ArticleAnnals of translational medicine2019
MiR-92a regulates endothelial progenitor cells (EPCs) by targeting GDF11 via activate SMAD2/3/FAK/Akt/eNOS pathway.
Article in Annals of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 22 citations in OpenAlex.
- GDF11-secreting cell transplant efficiently ameliorates age-related pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Depletion of microRNA-92a Enhances the Role of Sevoflurane Treatment in Reducing Myocardial Ischemia-Reperfusion Injury by Upregulating KLF4.Cardiovascular drugs and therapy · 2023Review
- Long noncoding RNA TUG1 induces angiogenesis of endothelial progenitor cells and dissolution of deep vein thrombosis.Thrombosis journal · 2022Article
- Clinical Parameters and Epigenetic Biomarkers of Plaque Vulnerability in Patients with Carotid Stenosis.International journal of molecular sciences · 2022Review
- Salvianic Acid A Regulates High-Glucose-Treated Endothelial Progenitor Cell Dysfunction via the AKT/Endothelial Nitric Oxide Synthase (eNOS) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Focal Adhesion Kinase Inhibitor Inhibits the Oxidative Damage Induced by Central Venous Catheter via Abolishing Focal Adhesion Kinase-Protein Kinase B Pathway Activation.BioMed research international · 2021Article
- Overexpression of circRNA circUCK2 Attenuates Cell Apoptosis in Cerebral Ischemia-Reperfusion Injury via miR-125b-5p/GDF11 Signaling.Molecular therapy. Nucleic acids · 2020Article
- The effect of fluid shear stress in hydrogen sulphide production and cystathionine γ-lyase expression in human early endothelial progenitor cells.Annals of translational medicine · 2020Article
- Genetically modified endothelial progenitor cells with hNotch1.ICN overexpression display facilitated angiogenesis.Annals of translational medicine · 2020Article
- Diagnostic value of miR-92a in asymptomatic carotid artery stenosis patients and its ability to predict cerebrovascular events.Diagnostic pathology · 2020Article
- MicroRNA Expression Profiling of Bone Marrow-Derived Proangiogenic Cells (PACs) in a Mouse Model of Hindlimb Ischemia: Modulation by Classical Cardiovascular Risk Factors.Frontiers in genetics · 2020Article
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7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe effects of miR-92a on EPCs are still poorly elucidated. This study aimed to investigate the effects of miR-92a on EPCs (Endothelial progenitor cells) in a model of hypoxia (HO) or high glucose (HG)-induced EPCs injury by targeting GDF11 (Differentiation growth factor 11).
methodsThe effects of miR-92a on EPCs subjected to HO or HG were investigated firstly. Subsequently, the action mechanism of miR-92a on EPCs by targeting GDF11 was elucidated. Proliferation, apoptosis, migration, angiogenesis was measured with MTT, flow cytometry, transwell, tube formation respectively. After 24 h, levels of reactive oxygen species (ROS) were measured by fluorescence intensity. LDH and NO (nitric oxide) levels were determined by ELISA. The expression of FLK-1 (fetal liver kinase 1) and vWF (von Willebrand factor) was detected by immunofluorescence. mRNA and protein expression levels were examined using PCR and western blotting respectively. The interaction between miR-92a and GDF11 was evaluated by dual-luciferase reporter assay.
resultsOur results showed that HO or HG increased apoptosis, production of LDH and generation of ROS, but decreased the ability of migration and tube formation and generation of NO in EPCs; inhibiting of miR-92a decreased HO or HG-induced injury of EPCs, whereas miR-92a over-expression had the opposite effect; the protective effects induced by inhibiting of miR-92a on EPCs could be reversed by GDF11 siRNA and the harmful effects induced by over-expression of miR-92a could be rescued by over-expression of GDF11, which showed that the harmful effects of miR-92a be related to its inhibition of GDF11 and subsequent inactivation of the SMAD2/3/FAK/Akt/eNOS signaling pathway.
conclusionsInhibiting miR-92a can protect EPCs from HO or HG-induced injury. The effect of miR-92a on EPCs are mediated by regulating of GDF11 and downstream SMAD2/3/FAK/Akt/eNOS signaling pathway.
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