ArticleExperimental and therapeutic medicine2019
miR-29a/b cluster suppresses high glucose-induced endothelial-mesenchymal transition in human retinal microvascular endothelial cells by targeting Notch2.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Improved wound healing by dual inhibition of miR-146a-5p and miR-29a-3p supports a network action of dysregulated miRNAs in diabetic skin.Diabetologia · 2026Article
- Endothelial-to-mesenchymal transition in the central nervous system: A potential therapeutic target to combat age-related vascular fragility.The Journal of pharmacology and experimental therapeutics · 2025Review
- Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Review
- 12-HETE activates Müller glial cells: The potential role of GPR31 and miR-29.Prostaglandins & other lipid mediators · 2024Article
- Experimental Models to Study Endothelial to Mesenchymal Transition in Myocardial Fibrosis and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Endothelial-to-mesenchymal transition: An underappreciated mediator of diabetic complications.Frontiers in endocrinology · 2023Review
- Endothelial to mesenchymal cell transition in diabetic retinopathy: targets and therapeutics.Frontiers in ophthalmology · 2023Review
- Mesenchymal Stem Cell-derived Nanovesicles as a Credible Agent for Therapy of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2022Article
- The Interaction Between Non-Coding RNAs and Calcium Binding Proteins.Frontiers in oncology · 2022Review
- A promising field: regulating imbalance of EndMT in cardiovascular diseases.Cell cycle (Georgetown, Tex.) · 2021Review
- PTH-induced EndMT via miR-29a-5p/GSAP/Notch1 pathway contributed to valvular calcification in rats with CKD.Cell proliferation · 2021Article
- MicroRNAs may provide new strategies in the treatment and diagnosis of diabetic retinopathy: Importance of VEGF.Iranian journal of basic medical sciences · 2021Review
- miR-29a-5p Alleviates Traumatic Brain Injury- (TBI-) Induced Permeability Disruption via Regulating NLRP3 Pathway.Disease markers · 2021Article
- miRNA, lncRNA and circRNA: Targeted Molecules Full of Therapeutic Prospects in the Development of Diabetic Retinopathy.Frontiers in endocrinology · 2021Review
- EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress.Frontiers in cell and developmental biology · 2021Review
- Increased miR-7641 Levels in Peritoneal Hyalinizing Vasculopathy in Long-Term Peritoneal Dialysis Patients.International journal of molecular sciences · 2020Article
- Calcium-Sensing Receptor Participates in High Glucose-Induced EndMT in Primary Human Aortic Endothelial Cells.Frontiers in physiology · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several studies have previously reported that endothelial cells contributed to pathological fibrosis in proliferative diabetic retinopathy (PDR) through endothelial-mesenchymal transition (EndMT); however, the precise mechanism of this interaction has not been completely elucidated. The present study investigated the expression of microRNA (miR)-29a/b cluster in human retinal microvascular endothelial cells (HRMECs) and examined its functional role in high glucose (HG)-induced EndMT. HRMECs were exposed to glucose at concentrations of 5, 15, 30 and 50 mM for 7 days and reverse transcription-quantitative polymerase chain reaction, western blotting and immunofluorescence were conducted to determine the expression of genes associated with miR-29a/b and EndMT. A luciferase reporter gene assay was also performed to confirm the association between miR-29a/b and neurogenic locus notch homolog protein 2 (Notch2). The expression levels of miR-29a/b, and endothelial markers vascular endothelial cadherin and cluster of differentiation 31 were decreased, whereas the expression levels of Notch2 and mesenchymal markers, including α-smooth muscle actin, fibroblast-specific protein 1 (also named S100 calcium binding protein A4, S100A4), fibronectin and SNAI1 were increased in HRMECs under HG (30 nM) conditions. In addition, Notch2 was identified as a target of miR-29a and miR-29b. Overexpression of miR-29a/b downregulated the expression of Notch2 and subsequently suppressed HG-induced EndMT. Taken together, the results of the present study revealed that the miR-29/Notch2 signaling pathway may participate in the regulation of HG-induced EndMT, and may serve as a potential molecular target during fibrosis in PDR.
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