellar growth.

overall_design: Fresh frozen cerebellum (130-180 mg) was sent to Active Motif for ChIP-seq using the following antibodies: H3K4me3 (Active Motif, cat#39159), H3K27Ac (Active Motif, cat #39133) and RNA Pol II (Active Motif, cat # 91151).  H3K27ac, H3K4me3, and POL2 peaks were called in two fetal hindbrain samples (male, 14 and 18 PCW, N=6 samples). Standard normalization was achieved by down-sampling the usable number of tags for each sample in a group to the level of the sample in the group with the fewest usable number of tags. This resulted in an equal number of tags within each group. Peaks were called using either MACS 2.1.0 or SICER algorithms. MACS default cutoff was pvalue 1e-7 for narrow peaks and 1e-1 for broad peaks. SICER default cutoff was FDR 1e-10 with gap parameter of 600 bp. Peak filtering was performed by removing false ChIP-Seq peaks as defined within the ENCODE blacklist. Super enhancers were predicted using Active Motif’s proprietary algorithm. Reads were aligned to hg38.

first: Kimberly

middle: A

last: Aldinger


title: GATA2 coordinates pluripotency exit and meiotic initiation in female fetal germ cells

city: Guangzhou

first: Zhenyi

last: Huang

state: GuangDong

address: ShaTaiNan Street 1023-1063,Baiyun

department: Development

institute: Southern Medical University


title: Neutralizing IL-22RA1 improves histological and molecular alterations associated with atopic dermatitis pathogenesis

city: Freiburg

first: Natalie

last: Garzorz-Stark

address: Hauptstraße 7

department: Department of Dermatology and Venereology

country: Germany

institute: University of Freiburg

summary: BACKGROUND: A subgroup of patients with atopic dermatitis (AD) do not show sufficient improvement with current systemic therapies, highlighting the heterogeneity of the chronic inflammatory skin disease and the need for novel treatments. OBJECTIVES: In this study, we investigated the pathogenic contribution of the IL-22/IL-22 receptor (IL-22RA1) axis to AD skin inflammation in in vitro, ex vivo, and in vivo models to evaluate the therapeutic potential of blocking this axis. METHODS: IL-22RA1 expression in AD skin was assessed by in situ hybridization. Inhibition of the IL-22/IL-22R signaling cascade was evaluated in a human AD in vitro model (3D skin equivalents) and a TPA mouse model using temtokibart, a humanized antibody directed against IL-22RA1. RESULTS: IL22RA1 was highly expressed in the epidermis of lesional AD skin versus non-lesional control skin; expression correlated positively with epidermal thickness and negatively with the barrier integrity marker loricrin. IL-22 stimulation in 3D skin equivalents induced a specific molecular signature associated with lack of terminal differentiation, altered lipid metabolism, and increased immune response. Inhibition of IL-22RA1 with temtokibart showed significant improvements in skin barrier integrity at the histological and molecular levels. IL-22RA1 inhibition in a skin inflammation mouse model with Zymo, a surrogate murine anti-IL-22RA1 monoclonal antibody for temtokibart, reduced local expression of Cxcl1 and S100a9. CONCLUSIONS: These findings suggest that the IL-22/IL-22RA1 axis functionally contributes to AD pathogenesis. Thus, blocking IL-22RA1 represents a potentially valuable new therapeutic option.

overall_design: Following digestion, lesional skin samples of Psoriasis (n=12) and Atopic Dermatitis (n=8) patients were introduced into the single cell sequencing workflow using the 10X Genomics platform.

first: Sophia

last: Wasserer

first: Thomas

last: Litman

first: Josephine

last: Hebsgaard

first: Manja

last: Jargosch

first: Christina

last: Hillig

first: Anna Caroline

last: Pilz

first: Tilo

last: Biedermann

first: Christophe

last: Blanchetot

first: Michael

last: Menden

first: Mette

last: Sidsel Mortensen

first: Tine

last: Skak-Nielsen

first: Malene

last: Bertelsen

first: Birgitte

last: Ursoe

first: Felix

last: Lauffer

first: Britta C

last: Martel

first: Kilian

last: Eyerich

first: Stefanie


title: The CRAC channel inhibitor Auxora interrupts inflammatory circuits between alveolar macrophages and T cells in patients with viral pneumonia

first: Alexander

middle: V

last: Misharin

state: Illinois

address: 303 E Superior St

department: Pulmonary and Critical Care

summary: Viral pneumonia is perpetuated by inflammatory circuits between activated T cells and monocyte-derived alveolar macrophages (MoAM). T cells and macrophages express ORAI1 and STIM1, which form calcium release-activated calcium (CRAC) channels that allow extracellular calcium entry in response to endoplasmic reticulum calcium store depletion. In a randomized, placebo-controlled, multicenter phase 2 trial (CARDEA), Auxora, a CRAC channel inhibitor, reduced all-cause 30-day mortality by 56% in patients with severe SARS-CoV-2 pneumonia1.  Here, we report a multi-omics analysis of serially collected alveolar samples from unvaccinated patients with severe SARS-CoV-2 pneumonia treated with Auxora versus placebo. We found reductions in plasma levels of the monocyte- and T cell-chemokines, CCL8 and CXCL10. Using PBMCs from healthy volunteers, we show Auxora directly targets T cells to inhibit the transcription of CCL8 and CXCL10 in monocyte-derived macrophages, supporting a mechanism for its effects and a potential intermediate biomarker of efficacy.

overall_design:
The trial was designed to enroll 4 patients each into three cohorts in a 3:1 drug:placebo ratio. The first cohort received Auxora or placebo for three days, the second cohort received Auxora or placebo for 4 days, and the third cohort received Auxora as a continuous infusion for 5 days. The dose of Auxora was 2.0 mg/kg (1.25 mL/kg) administered at 0 hour, a start of the first infusion and then 1.6 mg/kg (1 mL/kg) at 24 hours and 1.6 mg/kg (1 mL/kg) at 48 hours from the start of the first infusion. The dose of placebo was 1.25 mL/kg administered at 0 hour and then 1 mL/kg at 24 hours and 1 mL/kg at 48 hours. For all cohorts, a BAL procedure was performed within 12 hours before the first dose of Auxora or placebo and 24 hours after the last dose of Auxora or placebo.

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Missing raw data files due to patient privacy concerns.
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first: Marina

last: Casalino Matsuda

first: Vijeeth

last: Guggilla


title: Single-cell RNA sequencing of small intestinal organoid self-organization [scRNA-Seq]

city: Basel

first: Prisca

last: Liberali

address: Klingelbergstrasse 48

department: D-BSSE

country: Switzerland

institute: ETHZ

summary: The mouse small intestinal epithelium is composed of diverse cell types that interact to regulate signaling, cell patterning, and tissue form and function. The self-organization of small intestinal organoids, starting from a single cell (0 h) to a budded crypt-villus structure (96–108 h), recapitulates aspects of such multicellular intestinal morphogenesis. To characterize the cell states and lineage trajectories underlying organoid self-organization, we performed single-cell RNA sequencing of intestinal organoids in a high-resolution time course. Organoids derived from mouse duodenal epithelium were dissociated to single cells and seeded to initiate organoid formation, followed by sampling for sequencing at 12-hour intervals from 24 to 108 h. This dataset captures dynamic changes in cell state composition during organoid development. Early time points (24–36 h) reveal a population of reprogramming cells characterized by loss of mature lineage markers, followed by the emergence and differentiation of major intestinal lineages, including absorptive, secretory, and stem cell populations. A secretory progenitor population emerges by 48 h, which gives rise to both exocrine (Paneth and goblet cells) and endocrine lineages (enteroendocrine progenitors and differentiated enteroendocrine cell types). Absorptive and stem cell lineages continue their differentiation and maturation following their emergence at 48–72 h. Overall, this dataset provides a comprehensive resource for studying cell state transitions and lineage specification during intestinal organoid self-organization and recapitulates key features of epithelial differentiation observed in vivo.

overall_design: Single cell RNA-seq timecourse of mouse intestinal organoid regeneration at 12h intervals from 24h until 108h after seeding.

first: Nicole

last: Repina

first: Clara

last: Baader

first: Silvia

last: Barbiero

middle: B

last: Stadler


title: hLMR1, a hepatocyte-specific long noncoding RNA that represses amino acid catabolism through pre-mRNA interaction in human liver [RNA-seq]

city: St. Petersburg

first: Xiangbo

last: Ruan

state: Florida

address: 600 Fifth Street S

institute: Johns Hopkins University School of Medicine

summary: hLMR1 (human lncRNA metabolic regulator 1) is a human-specific lncRNA which promotes hepatic cholesterol biosynthesis. To systematically identify genes regulated by hLMR1, we performed high-throughput RNA sequencing on humanized mouse livers with or without hLMR1 knockdown.

