ArticlePloS one2013
Functional implications of microRNA-215 in TGF-β1-induced phenotypic transition of mesangial cells by targeting CTNNBIP1.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Identification of candidate microRNA biomarkers in diabetic nephropathy: a meta-analysis of profiling studies.Journal of nephrology · 2018Pooled it
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- Incretin-based therapy: a new horizon in diabetes management.Journal of diabetes and metabolic disorders · 2024Review
- The Role of MicroRNA in the Pathogenesis of Diabetic Nephropathy.International journal of molecular sciences · 2023Review
- Roles of microRNA-192 in diabetic nephropathy: the clinical applications and mechanisms of action.Frontiers in endocrinology · 2023Review
- Molecular profiling of urinary extracellular vesicles in chronic kidney disease and renal fibrosis.Frontiers in pharmacology · 2022Review
- Influence of high glucose in the expression of miRNAs and IGF1R signaling pathway in human myometrial explants.Archives of gynecology and obstetrics · 2021Article
- Advances in the Progression and Prognosis Biomarkers of Chronic Kidney Disease.Frontiers in pharmacology · 2021Review
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- miR-150-Based RNA Interference Attenuates Tubulointerstitial Fibrosis through the SOCS1/JAK/STAT PathwayMolecular therapy. Nucleic acids · 2020Article
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- Circulating miRNA-181b-5p, miRNA-223-3p, miRNA-210-3p, let 7i-5p, miRNA-21-5p and miRNA-29a-3p in patients with localized scleroderma as potential biomarkers.Scientific reports · 2020Article
- Article
- Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease.Frontiers in pharmacology · 2020Review
- Exosomal miRNA-215-5p Derived from Adipose-Derived Stem Cells Attenuates Epithelial-Mesenchymal Transition of Podocytes by InhibitingBioMed research international · 2020Article
- LNA-anti-miR-150 ameliorated kidney injury of lupus nephritis by inhibiting renal fibrosis and macrophage infiltration.Arthritis research & therapy · 2019Article
- Non-Coding RNAs as New Therapeutic Targets in the Context of Renal Fibrosis.International journal of molecular sciences · 2019Review
- Biogenesis, Stabilization, and Transport of microRNAs in Kidney Health and Disease.Non-coding RNA · 2018Review
- Genomics, microbiomics, proteomics, and metabolomics in bronchopulmonary dysplasia.Seminars in perinatology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesangial cell (MC) phenotypic transition is crucial for the progression of diabetic nephropathy. A major stimulus mediating high glucose-induced MC phenotypic transition is TGF-β1. Our current study focuses on microRNA-215 (miR-215) and investigates its role in TGF-β1-mediated MC phenotypic transition. Using real-time quantitative PCR (qRT-PCR) and northern blotting, we determined that the miR-192/215 family is dramatically upregulated under diabetic conditions both in vitro and in vivo. Gain- and loss-of-function approaches demonstrated that miR-215 inhibition significantly inhibited TGF-β1-induced mouse mesangial cell (MMC) phenotypic transition, whereas miR-215 upregulation promoted MMC phenotypic transition. Interestingly, these changes were not detected in cells that were treated with TGF-β1 and miR-192 mimics or inhibitors. These results suggest that miR-215 participates in TGF-β1-induced MMC phenotypic transition. Luciferase reporter assays were used to identify whether catenin-beta interacting protein 1 (CTNNBIP1) is a direct target of miR-215, which was predicted by bioinformatic analysis. Mechanistic studies revealed that CTNNBIP1 suppresses Wnt/β-catenin signaling and that miR-215 promotes β-catenin activation and upregulates α-SMA and fibronectin expression in TGF-β1-treated MMCs by targeting CTNNBIP1. In addition, in vivo miR-215 silencing with a specific antagomir significantly increased CTNNBIP1 protein expression, resulting in reduced β-catenin activity and decreased α-SMA and fibronectin expression in db/db mouse kidney glomeruli. Taken together, our findings indicate that miR-215 plays an essential role in MC phenotypic transition by regulating the CTNNBIP1/β-catenin pathway, which is related to the pathogenesis of diabetic nephropathy.
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