Journal
CELL CYCLE
Volume 20, Issue 5-6, Pages 490-507Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2021.1875665
Keywords
Liver fibrosis; HSCs activation; lncRNA Neat1; miR-148a-3p; 22-3p; cyth3
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Funding
- Education Reform Program for Central South University [2019jy195]
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In this study, the regulatory effects of lncRNA Neat1 on liver fibrosis and HSC activation were investigated. Neat1 was found to modulate Cyth3 expression by regulating miR-148a-3p and miR-22-3p, affecting liver fibrosis and HSC activation. These findings provide a deeper understanding of the pathogenesis of liver fibrosis and offer insights into the development of lncRNA-directed therapy.
Liver fibrosis is a common response to chronic liver injury, ultimately leading to cirrhosis. The activation of hepatic stellate cells (HSCs) plays a dominant role in liver fibrosis. The regulatory roles of long noncoding RNAs (lncRNAs) in multiple human diseases have been observed. This study was dedicated to investigating the regulatory effects of the lncRNA nuclear paraspeckle assembly transcript 1 (Neat1) on liver fibrosis and HSC activation. Upregulation of Neat1 and cytohesin 3 (Cyth3) and downregulation of miR-148a-3p and miR-22-3p were observed in mouse fibrotic liver tissues. Knockdown of Neat1 or Cyth3 attenuated liver fibrosis and collagen deposition in vivo and the activation of HSCs in vitro. An miR-148a-3p and miR-22-3p inhibitor facilitated HSC activation and collagen fiber expression. Neat1 directly targeted miR-148a-3p and miR-22-3p to modulate Cyth3 expression. Knockdown of Neat1 inhibited Cyth3 expression via the competing endogenous RNA (ceRNA) mechanism of sponging miR-148a-3p and miR-22-3p to regulate liver fibrosis and HSC activation. The ceRNA regulatory network may promote a better understanding of liver fibrogenesis, contribute to an original agreement of liver fibrosis etiopathogenesis and provide insights into the development of a novel domain of lncRNA-directed therapy against liver fibrosis.
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