overall_design: Adenoviruses carrying shRNA expression cassettes targeting hLMR1 or LacZ were injected into humanized liver mice. Total RNA was isolated from liver tissues and subjected to strand-specific RNA sequencing.

first: Marcos

middle: E

last: Jaso-Vera

first: Shohei

last: Takaoka

first: Lanuza A.P

last: Faccioli

first: Zhiping

last: Hu

first: Alejandro

last: Soto-Gutierrez


title: Tubular cell-specific PDGF-B drives fibrogenic niches in kidney fibrosis [RNA-seq_Aging]

city: Aachen

first: Barbara

middle: Mara

last: Klinkhammer

address: Pauwelsstrasse 30

department: Pathology

institute: RWTH Aachen University

summary: Kidney fibrosis is the underlying pathological process of chronic kidney disease, the mechanisms of which are still incompletely understood. Following a transcriptome-wide gene expression analysis of PDGF-B in murine and human kidney cells, we generated transgenic mouse lines with Pdgfb deletion in major expressing cells. Mice with Pdgfb deletion in kidney tubular epithelial cells showed significantly reduced activation and proliferation of peritubular fibroblasts and fibrosis in three models with tubular injury of different etiologies. We identified paracrine PDGF signaling as a key molecular mechanism of cellular crosstalk mediating the transition of kidney tubular injury to interstitial fibrosis via induction of profibrotic niches.

overall_design: Kidney cortex from aged mice with tubule(Pax8)-specific deletion of Pdgfb

middle: M

first: Eva

last: Buhl

first: Tim

last: Caspers

first: Sidrah

last: Maryam

first: Dickson

last: Wong

first: Michael

last: Godetier

first: David

last: Hoelscher

first: Roman

middle: D

last: Buelow

first: Rafael

last: Kramann

first: Sikander

last: Hayat

first: Jürgen

last: Floege

first: Peter

last: Boor


title: Tubular cell-specific PDGF-B drives fibrogenic niches in kidney fibrosis [RNA-seq_UUO]

overall_design: Kidney cortex from mice with tubule(Pax8)-specific deletion of Pdgfb after 5 days of unilateral ureteral obstruction (UUO)


title: The AC16 Cell Line Revisited: Integrated Cytogenetic, Genomic, and Transcriptomic Analysis Reveals a Highly Rearranged Near Tetraploid Genome

first: Ralf

last: Weiskirchen

address: Pauwelsstr. 30

department: IFMPEGKC

institute: RWTH University Hospital Aachen

summary: The human AC16 cell line was established in 2005 by fusing primary cells from adult human ventricular heart tissues with SV40 transformed, uridine auxotroph human fibroblasts devoid of mitochondrial DNA. This cell line is widely used as an in vitro model for studying cardiac biology, cardiotoxicity, and molecular mechanisms underlying cardiovascular diseases. However, despite its broad application, the detailed genetic and cytogenetic characteristics of this cell line has so far remained largely undefined. In the present study, we performed a comprehensive molecular and cytogenetic characterization of AC16 cells using multiple complementary approaches. Short tandem repeat profiling confirmed the AC16 reference profile deposited in the Cellosaurus database. Morphological examination by light and electron microscopy demonstrated a spindle-shaped, fibroblast-like morphology with a metabolically active cytoplasm containing numerous mitochondria, lysosomes, and extensive rough endoplasmic reticulum. Cytogenetic analyses using multicolor banding and inverted DAPI banding revealed an instable highly complex near-tetraploid karyotype with 90-100 chromosomes and numerous structural abnormalities, including deletions, derivative chromosomes, translocations, inverted duplications, and Robertsonian translocations. These findings were further supported by array comparative genomic hybridization, which demonstrated widespread genomic copy number alterations affecting nearly all chromosomes. This highlights that this cell line is rather suited as a cancer model than a model for normal heart cells. Next-generation sequencing confirmed the expression of several genes associated with cardiomyocyte function, including GJA1, GATA4, NFATC4, and CACNA1C, although classical cardiac markers such as TNNT2 and ACTN2 were absent or expressed at very low levels. Our findings reveal that AC16 cells possess a highly rearranged genome and exhibit a mixed molecular phenotype, emphasizing the importance of careful interpretation when using this cell line as a model for cardiac biology.

overall_design: mRNA bulk next-generation sequencing (NGS) was performed to assess the translational profile of the human AC16 cell line


title: SNHG29 knockdown by CRISPRi and shRNA in M07e acute myeloid leukemia cells

city: Frankfurt

first: Robert

last: Winkler

state: Hesse

address: Theodor-Stern-Kai 7

department: Department of Pediatrics

institute: Goethe University Frankfurt

summary: The long non-coding RNA SNHG29 has been identified as a candidate essential gene in acute myeloid leukemia (AML) through a genome-wide CRISPRi depletion screen. To characterize the transcriptomic consequences of SNHG29 loss, we performed RNA-seq in M07e AML cells following SNHG29 knockdown using two independent methods: CRISPRi (two sgRNAs targeting the SNHG29 promoter, with Luciferase-targeting sgRNA as control) and shRNA (two shRNAs targeting SNHG29, with scrambled shRNA as control). Three biological replicates were generated per condition. Differential expression analysis was performed using DESeq2.

overall_design: M07e cells were transduced with CRISPRi or shRNA constructs targeting SNHG29 or non-targeting controls (firefly luciferase). Three biological replicates per condition. Total RNA was extracted on days 3 (shRNA) or 7 (CRISPRi) post-transduction using the RNeasy Plus Mini Kit (Qiagen). rRNA-depleted libraries were sequenced on an Illumina NovaSeq 6000 (150 bp paired-end; Novogene). Reads were processed using the nf-core/rnaseq pipeline v3.18, aligned to hg38 with STAR 2.7.11b and quantified with Salmon 1.10.3 against the Ensembl transcriptome version 108. Differential expression analysis was performed using DESeq2 1.46.0.

first: Bruno

last: Griesler

first: Wolfgang

last: Sippl

first: Reinier

last: Boon

first: Ilka

last: Wittig

first: Marie-Laure

last: Yaspo

first: Stefan

last: Hüttelmaier

first: Raj

last: Bhayadia

first: Dirk

last: Heckl

first: Jan-Henning

last: Klusmann


title: Short-term toxic effects of Potassium peroxymonosulfate on Chlorella pyrenoidosa: due to its rapid degradation

city: Yang Zhou

first: Yi

last: Du

address: Shuangqiao Street

institute: Yang Zhou University

summary: The widespread use of potassium peroxymonosulfate (PMS) in aquaculture raises concerns about its ecological risks. This study evaluated acute toxicity of PMS to Chlorella pyrenoidosa over 24-96 h to establish a 96 h EC₅₀. Chronic exposure groups (0, 1.70, 3.40, 8.49 mg/L, corresponding to 0, 0.1, 0.2, and 0.5 of the EC₅₀) were cultured for 12 days. Cell growth, oxidative stress, ultrastructure, chlorophyll fluorescence, and transcriptomic genes were measured on days 0, 3, 6, 9, and 12. PMS decomposition products were monitored and correlated with physiological and Biochemical responses. PMS rapid decomposition increased breakdown products, inhibiting algal growth during days 0-3 and causing surface wrinkling, plasmolysis, chloroplast damage, and thylakoid disarray. Oxidative stress rose and growth_x001e_related genes were down_x001e_regulated. After day 6, with the cessation of PMS decomposition and the subsequent reduction in its byproducts, growth recovered, cellular structures were restored, oxidative stress decreased, and ribosome‑related genes were up_x001e_regulated. These findings contribute to the assessment of the potential risks of PMS to C.pyrenoidosa and provide new insights for the application of PMS in aquaculture practices.

overall_design: This study evaluated acute toxicity of PMS to Chlorella pyrenoidosa over 24-96 h to establish a 96 h EC₅₀. Chronic exposure groups (0, 1.70, 3.40, 8.49 mg/L, corresponding to 0, 0.1, 0.2, and 0.5 of the EC₅₀) were cultured for 12 days,each group at least rep 3 times. Cell growth, oxidative stress, ultrastructure, chlorophyll fluorescence, and transcriptomic genes were measured on days 0, 3, 6, 9, and 12.


