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PAR-CliP - A Method to Identify Transcriptome-wide the Binding Sites of RNA Binding Proteins
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linc-SCRG1 accelerates liver fibrosis by decreasing RNA-binding protein tristetraprolin

Jun-Cheng Wu1, Sheng-Zheng Luo1, Ting Liu1

  • 1Department of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|September 19, 2018
PubMed

Insights

Long noncoding RNA linc-SCRG1 accelerates liver fibrosis by reducing tristetraprolin (TTP). Inhibiting linc-SCRG1 may offer a new therapy for liver fibrosis by inactivating hepatic stellate cells.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Gastroenterology

Background:

  • Long noncoding RNAs (lncRNAs) play crucial roles in various biological processes, but their specific functions in liver fibrosis remain largely unexplored.
  • Liver fibrosis is a complex pathological process characterized by excessive accumulation of extracellular matrix in the liver, potentially leading to cirrhosis.

Purpose of the Study:

  • To investigate the biological role of the long noncoding RNA linc-SCRG1 in the pathogenesis of human liver fibrosis.
  • To elucidate the molecular mechanism by which linc-SCRG1 influences hepatic stellate cell activation and liver fibrosis progression.

Main Methods:

  • Microarray analysis and quantitative PCR were used to assess linc-SCRG1 expression in human cirrhotic tissues and activated LX2 cells.
  • RNA interference (siRNA) was employed to knockdown linc-SCRG1 and evaluate its effects on LX2 cell activation, apoptosis, proliferation, and invasion.
  • RNA-binding protein immunoprecipitation (RIP) and Western blotting were used to investigate the interaction between linc-SCRG1 and tristetraprolin (TTP).

Main Results:

  • linc-SCRG1 was significantly upregulated in human cirrhotic tissues and correlated with fibrosis progression.
  • Knockdown of linc-SCRG1 reversed TGF-β1-induced activation of LX2 cells, inhibiting proliferation, promoting apoptosis, and reducing invasion.
  • linc-SCRG1 directly binds to TTP, leading to decreased TTP mRNA stability and protein levels, thereby promoting liver fibrosis by repressing TTP's inactivation effect on hepatic stellate cells.

Conclusions:

  • linc-SCRG1 acts as a pro-fibrotic factor by destabilizing TTP, a key regulator of hepatic stellate cell phenotypes.
  • Inhibition of linc-SCRG1 presents a potential therapeutic strategy for treating human liver fibrosis by reactivating TTP-mediated inactivation of hepatic stellate cells.
Keywords:
TTPhepatic stellate celllong noncoding RNA

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