ArticleAmerican journal of physiology. Renal physiology2023
The miR-143/145 cluster induced by TGF-β1 suppresses Wilms' tumor 1 expression in cultured human podocytes.
Article in American journal of physiology. Renal physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- MiR-145-5p modulates collagen production and fibroblast behaviour after cardiac injury partially via COL5A1.Basic research in cardiology · 2026Article
- Article
- Advances in focal segmental glomerulosclerosis research: genetic causes to non-coding RNAs.Molecular biology reports · 2025Review
- Upregulated PCAT-1 predicts poor prognosis and reduced immune cell infiltration in head and neck squamous cell carcinoma through the miR-145-5p / FSCN-1 axis.Molecular biology reports · 2025Article
- Downregulation of hsa-miR-100-5p May Be a Protective Factor in the Early Stages of Nephropathy in Type 1 Diabetes Mellitus.International journal of molecular sciences · 2024Article
- Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor (TGF)-β1 contributes to podocyte injury in various glomerular diseases, including diabetic kidney disease, probably at least in part by attenuating the expression of Wilms' tumor 1 (WT1). However, the precise mechanisms remain to be defined. We performed miRNA microarray analysis in a human podocyte cell line cultured with TGF-β1 to examine the roles of miRNAs in podocyte damage. The microarray analysis identified miR-143-3p as the miRNA with the greatest increase following exposure to TGF-β1. Quantitative RT-PCR confirmed a significant increase in the miR-143-3p/145-5p cluster in TGF-β1-supplemented cultured podocytes and demonstrated upregulation of miR-143-3p in the glomeruli of mice with type 2 diabetes. Ectopic expression of miR-143-3p and miR-145-5p suppressed WT1 expression in cultured podocytes. Furthermore, inhibition of Smad or mammalian target of rapamycin signaling each partially reversed the TGF-β1-induced increase in miR-143-3p/145-5p and decrease in WT1. In conclusion, TGF-β1 induces expression of miR-143-3p/145-5p in part through Smad and mammalian target of rapamycin pathways, and miR-143-3p/145-5p reduces expression of WT1 in cultured human podocytes. miR-143-3p/145-5p may contribute to TGF-β1-induced podocyte injury.
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