title: Profiling of microRNAs in extracellular vesicles derived from mouse normal hepatocyte line AML12

city: Columbus

first: Xinlei

last: Li

state: OH

address: 700 Children's Dr

department: CCTR

institute: Nationwide Children's Hospital

summary: Previously we have shown that AML12 cell-derived extracellular vesicles (EVs) exhibit anti-fibrotic effects in human hepatic stellate cells in vitro and during toxin-induced liver injury in mice. The mechanisms by which AML12 EVs ameliorate liver fibrosis have not been fully investigated and microRNAs are among the EV payload components that are delivered to recepient cells to regulate their functionsl properties. In this study, EVs were isolated by differential centrifugation of culture supernatants from AML12 cells that ahd been maintained in serum-free conditions. The EVs were characterized by Nanosight Tracking Analysis and Western blot. Three different batches of AML12 EVs were used to isolate total RNAs by QIAGEN miRNeasy kit, and approximately 200 ng of RNAs were subjected to small RNA-seq. A total of 224 miRNAs were identified, with miR-122-5p, miR-378a-3p, miR-210-3p, miR-320-3p, and miR-125a-5p ranked as the top five most abundant miRNAs.

overall_design: AML12 cells were cultured with serum-free DMEM/F12 medium with supplements for 48 hr for supernatant collection and EV isolation. Three batches of AML12 EVs were used to isolate RNA, which was subjected to small RNA-seq.

first: Li

last: Xinlei

first: Chen

last: Ruju

first: Kemper

last: Sherri

first: Xu

last: Zhaohui

first: Brigstock

last: David


title: Radiation Induces Persistent Dysregulation and Functional Impairment in CD8+ T Cell Immunity

city: Washington

first: Henghong

state: DC

address: 3700 Reservoir Rd. NW

department: Oncology

institute: Georgetown University

summary: In addition to immediate cell lethality, radiation exposure has longer term effects on the immune system, particularly T lymphocytes, causing persistent functional abnormalities post-exposure. Uncertainties remain regarding the long-lasting consequences on T cell immunity in acute-radiation-syndrome survivors and the underlying mechanisms. Here, we investigated delayed effects of acute radiation exposure on CD8+ T cell immunity using the Listeria monocytogenes infection model. Impaired CD8+ T cells activation, reduced terminal effector formation upon infection, and exacerbated listeriosis were found in mice at four weeks post-irradiation with sublethal doses. To elucidate how radiation affects the functionality of CD8+ T cells at various differentiation stages, we performed single-cell transcriptomic profiling. Irradiation altered cluster distribution pre-infection and impaired terminal effector and memory precursor effector formation post-infection. Differential gene analysis highlights radiation-induced gene expression changes, including cytokines and mitochondrial proteins, in a cluster-specific manner post-infection. The study demonstrates dysfunction of newly replenished naïve T cells, which results in impaired CD8+ T cell immunity after irradiation.

overall_design: Following total body irradaition C57BL/6J male mice were infected with Listeria monocytogenes expressing OVA peptide. At different time points CD8+ T cells were isolated and analyzed by scRNA-seq.

first: Anika

last: Kot

first: Yun-Tien

last: Lin

first: Heng-Hong


title: STAT1-GCLM axis promotes B-cell expansion in adenoid hypertrophy

city: guangzhou

first: mengye

last: he

state: guangdong

address: guangzhou

institute: guangzhoucunzhongkeji

summary: Adenoid hypertrophy (AH) is a chronic inflammatory disorder characterized by pathological enlargement of nasopharyngeal lymphoid tissue, yet the mechanisms driving its progression remain unclear. Here, an LPS-induced inflammatory model was established in human immortalized B lymphoblastoid cells (B-LCLs). LPS stimulation increased IL-6 and TNF-α secretion and enhanced Ki67 expression, indicating an activated proliferative phenotype. RNA-seq analysis revealed marked transcriptional reprogramming, with significant enrichment of STAT signaling, glutathione metabolism, and ferroptosis-related pathways. Further experiments showed that inflammatory stimulation promoted STAT1 phosphorylation and nuclear translocation, whereas pharmacological inhibition of STAT signaling suppressed B-cell proliferation and partially reversed the inflammatory transcriptional program. Functionally, STAT inhibition partially reduced ATP production but further increased ROS accumulation, suggesting that STAT signaling contributes to both metabolic activation and redox maintenance. Mechanistically, GCLM was identified as a downstream target of STAT1 through differential gene overlap analysis and was validated by qPCR, western blotting, clinical sample analysis, and ChIP-qPCR. GCLM expression was elevated in the inflammatory model and in stage IV AH tissues, while STAT inhibition reduced GSH levels and enhanced ferroptosis-related changes. Consistently, GCLM knockdown decreased GSH content, increased lipid peroxidation, and altered ferroptosis-associated protein expression. Collectively, these findings demonstrate that the STAT1-GCLM axis sustains glutathione-dependent redox homeostasis and suppresses ferroptosis in B cells, thereby promoting AH progression.

overall_design:
Experimental Design: Role of STAT1-GCLM Axis in B-cell Ferroptosis during AH.
Objective: To investigate if the STAT1-GCLM axis regulates redox homeostasis to suppress ferroptosis in B cells, thereby facilitating Atherosclerotic Hyperlipidemia (AH) progression.
Sample Groups
Clinical: Healthy controls versus AH patients (Stage IV).
Cellular: Normal B cells, inflammatory model (ox-LDL/LPS), STAT inhibitor treatment, and GCLM knockdown (siRNA).
Key Methodologies
Gene/Protein Expression: qPCR and Western Blotting for GCLM, STAT1, and ferroptosis markers (GPX4, ACSL4).
Mechanistic Validation: ChIP-qPCR to confirm STAT1 binding to the GCLM promoter.
Redox & Ferroptosis Assays: Measurement of GSH levels and lipid peroxidation (MDA).
Expected Outcomes Elevated GCLM expression in inflammation and advanced AH. Inhibition of STAT1 or GCLM will deplete GSH, increase lipid ROS, and induce ferroptosis, confirming the axis's protective role in B cells.

first: Shilei

last: Pu

first: Ying

last: Zhu

first: Weitian

last: Zhang


title: Molecular Rejection Signatures in Pancreas Transplant Biopsies

city: Praha 4

first: Petra

last: Hruba

address: Videnska 1958

department: Transplant Laboratory

country: Czech Republic

institute: Institute for Clinical and Experimental Medicine

summary: This retrospective, single-center study included 124 pancreas allograft biopsies obtained between April 2019 and May 2025. Biopsies were analyzed using a kidney-derived Molecular Microscope® Diagnostic System (MMDx) classifier, and molecular classifications were compared with histology and related to pancreas graft survival. MMDx classified 93 biopsies (75%) as no rejection, 13 (10%) as subthreshold rejection, and 18 (15%) as rejection, whereas histology identified rejection in 65 of 112 biopsies (58%) and 25 (22%) as indeterminate cases. Concordance between histology and MMDx was low (Cohen’s κ = 0.14, p<0.001). Acute cellular histologic grading correlated strongly with multiple molecular scores, including interstitial inflammation (ρ=0.60, p=3.4×10⁻12), TCMR (ρ=0.55, p<3.2×10⁻10), acute kidney injury (ρ=0.48, p=7.4×10⁻8), and overall inflammation (ρ=0.46, p=4.4×10⁻7). Both subthreshold rejection (HR=4.41, 95% CI 1.29–15.1, p=0.018) and MMDx-defined rejection (HR=6.52, 95% CI 2.36–18.03, p=0.0003) were associated with significantly worse three-year graft survival compared to no rejection, whereas histologic classification showed no significant prognostic impact. Molecular assessment using a kidney-derived MMDx classifier provides complementary prognostic information beyond histology in pancreas transplantation.

overall_design: Whole-genome mRNA profiling was performed with Affymetrix microarrays (PrimeView Human Gene Expression, Applied Biosystems)  in 124  pancreas transplant patients collected between April 2019 and May 2025.  The primary aim of the study was to evaluate whether the existing kidney-derived rejection signatures are applicable to pancreas tissue.

first: Eva

last: Girmanova

first: Marek

last: Kollar

first: Martina

last: Mackova

last: Mrazova

first: Mariia

last: Bibik

first: Ludek

last: Voska

first: Martin

last: Kment

first: Ondrej

last: Viklicky

first: Philip F

last: Halloran

first: Peter

last: Girman


title: Peristaltic forces drive tumor cell invasion in colorectal cancer [bulk RNA-seq]

city: Los Angeles

first: Shannon

last: Mumenthaler

state: California

address: 12414 Exposition Blvd

department: Translational Research

institute: Ellison Medical Institute

summary: Mechanical forces are known to influence the progression of cancer, however, the impact of naturally occurring physical forces remains less well understood. With the advent of organ-on-chip (OOC) technology, preclinical models can now incorporate human-relevant physiological forces and allow for more precise investigation of their effects.  In this study, we explore how the peristaltic motions of the gut influence the early metastatic spread of colorectal cancer (CRC).  Specifically, we use a CRC OOC model consisting of tumor epithelial and endothelial channels separated by a porous membrane to investigate, through live cell imaging and ‘omics-based approaches, how peristaltic compressions enhance the invasiveness of colorectal cancer cells. scRNA-seq analysis revealed that invaded tumor cells exhibited significantly higher expression of mechanosensitive genes compared to non-invaded cells. Among the enriched genes was the mechanosensitive calcium ion channel, PIEZO1.  Knockdown of PIEZO1 disrupted YAP1-mediated mechanotransduction and reduced invasive capability. In contrast, exposure to peristaltic contractions enhanced invasiveness.  Analysis of publicly available datasets confirmed that elevated tumor mechanosensitive gene expression is associated with poorer clinical outcomes.  These findings reveal how physiological mechanical forces drive the invasive behavior of mechanosensitive CRC tumors.

