title: MicroRNAs modulating angiogenesis: miR-129-1 and miR-133 act as angio-miR in HUVECs.
abstract: The sprouting of new blood vessels by angiogenesis is critical in vascular development and homeostasis. Aberrant angiogenesis leads to enormous pathological conditions such as ischemia and cancer. MicroRNAs (also known as miRNAs or miRs) play key roles in regulation of a range of cellular processes by posttranscriptional suppression of their target genes. Recently, new studies have indicated that miRNAs are involved in certain angiogenic settings and signaling pathways use these non-coding RNAs to promote or suppress angiogenic processes. Herein, VEGFR2 and FGFR1 were identified as miR-129-1 and miR-133 targets using bioinformatic algorithms, respectively. Afterwards, using luciferase reporter assay and gene expression analysis at both mRNA and protein levels, VEGFR2 and FGFR1 were validated as miR-129-1 and miR-133 targets. In addition, we showed that miR-129-1 and miR-133 suppress angiogenesis properties such as proliferation rate, cell viability, and migration activity of human umbilical vein endothelial cells (HUVEC) in vitro. We conclude that these miRNAs can suppress key factors of angiogenesis by directly targeting them. These results have important therapeutic implications for a variety of diseases involving deregulation of angiogenesis, including cancer.
authors.affiliation: Department of Hematology, School of Medical Sciences, Terbiat Modares University, P.O. Box: 14115-331, Tehran, Iran.
authors.forename: Mina
authors.initials: M
authors.lastname: Soufi-Zomorrod
authors.affiliation: Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: Abbas
authors.initials: A
authors.lastname: Hajifathali
authors.affiliation: Stem Cell Technology Research Center, Tehran, Iran.
authors.forename: Fatemeh
authors.initials: F
authors.lastname: Kouhkan
authors.affiliation: Shahid Beheshti University of Medical Science, Tehran, Iran.
authors.forename: Mahshid
authors.initials: M
authors.lastname: Mehdizadeh
authors.affiliation: Stem Cell Technology Research Center, Tehran, Iran.
authors.forename: Seyed Mohammad Ali Hosseini
authors.initials: SM
authors.lastname: Rad
authors.affiliation: Department of Hematology, School of Medical Sciences, Terbiat Modares University, P.O. Box: 14115-331, Tehran, Iran. soleim_m@modares.ac.ir.
authors.forename: Masoud
authors.initials: M
authors.lastname: Soleimani
mesh_terms: D002460:Cell Line; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D002470:Cell Survival / Q000235:genetics; D015870:Gene Expression / Q000235:genetics; D061307:Human Umbilical Vein Endothelial Cells / Q000473:pathology*; D006801:Humans; D035683:MicroRNAs / Q000235:genetics*; D009389:Neovascularization, Pathologic / Q000235:genetics* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics; D051496:Receptor, Fibroblast Growth Factor, Type 1 / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000235:genetics
chemical_list: D035683:MicroRNAs; D012333:RNA, Messenger; C496348:FGFR1 protein, human; D051496:Receptor, Fibroblast Growth Factor, Type 1; D040301:Vascular Endothelial Growth Factor Receptor-2
keywords: Angiogenesis; FGFR1; HUVEC cells; MiR-129-1; MiR-133; VEGFR2