ArticleOxidative medicine and cellular longevity2021
hsa-miR-199b-3p Prevents the Epithelial-Mesenchymal Transition and Dysfunction of the Renal Tubule by Regulating E-cadherin through Targeting KDM6A in Diabetic Nephropathy.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Beyond hyperglycemia: histone modification-mediated epigenetic dysregulation in diabetic retinopathy and nephropathy.Diabetology & metabolic syndrome · 2026Review
- Circ_0070987 Promotes Pyroptosis of Ovarian Granulosa Cells in Polycystic Ovarian Syndrome Through the miR-139-5/CDH1 Axis.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- miR-539-5p Regulates Irritable Bowel Syndrome Pathological Processes by Targeting KDM6A.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- Decidual/placental and first trimester plasma levels of hsa-miR-199a-3p|hsa-miR-199b-3p and hsa-miR-3150b-3p are associated with insulin secretion in pregnancy.Frontiers in endocrinology · 2025Article
- COL1A1, COL1A2, CHN1, and FN1 Promote Tumorogenesis and Act as Markers of Diagnosis and Survival in Gastric Cancer Patients.Current pharmaceutical biotechnology · 2025Article
- Long non-coding RNA H19 mediates the miR-29b/transforming growth factor-β1/Drosophila mothers against decapentaplegic 3 signalling pathway to promote bladder fibrosis in diabetic rats.International urology and nephrology · 2024Article
- MicroRNA193a: An Emerging Mediator of Glomerular Diseases.Biomolecules · 2023Review
- Pathomechanisms of Diabetic Kidney Disease.Journal of clinical medicine · 2023Review
- hsa-miR-199b-3p suppresses osteosarcoma progression by targeting CCDC88A, inhibiting epithelial-to-mesenchymal transition, and Wnt/beta-catenin signaling pathway.Scientific reports · 2023Article
- The Role of Histone Modifications in the Pathogenesis of Diabetic Kidney Disease.International journal of molecular sciences · 2023Review
- Review
- Histone Modifications and Non-Coding RNAs: Mutual Epigenetic Regulation and Role in Pathogenesis.International journal of molecular sciences · 2022Review
- GSK-J4, a Specific Histone Lysine Demethylase 6A Inhibitor, Ameliorates Lipotoxicity to CardiomyocytesFrontiers in cardiovascular medicine · 2022Article
- Epithelial-mesenchymal transition in organ fibrosis development: current understanding and treatment strategies.Burns & trauma · 2022Review
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. The association between epithelial-mesenchymal transition (EMT) and fibrosis is quite ascertained, but its link to eventual tubule dysfunction is missing. Here, we show that human microRNA- (hsa-miR-) 199b-3p protects renal tubules from diabetic-induced injury by repressing KDM6A, a histone lysine demethylase regulating E-cadherin expression. Lower E-cadherin expression is related to a higher level of KDM6A, while E-cadherin is promoted upon treatment with the KDM6A inhibitor GSK-J4 in both high glucose- (HG-) induced HK2 cells and the kidneys from streptozotocin- (STZ-) induced type 1 diabetic mice. However, overexpression or RNA silencing of E-cadherin fails to alter KDM6A expression. We also show that the upregulation of KDM6A is associated with the increased methylation level of the E-cadherin promoter. Then, the target prediction results and a dual-luciferase assay show that hsa-miR-199b-3p is a new miRNA that targets KDM6A. Overexpression of hsa-miR-199b-3p increases E-cadherin expression and prevents EMT through repressing KDM6A expression in HG-induced HK2 cells. In contrast, inhibitor-induced hsa-miR-199b-3p knockdown has opposite effects, as it decreases E-cadherin level and worsens EMT, accompanied by increased levels of KDM6A. Besides, Mir199b-knockout mice without mmu-miR-119b-3p expression exhibit more renal tubule dysfunction and more serious kidney tissue damage upon treatment with STZ. These results demonstrate that hsa-miR-199b-3p improves E-cadherin expression and prevents the progression of DN through targeting KDM6A. miR-199b-3p could be a future biomarker or target for the diagnosis or treatment of DN.
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