overall_design: Following a six day period of exposure to peristaltic stretch on our organ-on-chip model, organoid cells were directly lysed and had RNA extracted for RNA sequencing

first: Curran A.

last: Shah

first: Carly

last: Strelez

first: Rachel

last: Perez

first: Christopher

last: Cherry

first: Heinz-Josef

last: Lenz

first: Shannon M.


title: Static Magnetic Fields Exposure Allievates Liver Injury via Promoting Ca 2+ Influx and Cellular Respiration

city: Xi'an

first: Xuan

last: Han

state: ShaanXi

address: Medical department of Xi'an JiaoTong University

institute: Xi'an Jiaotong University

summary: Magnetic fields influence a wide range of biological processes, from animal navigation to human cellular metabolism. Despite these diverse effects, the therapeutic mechanisms of static magnetic fields (SMFs) remain poorly understood. Here we show that SMFs exposure markedly ameliorates drug-induced liver injury in mice, including both acetaminophen- and CCl4-induced models. SMFs treatment reduced serum aminotransferases, limited collagen deposition, and improved hepatocyte survival in vitro and in vivo. Multi-omics analyses revealed pronounced metabolic reprogramming, characterized by enhanced ATP production, increased oxygen consumption, and elevated mitochondrial membrane potential. These findings indicate that SMFs promote cellular respiration and stabilize hepatic energy homeostasis under injury conditions. At the mechanistic level, SMFs increased intracellular Ca2+ influx via activation of the Piezo1 channel and enhanced malate–aspartate shuttle activity through malate dehydrogenase 1 (MDH1). Together, our study establishes SMFs as a potent modulator of hepatocyte metabolism and highlights their promise as a non-invasive therapeutic strategy for liver disease.

overall_design: RNA-seq profiling of wild type AML12 cells treated with or without static magnetic field

first: Yi

last: Lyu


title: Bulk RNA-seq of young, pre-senescent, and senescent colonic fibroblasts

city: Suwon

first: Soon Sang

last: Park

address: Worldcup-Ro 206

country: South Korea

institute: Ajou University School of Medicine

overall_design: Human primary colonic fibroblasts (HCoFi) is serially replicated in a in vitro culture model.

first: Young-Kyoung

last: Lee

first: Tae Jun


title: Cucurbitacin B induces immunogenic cell death in cutaneous melanoma via ROS-STAT3-(EIF2α-ATF4/IRE1-XBP1) pathway mediated endoplasmic reticulum stress

city: Luzhou

first: Mengdie

last: Xu

address: Taiping str.25

institute: The Affiliated Hospital of Southwest Medical University

summary: Identify the differentially expressed genes in melanoma cells after CuB treatment and identify the core biological pathways

overall_design: melanoma mRNA profiles of A375 cell treated with DMSO or CuB were generated by deep sequencing, in triplicate


title: CRISPRi lncRNA depletion screen in acute myeloid leukemia cell lines

first: Robert

last: Winkler

summary: To identify long non-coding RNAs (lncRNAs) essential for proliferation and survival of acute myeloid leukemia (AML) cells, we performed a genome-wide CRISPRi depletion screen using a custom CRISPRi lncRNA library. Six AML cell lines (K562, THP-1, ML-2, SKNO-1, M07e, NOMO-1) were screened with two biological replicates each. sgRNA representation was measured at baseline (Day 0) and after 18 population doublings. Screen hits were identified using the MAGeCK MLE algorithm with copy number variation correction.

overall_design: AML cell lines stably expressing dCas9-KRAB.MeCP2 were transduced with a custom CRISPRi lncRNA sgRNA library at 30% efficacy and cultured for 18 population doublings, ensuring a library representation of at least 1000-fold was maintained throughout. Genomic DNA was extracted from samples at the beginning and end of the screen. The integrated sgRNA cassettes were amplified by PCR, gel-purified, and sequenced on an Illumina HiSeq 2000 instrument (50 bp single-end). sgRNA counts were quantified using MAGeCK count.

first: Bruno

last: Griesler

first: Wolfgang

last: Sippl

first: Reinier

last: Boon

first: Ilka

last: Wittig

first: Marie-Laure

last: Yaspo

first: Stefan

last: Hüttelmaier

first: Raj

last: Bhayadia

first: Dirk

last: Heckl

first: Jan-Henning

last: Klusmann


title: Comparative lipidomic and transcriptomic profiling reveals distinct fatty acid utilization in T and B cells across mouse and human

city: kisarazu

first: Keiko

last: Nakano

state: chiba

address: kazusa-kamatari 2-6-7

country: Japan

institute: Kazusa DNA Research institute

summary: Lipid metabolism is increasingly recognized as a critical determinant of immune cell differentiation and function, yet the metabolic programs that distinguish closely related adaptive immune cell subsets remain incompletely defined. Here we demonstrate that T and B cells employ distinct fatty acid utilization strategies across species. Integrated lipidomic and transcriptomic analyses of mouse and human lymphocytes revealed enrichment of long-chain phospholipid species in T cells, including prominent increases in arachidonic acid–containing lipids, accompanied by elevated expression of fatty acid elongation–associated genes including Elovl5. In contrast, B cells preferentially accumulated phospholipids with shorter and/or more unsaturated acyl chains, notably with consistent enrichment of eicosapentaenoic acid–containing lipids, together with increased expression of genes involved in fatty acid uptake, desaturation, and phospholipid remodeling, including Cd36, Scd1, and Lpgat1. Acyl-chain pairing analyses further uncovered distinct organizational patterns in lipid assembly, and cross-species comparisons revealed both conserved features and marked species-specific divergence, highlighting shared metabolic principles in mouse and human lymphocytes. Our data indicate that differential fatty acid elongation, uptake, and remodeling programs shape lineage-specific lipid architectures and contribute to metabolic specialization in adaptive immune cells.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Related to Fig 3 and 4. RNA-seq was performed to investigate differences in the role of fatty acid metabolism in regulating gene expression between T and B cells.

first: Kiyoe

last: Sumi

first: Keisuke

last: Miyako

first: Arisa

last: Ito

first: Toshiyuki

last: Kobayashi

last: Yamamoto

first: Yukie

last: Iwao

first: Toshio

last: Kanno

first: Takaharu

last: Kimura

first: Satoru

last: Yokoyama

first: Kazuko

last: Yamada

first: Hikari

middle: K

last: Asou

first: Mayumi

last: Maruyama

first: Yoko

last: Suzuki

first: Yusuke

last: Kawashima

first: Osamu

last: Ohara

last: Endo


title: Sphingosine kinase 2 regulates adipocyte browning and whole-body metabolism [CUT&Tag]

city: Richmond

first: Christopher

last: Green

state: Virginia

address: 1101 E. Marshall St.

institute: Virginia Commonwealth University

summary: Obesity increases circulating levels of the bioactive sphingolipid metabolite sphingosine-1-phosphate (S1P).  Here, we identify adipocyte-expressed sphingosine kinase 2 (SPHK2), an enzyme that produces S1P, as a regulator of adipose tissue browning. Mice with adipocyte-specific deletion of Sphk2 were protected from Western diet-induced obesity concomitantly with elevated energy expenditure and browning of subcutaneous fat and enhanced expression of Ucp1 and key thermogenic genes, resulting in reduced adiposity and hepatic steatosis, improved glucose tolerance and insulin sensitivity. Mechanistically, obesogenic diet promoted nuclear localization of SPHK2 in adipocytes, where it cooperated with transcription factors to suppress the thermogenic transcriptome. Adipocyte SPHK2 was responsible for maintaining homeostatic circulating S1P levels and driving the pathogenic rise of S1P in response to obesogenic diet. Our findings reveal a distinct role of adipocyte SPHK2 in regulation of the thermogenic program important for whole-body metabolic homeostasis and energy expenditure and highlights SPHK2 as a potential therapeutic target for treatment of metabolic disorders.

overall_design: CUT&Tag (Cleavage Under Targets and Tagmentation) sequencing to profile genome-wide histone acetylation at H3K9 and H3K27 in male wild-type and adipocyte-specific Sphk2 deleted subcutaneous white adipose tissue after eighteen weeks on a high fat, high sugar Western diet.

