ArticleBiochemical genetics2021
MicroRNA-363-3p Inhibits the Expression of Renal Fibrosis Markers in TGF-β1-Treated HK-2 Cells by Targeting TGF-β2.
Article in Biochemical genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- Cadmium exposure induces renal fibrosis by inhibiting hsa_circ_0075684/miR-363-3p/KLF4 signaling pathway.Scientific reports · 2026Article
- Article
- miR‑363‑3p attenuates the oxygen‑glucose deprivation/reoxygenation‑induced neuronal injuryMolecular medicine reports · 2022Article
- Human umbilical cord mesenchymal stem cell-derived exosomal miR-335-5p attenuates the inflammation and tubular epithelial-myofibroblast transdifferentiation of renal tubular epithelial cells by reducing ADAM19 protein levels.Stem cell research & therapy · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to explore the role of miR-363-3p in renal fibrosis (RF) in vitro. HK-2 cells were treated with transforming growth factor (TGF)-β1 for 72 h to establish an in vitro model of RF. Subsequently, western blot analysis and reverse transcription-quantitative PCR were used to detect the protein and mRNA expression levels of RF markers in TGF-β1-treated HK-2 cells, respectively. The results showed that the protein and mRNA expression levels of TGF-β2, α-smooth muscle actin (SMA), fibronectin, vimentin, collagen II and N-cadherin were increased, while the protein and mRNA expression levels of E-cadherin were decreased in TGF-β1-treated HK-2 cells. The level of miR-363-3p was significantly decreased in TGF-β1-treated HK-2 cells. TargetScan indicated that TGF-β2 was a direct target gene for miR-363-3p, which was further verified using dual luciferase reporter gene assays. Further analyses revealed that the increased protein and mRNA expression levels of TGF-β2, α-SMA, fibronectin, vimentin, collagen II, N-cadherin, increased phosphorylated-Smad3 protein level, and decreased E-cadherin protein and mRNA expression in TGF-β1-treated HK-2 cells were significantly reversed by miR-363-3p mimics. However, all the effects were suppressed by a TGF-β2-plasmid. The results suggested that miR-363-3p plays a protective role in RF by regulating the TGF-β2/Smad3 signaling pathway.
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Registered trials
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