MicroRNA-363-3p Inhibits the Expression of Renal Fibrosis Markers in TGF-ß1-Treated HK-2 Cells by Targeting TGF-ß2.
Biochem Genet
; 59(4): 1033-1048, 2021 Aug.
Article
em En
| MEDLINE
| ID: mdl-33630202
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)-ß1 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-ß1-treated HK-2 cells, respectively. The results showed that the protein and mRNA expression levels of TGF-ß2, 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-ß1-treated HK-2 cells. The level of miR-363-3p was significantly decreased in TGF-ß1-treated HK-2 cells. TargetScan indicated that TGF-ß2 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-ß2, α-SMA, fibronectin, vimentin, collagen II, N-cadherin, increased phosphorylated-Smad3 protein level, and decreased E-cadherin protein and mRNA expression in TGF-ß1-treated HK-2 cells were significantly reversed by miR-363-3p mimics. However, all the effects were suppressed by a TGF-ß2-plasmid. The results suggested that miR-363-3p plays a protective role in RF by regulating the TGF-ß2/Smad3 signaling pathway.
Palavras-chave
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
MicroRNAs
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Fator de Crescimento Transformador beta1
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Fator de Crescimento Transformador beta2
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Túbulos Renais Proximais
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Revista:
Biochem Genet
Ano de publicação:
2021
Tipo de documento:
Article
País de afiliação:
China