first: Ryan

last: Brown

first: Christiane

last: Carter

first: Katarzyna

last: Tyc

first: Sarah

last: Spiegel


title: Letrozole alters transcriptomic profiles in infrapatellar fat pad from female mice: Possible involvement of aromatase inhibitor-induced arthralgias

city: Suzhou

first: Xiaoyu

last: Lin

address: No. 100, Chongwen Road, Suzhou Industrial Park

institute: Suzhou Institute of Systems Medicine

summary: Letrozole, is an aromatase inhibitors (AIs) preventing estrogen synthesis from testosterone, and it induces many side effects, known as the aromatase inhibitor-associated musculoskeletal syndrome (AIMSS), including arthralgias. The infrapatellar fat pad (IFP), rectus femoris and tendon are critical structural and functional components of the knee musculoskeletal system. The IFP is metabolically active and acts as a key regulator of joint inflammation and homeostasis. Meanwhile, rectus femoris and tendon tissues are highly susceptible to estrogen fluctuation and inflammatory insult, making them pivotal peripheral targets closely linked to the onset and progression of AIMSS. However, how letrozole intervention induces pathological and molecular alterations in these three key tissues remains unclear. Given the above research gaps,We integrated transcriptomic profiling to characterize molecular signatures underlying letrozole-related musculoskeletal injury. This work aims to uncover the potential aetiological mechanisms of AIMSS and identify novel molecular biomarkers and therapeutic targets for the early prevention and clinical intervention of AIMSS.

overall_design: RNA _Seq library constructioniwith rigorous auaity contro ait each step,Startina fom RNA aualityassessment , followed by efficient mRNA enrichment, precise library size selection during fragmentationand adapter ligation, and final library quantifcation and quality validation before sequencing on the illumina platform.

first: Shuping

last: Mo


title: Rewiring of the transcriptome of breast cancer cells in 3D organotypic cultures promotes cancer progression through SNHG7/miR-486-3P/HIF1A axis

city: Mexico City

first: Yarely M.

last: Salinas-Vera

address: Av Instituto Politécnico Nacional 2508, San Pedro Zacatenco, Gustavo A. Madero, 07360 Mexico City, CDMX

department: Biochemistry

country: Mexico

institute: Centro de Investigación y de Estudios Avanzados del IPN

summary: Three-dimensional (3D) organotypic cell cultures more accurately recapitulate the spatial architecture, biological, and epigenetic features of tumors than traditional two-dimensional (2D) monolayer models, thus representing an innovative approach in cancer research. However, the impact of the 3D microenvironment on the reprogramming of non-coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs in breast cancer cells, remains unexplored. To fill this knowledge gap, we performed RNA sequencing to identify the differential transcriptome of 3D versus 2D cell cultures and novel potential therapeutic targets. Our data showed that the Hs-578T breast cancer cells grew as stellated 3D structures over an extracellular matrix protein- enriched scaffold. Expression profiling data revealed that 88 lncRNAs, 218 microRNAs, and 2,806 mRNAs were modulated in Hs-578T cells under 3D conditions. Regulated protein-encoding genes were found to be associated with cell proliferation, migration, and chemoresistance. Interestingly, coregulatory network analyses reveal a positive regulation of a set of hypoxia-responsive genes related to the lncRNA-SNHG7/miR-486-3p/HIF1A axis in 3D cultures. SNHG7 and HIF1A expression were upregulated, whereas miR-486-3p was downregulated in 3D cultures, correlating with poor overall survival in cancer patients. Functional studies in the 3D environment indicate that the knockdown of SNHG7 abolishes cell proliferation and invasion, while activating apoptosis, thereby sensitizing cancer cells to cisplatin. Furthermore, a significant increase in hypoxic internal regions was found in SNHG7-deficient 3D structures. In conclusion, our data suggested that the 3D architecture of cells reprograms the transcriptional programs of breast cancer cells. Importantly, SNHG7 plays a key role in cancer progression, representing a promising novel therapeutic target for breastcancer.

overall_design: Transcriptomic profiling by RNA-seq was performed on Hs578T breast cancer cells cultured in 2D and 3D conditions. LncRNAs, miRNAs and mRNAs were analysed to identify differences in gene expression associated with the 3D microenvironment.

first: Yarely

first: Jesús

last: Valdés

first: Yussel

last: Pérez-Navarro

first: Stephanie

middle: I

last: Nuñez-Olvera

first: Mercedes

last: Bermúdez

first: Eloisa

last: Ibarra-Sierra

first: María

last: Álvarez-Sánchez

first: Nancy

last: Martínez-Rodríguez

first: Macrina

last: Silva-Cázares

first: Laurence

last: Marchat

first: Cesar

last: López-Camarillo


title: RNA Sequencing Reveals Differential Gene Expression in Human Brain Microvascular Endothelial Cells (HBMECs) Subjected to Oxygen-Glucose Deprivation/Reperfusion (OGD/R)

city: Wuhan

first: Haipeng

last: Wang

address: Shizishan Rd, Wuhan, Hubei

institute: Huazhong Agriculture Unversity

summary: Human brain microvascular endothelial cells (HBMECs) are a critical component of the blood-brain barrier (BBB), and their stability is paramount for BBB integrity, particularly under pathological stress such as ischemic stroke. This study employed an *in vitro* model of ischemia-reperfusion injury using oxygen-glucose deprivation followed by reperfusion (OGD/R) on cultured HBMECs. To comprehensively characterize the transcriptional response, we performed high-throughput RNA sequencing (RNA-seq) on both OGD/R-treated and control (normoxic) HBMEC samples. Our analysis identified a significant number of differentially expressed genes (DEGs) associated with the OGD/R challenge. These DEGs encompass genes involved in key biological processes pertinent to endothelial cell dysfunction, BBB disruption, inflammatory responses, oxidative stress, apoptosis, and potential protective/repair mechanisms. This dataset provides a detailed transcriptional profile of HBMECs undergoing simulated ischemia-reperfusion injury. It serves as a valuable resource for elucidating the molecular mechanisms underlying BBB compromise in ischemic stroke and for identifying novel potential therapeutic targets aimed at preserving BBB function and mitigating neuronal damage.

overall_design: RNA-seq analysis of HBMEC cultured in normal condition and after OGD/R treatment

first: Zhiqiang

last: Dong


title: Effects and mechanisms of blueberry extract on improving age-related sperm motility in mice by alleviating inflammatory responses

city: Nanjing

first: Lu

last: Guo

email: 3230204169@qq.com, luguo280@gmail.com

state: Jiangsu

address: Xuanwu District of Nanjing City, Jiangsu Province.

department: College of Animal Science and Technology

institute: Nanjing Agricultural University

summary: Aging leads to progressive decline in male fertility, characterized by structural degeneration of the seminiferous epithelium and oxidative imbalance. Objective: This study aimed to evaluate the efficacy of Blueberry Extract (BBE) in ameliorating reproductive aging and to elucidate the underlying molecular mechanisms involving cell fate determination. Methods: Aging male ICR mice (8 months old) were treated with varying doses of BBE. Testicular histology, sperm quality, and expression of key germ cell markers were analyzed. Results: BBE administration significantly alleviated body weight loss, reduced seminiferous tubule vacuolization, and improved sperm motility parameters in aging mice. Immunofluorescence and Western Blot analyses revealed that BBE successfully reconstituted the germline population, as evidenced by the upregulation of DDX4. Notably, a dose-dependent divergence in cellular fate was observed: high-dose BBE significantly promoted the self-renewal of PLZF+ spermatogonial stem cells (SSCs), whereas low/medium doses preferentially upregulated STRA8 to drive meiotic differentiation. This cell fate remodeling was associated with a "U-shaped" regulation of the cell cycle regulator CCND1 and enhanced SIRT1 expression. Conclusion: BBE mitigates age-related spermatogenic failure by orchestrating a delicate balance between SSC self-renewal and differentiation via the SIRT1 pathway. These results position BBE as a promising functional food ingredient for preserving male reproductive health.

overall_design: In this study, 8-month-old male ICR mice were utilized to simulate natural reproductive senescence. The animals were randomly assigned into four groups: the model group and three BBE treatment groups. The model group received physiological saline, while the treatment groups were administered BBE at doses of 50, 100, and 200 mg/kg/day, respectively, via daily intragastric gavage. Following the treatment period, samples were collected for multi-dimensional analysis, including sperm motility assessment (CASA), testicular morphological observation (H&E staining), and protein expression analysis (Western Blot and Immunofluorescence).

