Knockdown of Fstl1 attenuates hepatic stellate cell activation through the TGF-β1/Smad3 signaling pathway
Autor: | Hui Guo, Xiangjin Liu, Hongye Shang |
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Rok vydání: | 2017 |
Předmět: |
Liver Cirrhosis
0301 basic medicine Cancer Research Follistatin-Related Proteins Biochemistry Collagen Type I Transforming Growth Factor beta1 03 medical and health sciences Hepatic Stellate Cells Genetics Humans Smad3 Protein RNA Small Interfering Molecular Biology Cells Cultured Cell Proliferation Gene knockdown 030102 biochemistry & molecular biology biology Hepatic stellate cell activation Actins Up-Regulation 030104 developmental biology Oncology Cancer research biology.protein Hepatic stellate cell Molecular Medicine Phosphorylation RNA Interference Signal transduction Hepatic fibrosis Signal Transduction Follistatin Transforming growth factor |
Zdroj: | Molecular Medicine Reports. 16:7119-7123 |
ISSN: | 1791-3004 1791-2997 |
DOI: | 10.3892/mmr.2017.7445 |
Popis: | Follistatin‑like 1 (Fstl1) is a secreted glycoprotein that belongs to the follistatin and SPARC (secreted protein, acidic and rich in cysteine) families and was identified to serve a critical role in lung fibrosis. However, the role of Fstl1 in liver fibrosis remains undefined. Therefore, the aim of the present study was to investigate the role of Fstl1 in liver fibrosis. The results indicated that Fstl1 was highly expressed in human hepatic fibrosis tissues and activated hepatic stellate cells (HSCs). Furthermore, knockdown of Fstl1effectively suppressed HSC proliferation and the protein expression levels of α‑SMA and collagen I in transforming growth factor (TGF)‑β1‑treated HSCs. Mechanistically, knockdown of Fstl1 remarkably decreased the phosphorylation level of Smad3 in TGF‑β1‑induced HSCs. Taken together, the present study demonstrated that Fstl1serves an important role in liver fibrosis and target deletion of Fstl1 attenuated HSCs activation through suppressing TGF‑β1/Smad3 signaling pathway. Therefore, Fstl1 may be a potential therapeutic target for the treatment of liver fibrosis. |
Databáze: | OpenAIRE |
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