first: Ziang

last: Zhang

first: Feifei

last: Li

first: Hairui

last: Tian


title: SMD2 reads pseudouridines to regulate mRNA splicing and promote tumorigenesis [PAR-CLIP]

city: Shanghai, P.R. China

first: weiying

last: meng

address: 1239 Siping Road, Shanghai, P.R. China

institute: Tongji University

summary: Pseudouridines (Ψ) in mRNA are linked to alternative splicing, but their regulatory mechanisms remain unclear due to the lack of identified reader proteins. Here, we identify SMD2, a core spliceosomal component, as a direct Ψ reader. Using in vitro and ex vivo assays, we show that SMD2 preferentially binds Ψ over unmodified uridines. SMD2 collaborates with PUS family enzymes to regulate alternative splicing by binding Ψ near exon-intron boundaries, modulating the splicing of numerous pre-mRNAs. Notably, the gene encoding SMD2, SNRPD2, is overexpressed across multiple cancers and is essential for tumor cell proliferation through the maturation of key transcripts. These findings uncover a direct mechanistic link between Ψ and spliceosomal function, establishing SMD2 as a critical regulator of Ψ-mediated splicing and a potential cancer therapeutic target.

overall_design: Since RIP-seq is prone to false-positive interactions despite stringent washing conditions, we next employed photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation followed by high-throughput sequencing (PAR-CLIP-seq) to validate the interaction between Ψ and SMD2.

first: Weiying

last: Meng

first: Moping

last: Xu

first: Shuxia

last: Sun

first: Zhiyan

first: Jiejun

last: Shi


title: Identification of a silencer-like non-coding RNA transcribed from a region on the super-enhancer conferring B-cell lymphomagenesis

city: Matsudo City

first: Jinichi

last: Mori

state: Chiba

address: 107-1 Kanegasaku

institute: Chibanishi General Hospital

summary: Super-enhancers (SEs) orchestrate lineage-specific transcriptional programs and are frequently co-opted in cancer to sustain oncogenic gene expression. However, the functional complexity of SE-derived non-coding RNAs in B-cell lymphoma remains poorly understood. Here, we identify a lymphoma-specific SE located between the RGS1 and RGS13 loci (RGS-SE) through integrative in silico analysis of diffuse large B-cell lymphoma (DLBCL) enhancer landscapes. CRISPR/Cas9-mediated deletion of RGS-SE markedly impaired proliferation of Burkitt lymphoma cells and suppressed xenograft tumor growth, establishing its oncogenic relevance. Capture Hi-C revealed physical interactions between RGS-SE and the promoters of both RGS1 and RGS13, indicating a cis-regulatory architecture. Unexpectedly, transcriptomic analyses demonstrated that RGS-SE deletion increased RGS1 expression while modestly affecting RGS13, suggesting non-canonical regulatory activity. We further identified an SE-derived non-coding RNA (RGS-ncRNA) whose site-specific induction suppressed RGS1 transcription, whereas CRISPR interference modestly de-repressed it. Chromatin profiling revealed enrichment of H3K27me3 and PRC2 components within the RGS-ncRNA-coding region, consistent with silencer-like properties. Collectively, our findings uncover an oncogenic SE-ncRNA axis that functions not only as a classical enhancer but also as a PRC2-associated repressive module, expanding the conceptual framework of SE biology.

overall_design: RNA-seq and ATAC-seq were performed on wild-type and RGS-SE knockout (CRISPR/Cas9) Raji Burkitt lymphoma cells. RGS-SE knockout cells were generated by CRISPR/Cas9-mediated deletion of the super-enhancer region between RGS1 and RGS13 on chromosome 1. Each condition (wild-type and RGS-SE knockout) includes 2 biological replicates. Library preparation and sequencing were performed by DNAFORM Inc.

first: Mori

last: Jinichi

first: Sawada

last: Takahiro

first: Kanemoto

last: Yoshiaki

first: Kashimura

last: Miho

first: Nojiri

last: Koki

first: Kurokawa

last: Tomohiro

first: Sugimoto

last: Kotaro

first: Chiba

last: Hideki

first: Osato

last: Naoki

first: Hamada

last: Michiaki

first: Kato

last: Shigeaki


title: Bioinformatics analysis of lncRNA and mRNA differentially expressed in patients with cervical cancer [Agilent array]

city: zunyi

first: Xiaohua

last: An

state: guizhou

address: No. 149, Dalian Road, Huichuan District

department: Department of Clinical Laboratory

institute: The Third Affiliated Hospital of Zunyi Medical University

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

summary: To verify the expression profile of long non-coding RNAs (lncRNAs) and mRNAs in cervical cancer, identify their clinical significance in HPV16-associated cervical cancer, and annotate the biological function of mRNAs.

overall_design: Three pairs of cancerous and paracancer tissues were selected in cervical squamous cell carcinoma (IB2 stage), high-throughput sequencing was utilized to determine the expression levels of lncRNAs and mRNAs.


title: Spatial transcriptomic analysis of rat gut tissue reveals transcriptional changes associated with high-fat diet and tirzepatide treatment

city: Saskatoon

first: Changting

last: Xiao

state: SK

address: 107 Wiggins Rd

institute: University of Saskatchewan

summary: This study investigates spatial gene expression changes in rat gut tissue under different dietary and treatment conditions using 10x Genomics Visium spatial transcriptomics. Four experimental groups were analyzed: control diet with PBS treatment (CD_PBS), control diet with tirzepatide treatment (CD_TZP), high-fat diet with PBS treatment (HFD_PBS), and high-fat diet with tirzepatide treatment (HFD_TZP).  Spatial transcriptomic libraries were generated using the 10x Genomics Visium platform and sequenced on an Illumina sequencing platform. Raw sequencing data were processed using the SpaceRanger pipeline to generate gene-barcode matrices and spatial coordinates. Downstream analyses included cell type annotation, differential gene expression analysis, and gene ontology enrichment analysis.  These data provide insight into the spatial molecular mechanisms associated with metabolic disease and therapeutic intervention.

overall_design: Four rat gut tissue samples representing different diet and treatment conditions were analyzed using spatial transcriptomics. Samples included CD_PBS, CD_TZP, HFD_PBS, and HFD_TZP. Spatial gene expression libraries were prepared using 10x Genomics Visium and sequenced using paired-end sequencing. Differential expression analysis was performed between treatment groups, particularly HFD_TZP vs HFD_PBS.

first: Ying

last: Wang

first: Tao


title: Transcriptome regulation by miR-210 in hypoxic glomerular endothelium [miRNA-Seq]

city: Singapore

first: Chong Yun

last: Pang

address: 60 Nanyang Dr, School of Biological Sciences

institute: Nanyang Technological University

summary: Hypoxia occurs in both acute and chronic kidney diseases. Despite the central role of tubular injury in acute kidney injury (AKI), a hallmark feature is a reduction in glomerular filtration rate. There is now an increasing interest in the effect of direct injury to the renal vasculature and its potential role in the pathogenesis of AKI. In this study, we profiled glomerular endothelial miRNA and mRNA changes in response to hypoxia in vitro. We identified significant induction of a hypoxia associated miRNA, miR-210-3p, which enhanced cellular glycolytic capacity. Furthermore, integrated transcriptomic analysis identified HIF1A and TFRC as putative miR-210-3p targets. This was corroborated by the strong correlation in glomerular endothelial TfR1 and HIF-1α protein expression in kidney tissue samples. Collectively, our study uncovered a compensatory mechanism in which miR-210-3p supports glomerular endothelial adaptation by modulating bioenergetics, thereby fine-tuning hypoxia responses and limiting cellular injury.

overall_design: Primary glomerular endothelial cells cultured in hypoxic incubator for 4, 12 and 24 hours to mimic renal ischemia. Subsequently, total RNA was extracted for RNA-seq and miRNA seq.

first: Jenny

last: Gilmour

first: Simon

last: Satchell

first: John

last: Kirby

first: Neil

middle: S

last: Sheerin

first: Simi

last: Ali


title: ICAM1 expression and associated clinical parameters as predictive biomarkers for acute celluar rejection

city: Kunming

first: Fen

last: Huang

address: 727 Jingming Rd

institute: Ku

summary: Background: Acute cellular rejection (ACR) remains a significant complication after liver transplantation (LT). To identify pre-transplant biomarkers and elucidate the underlying immune mechanisms predisposing recipients to ACR, LT recipients were enrolled. Methods: Clinical parameters were analyzed pre- and post-LT. Single-cell RNA sequencing (scRNA-seq) was performed on pre-LT liver biopsies to characterize the immune microenvironment. Functional assays were performed in vitro and in vivo. Results: Pre-LT hepatitis virus infection was an independent risk factor for ACR. scRNA-seq revealed a distinct pre-LT immune landscape in patients who developed into ACR with a reduced proportion of T/NK cells but an enrichment of highly cytotoxic NK subsets (e.g., NK⁺_GNLY⁺), which was associated with downregulation of key adhesion molecules, particularly the ICAM1-ITGB2 (LFA-1) axis. ICAM1 knockdown impaired macrophage migration and synapses formation in vitro and suppressed the MAPK-ERK pathway. Clinically, low intrahepatic ICAM1 expression pre-LT correlated with diminished leukocyte infiltration (CD45⁺, CD18⁺), increased post-transplant collagen deposition, and more severe ACR. Furthermore, recipient ICAM1 levels strongly correlated with distinct serum parameter profiles, negatively with early post-LT ALT and positively with pre-LT bilirubin levels. Conclusion: Results suggest that a pre-LT state of dysregulated cytotoxicity and impaired immune cell adhesion/migration, characterized by low ICAM1 expression and a suppressed MAPK pathway, predisposes patients to ACR. ICAM1 expression, combined with specific bilirubin and liver enzyme profiles, emerges as a promising integrated biomarker for predicting rejection risk.

first: Siming

last: Qu

first: Huichan

last: Liu

first: Yang

last: Sun

first: Zhong

last: Zeng


title: GATA2 coordinates pluripotency exit and meiotic initiation in female fetal germ cells [scRNA-seq]

city: Guangzhou

first: Zhenyi

address: ShaTaiNan Street 1023-1063,Baiyun

institute: Southern Medical University

summary: NOT PROVIDED; REQUESTED

overall_design: NOT PROVIDED; REQUESTED

first: Xiaoyang

last: Zhao

first: Manman

last: Cui


title: Dual regulation of CXCR6+CD8+ T cells drives immune exhaustion in the progression of prostate cancer [PB-Cre; Pten knockout and WT]

city: Shanghai

first: Xingming

last: Zhang

address: No. 270, Dong'an Road, Xuhui District, Shanghai

institute: Fudan University Shanghai Cancer Center

summary: Prostate cancer (PCa) is widely recognized as an immunologically "cold" malignancy, characterized by limited responsiveness to immune checkpoint blockade. To disclose the mechanisms underlying immune exclusion, we performed single-cell RNA sequencing (scRNA-seq) of tumor-infiltrating immune cells from patients with PCa and identified a previously unappreciated subset of CXCR6+CD8+ cytotoxic T lymphocytes (CXCR6+ CTLs). Notably, the abundance of these cells was inversely correlated with Gleason Score (GS), indicating progressive depletion in advanced stages of PCa. Mechanistically, this depletion is modulated by dual converging pathways. On the one hand, reduced infiltration of M1-like macrophages in higher-grade tumors leads to diminished production of CXCL16, thereby impairing the recruitment of CXCR6⁺ CTLs; On the other hand, IL-10 derived from the tumor microenvironment, partly from M2-like macrophages, downregulates CXCR6 expression via the IL10–FOXO1–KLF2 transcriptional axis. SCENIC analysis and further identified KLF2 as a central transcriptional regulator governing CD8⁺ T cell fate, reinforcing its role in T cell dysfunction. Collectively, our findings delineate a multifaceted mechanism of T cell exclusion in advanced PCa and suggest that targeting the transcriptional axis to restore CXCR6⁺ CTL infiltration or sustain CXCR6 expression in CD8+ T cell, when combined with anti-PD1 therapy, may potentiate anti-tumor immunity and surmount resistance to immunotherapy in this disease.

overall_design: To confirm whether the level of IL-10 is elevated in the PCa microenvironment, we performed bulk RNA-seq on prostate tissues from Pb-Cre, Ptenflox/flox mice (T) and wild-type (WT) controls (n = 3/group). Differential expression analysis (cut offs |log2FC| ≥ 1.5, FDR < 0.05) revealed widespread transcriptional reprogramming in Pten-null prostates. Notably, Il10 was markedly upregulated in tumors together with canonical M2‐like macrophage markers (Mrc1, Cd163) and myeloid/immune-regulatory genes (C1qa/b/c, C3, Ccl2).

first: Leilei

last: Du

first: Wenfeng


title: CircROBO2 Orchestrates Osimertinib Resistance Through miR-625-5p/PDGFB-Mediated MAPK Activation in Non-Small Cell Lung Cancer

city: Lanzhou

first: Miao

last: He

state: Gansu

address: No.82, Cuiyingmen street, Chengguan District

institute: Lanzhou University Second Clinical Medical School: Lanzhou University Second Hospital

summary: Background: The emergence of acquired resistance to osimertinib represents a formidable therapeutic challenge in the management of non-small cell lung cancer (NSCLC). While circular RNAs (circRNAs) have been increasingly recognized as crucial modulators of chemotherapeutic resistance, their specific involvement in osimertinib resistance mechanisms remains poorly elucidated. Methods: We established osimertinib-resistant NSCLC cell lines (HCC4006OR) through prolonged drug exposure and conducted comprehensive transcriptome sequencing to identify differentially expressed circRNAs. The molecular characteristics and functional implications of circROBO2 were systematically investigated utilizing an array of cellular and molecular biological methodologies. Advanced molecular dynamics simulations were implemented to elucidate the potential molecular interactions between PDGFB and osimertinib. Results: We identified circROBO2 as significantly upregulated in osimertinib-resistant HCC4006OR cells. Functional studies revealed that circROBO2 enhances cell survival, proliferation, and invasion while suppressing apoptosis under osimertinib treatment. Mechanistically, circROBO2 functions as a molecular sponge for miR-625-5p, resulting in elevated PDGFB expression and subsequent activation of the MAPK pathway, particularly the RAF/MEK/ERK cascade. Targeting this pathway through circROBO2 knockdown or miR-625-5p overexpression partially restored osimertinib sensitivity in resistant cells. Molecular dynamics simulations suggested potential direct interactions between PDGFB and osimertinib, providing additional insights into the resistance mechanism. Conclusions: Our study identifies a novel circROBO2/miR-625-5p/PDGFB regulatory axis in osimertinib resistance and positions circROBO2 as a potential therapeutic target and biomarker for NSCLC treatment.

overall_design: circRNA-, miRNA-, mRNA-seq of Human derived non-small cell lung cancer cells under Mock and  Drug resistance experiment group


title: DNA methylation predicts hippocampus-dependent long-term memory, but not memory updating

city: Irvine

first: Jiachun

last: Li

state: CA

address: Samueli School of Engineering University of California, Irvine

institute: University of California Irvine

summary: DNA methylation-based epigenetic clocks estimate biological age and (in combination with clinical biomarkers) can predict complex behavioral phenotypes. We established a methylation clock highly predictive of chronological age, as well as two methylation predictors for long-term memory performance. CpG sites that accurately predicted chronological age were distinct from sites predictive of long-term memory performance, suggesting specific methylation signatures underlie cognitive function independent of aging.

overall_design: Mice were anesthetized through intraperitoneal (IP) injection of sodium pentobarbital (50mg/mL) and perfused transcardially with ice-cold PBS, pH 7.4, using a peristaltic perfusion pump (Thermo Fisher Scientific, Waltham, MA) 24 hours after the final 48hr Test session (Fig. 1A). All tissue collection proceeded within the same 2-hour time window as the behavior in order to avoid circadian effects. To do so, a maximum of two cohorts (two age groups) underwent behavior and subsequently tissue collection to ensure all procedures fell within the time window. Upon successful perfusion, the dorsal hippocampus was bilaterally dissected and flash frozen in isopentane. All samples were processed simultaneously to avoid batch effects.

first: Carlene

last: Chinn

first: Joseph

last: Picone

first: Maria

middle: F

last: de Albuquerque

first: Timothy

last: Downing

first: Marcelo

last: Wood


title: Epigenomic profiling of human developing cerebellum [EM-seq]

city: Toronto

first: Shraddha

last: Pai

state: ON

address: 160 College Street, Room 602

institute: University of Toronto

summary: The cerebellar rhombic lip neural progenitor niche of the prenatal hindbrain is an anatomical structure critical for cerebellar glutamatergic neurogenesis.  Humans have elaborated the rhombic lip niche to include a rhombic lip subventricular zone (RL-SVZ) not seen in mice or macaques. Although developmental disruptions of this progenitor zone can cause cerebellar growth abnormalities – from malformations to tumors – the gene regulatory networks underpinning this unique progenitor niche are unknown. Here we provide a predicted gene regulatory network for the human cerebellar rhombic lip, inferred from epigenomic maps of the developing human cerebellum. We generated DNA methylomes of neuroanatomically-dissected mid-gestation human rhombic lip ventricular zone and RL-SVZ (N=9 samples; 15-16 post conception weeks) using low-input Enzymatic MethylSeq.  We also mapped histone modifications marking active promoters and enhancers in the whole mid-gestation human fetal cerebellum (N=6 samples; 14 and 18 post-conception weeks). Integrating these data, we identified 9,855 differentially-methylated regions (DMR) which converge on binding sites of over three hundred transcription factors, including master regulators of rhombic lip neurogenesis, ATOH1, NEUROD1, and NEUROD2. DMRs hypomethylated in the RL-SVZ are enriched in active enhancers and in human accelerated regions, and are depleted in active promoters. We inferred 81,844 transcription factor-enhancer-gene links, covering 41 transcription factors active in the rhombic lip, and 4,610 target genes that include drivers of cerebellar neurogenesis and pediatric hindbrain cancer. Twenty-five DMRs overlap human accelerated regions located near genes associated with intellectual disability, autism spectrum disorders, and neurological deficits. DMRs are also statistically enriched in copy number aberrations in medulloblastoma, a malignant pediatric hindbrain cancer with subtypes hypothesized to originate in the rhombic lip. Close to one-quarter of the DMRs overlap known copy number aberrations in medulloblastoma, nominating potential enhancer and promoter elements impacted by these genomic aberrations. Collectively, our data provide a rich resource to start decoding the functional impact of non-coding variation on gene regulation in the developing cerebellum and on genomic dysregulation in diseases of cerebellar growth.

overall_design: We received frozen mid-gestation human hindbrains from the University of Maryland Brain and Tissue Bank. Tissue cryosectioning and immunohistochemistry was performed by the University Health Network Pathology Research Program Laboratory. Brain tissue was cryosectioned on the mid-sagittal plane and stained for cresyl violet, SOX2 (CST Sox2 (D6D9) XP Rabbit mAb #3579) and KI67 (Dako #M7240 Mouse monoclonal antibody). The rhombic lip was identified at the edge of the fourth ventricle by its size and prominent KI67+ staining. Selected sections were stained with CD34 (Dako #M7165 Monoclonal Mouse Anti-Human) and GFAP (Dako #Z334) to identify the vascular bed that separates the rhombic lip ventricular zone and subventricular zone. Using immunohistochemistry, we identified the rhombic lip ventricular (SOX2+ KI67+) and subventricular (SOX2- KI67+) zone in each sample. We used laser capture microdissection (LCM) to isolate tissue separately from the rhombic lip ventricular zone and subventricular zone. LCM was performed by the Ontario Institute for Cancer Research Tissue Portal using the Leica LMD6 instrument; cresyl violet was used to visualize the tissue. We extracted nucleic acid from each tissue compartment, and generated DNA methylome profiles using the Enzymatic Methyl-seq assay (EM-seq; NEBNext Enzymatic Methyl-seq; Illumina NovaSeq 6000 and NovaSeq X; 150bp paired-end reads; OICR Genomics Core).


title: Static Magnetic Fields Exposure Allievates Liver Injury via Promoting Ca 2+ Influx and Cellular Respiration [scRNA-Seq]

city: Xi'an

first: Xuan

last: Han

address: Medical department of Xi'an JiaoTong University

institute: Xi'an Jiaotong University

summary: Magnetic fields influence a wide range of biological processes, from animal navigation to human cellular metabolism. Despite these diverse effects, the therapeutic mechanisms of static magnetic fields (SMFs) remain poorly understood. Here we show that SMFs exposure markedly ameliorates drug-induced liver injury in mice, including both acetaminophen- and CCl4-induced models. SMFs treatment reduced serum aminotransferases, limited collagen deposition, and improved hepatocyte survival in vitro and in vivo. Multi-omics analyses revealed pronounced metabolic reprogramming, characterized by enhanced ATP production, increased oxygen consumption, and elevated mitochondrial membrane potential. These findings indicate that SMFs promote cellular respiration and stabilize hepatic energy homeostasis under injury conditions. At the mechanistic level, SMFs increased intracellular Ca2+ influx via activation of the Piezo1 channel and enhanced malate–aspartate shuttle activity through malate dehydrogenase 1 (MDH1). Together, our study establishes SMFs as a potent modulator of hepatocyte metabolism and highlights their promise as a non-invasive therapeutic strategy for liver disease.

overall_design: RNA-seq profiling of wild type AML12 cells treated with or without static magnetic field

first: Yi

last: Lyu


title: Cytokine-induced Expandable Memory NK Cells with Significant Metabolic, Epigenetic Remodeling, and Persistence Properties

first: Hongye

last: Wang

address: 1239 Siping Road, Yangpu District, Shanghai

summary: Recent investigations have indicated that NK cells induced overnight with IL-12/15/18 cytokines possess memory-like characteristics (refers as CIML NK, cytokine induced memory-like NK cells), demonstrating enhanced effector function and prolonged persistence. Preclinical studies and very early clinical trials revealed the promising clinical activity of CIML NK cells in the treatment of hematological malignancies, especially acute myelocytic leukemia (AML). However, the current manufacturing method for CIML NK cells do not endow these cells the ability to expand robustly ex vivo. The low production efficiency limits their clinical application. In this study, we established a novel expansion platform for these memory-like NK cells. This method can effectively and stably expand healthy donor-derived Peripheral NK (PBNK) cells by more than 200-fold within two weeks, with a purity exceeding 95%. Importantly, these ex vivo expanded NK (ExNK) cells exhibited hypomethylated state in the CNS-1 region (Conserved Noncoding Sequence 1) of IFNG gene, stronger metabolic ability, and enhanced effector function when compared to CIML NK cells. Based on these features, we named these expanded NK cells but still possess memory-like characteristics as mExNK (memory-like expanded NK cells). Bulk mRNA-seq further firmly uncovered a high similarity between mExNK and CIML NK cells, with both highly expressing genes being related to proliferation, metabolism, and memory. Furthermore, we also test that these mExNK cells are superior much more than conventional expanded ExNK cells (cExNK). Taken together, the method described herein showed an enhanced expansion efficiency for human memory NK cells and would facilitate their clinic applications in cancer therapy.

overall_design: RNA-seq profiling of PBNK (human peripheral blood NK) cells at D0, CIML NK (cytokine induced memory-like NK) cells at D5, mExNK (memory-like expanded NK) cells at D14, cExNK (conventional expanded NK) cells at D14;


title: GATA2 coordinates pluripotency exit and meiotic initiation in female fetal germ cells [CUT&Tag]

first: Zhenyi

last: Huang

state: GuangDong

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

overall_design: Refer to individual Series

first: Jiexiang

first: Xinyan

last: Yang


title: GATA2 coordinates pluripotency exit and meiotic initiation in female fetal germ cells [ATAC-Seq]

first: Xiaoyang

last: Zhao

first: Manman


title: Astrocytic Regulation of aberrant perineuronal net formation in Mecp2-null Neocortex

city: Syracuse

first: Jessica

middle: L.

last: MacDonald

state: NY

address: 107 College Place

department: Biology

institute: Syracuse University

summary: Rett syndrome (RTT), caused by mutations in MECP2, is a complex neurological disorder characterized by myriad physiological disruptions, including early closure of the critical period of developmental plasticity and precocious formation of perineuronal nets (PNNs). PNNs are lattice-like substructures of extracellular matrix (ECM) that enwrap specific subpopulations of neurons. PNNs are essential in the modulation of neuronal plasticity and brain maturation, and their enzymatic disruption can partially restore plasticity in adults and improve memory. Although precocious PNN formation is well-established in RTT, there is little known of the cellular, molecular, or biochemical underpinnings of their precocious formation. Further, whether precocious PNN formation is due to cell-autonomous or non-cell-autonomous mechanisms is not fully understood. While PNNs form on subsets of neurons throughout the brain, astrocytes secrete many ECM components that form PNNs, and they play a central role in controlling closure of the critical period. We have found increased expression of both neuron- and astrocyte-derived PNN components in the developing Mecp2-null cortex, and demonstrate that PNNs are structurally and biochemically mature at an earlier developmental stage. Further, Mecp2-null astrocyte conditioned media induces the expression of the key PNN component Hapln1 and causes enhanced PNN formation on wildtype neurons. This suggests that Mecp2-null astrocytes play a key role in the precocious formation of PNNs in RTT. These results provide essential insight into the mechanisms and structure of aberrant PNNs in Mecp2-null cortex, and identify potential new avenues for targeted rescue or reversal of the precocious closing of the critical period in RTT.

overall_design: RNA-seq profiling to determine changes in the transcriptome of neurons in response to astrocyte conditioned media, and to determine whether Mecp2 mutant astrocyte conditioned media (KO ACM) induces distinct neuronal transcriptome changes than wildtype astrocyte conditioned media (WT ACM).

first: Ashis

last: Sinha

first: Angelica

last: Kowalchuk

first: Nasim

last: Khatibi