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Novel protein C6ORF120 promotes liver fibrosis by activating hepatic stellate cells through the PI3K/Akt/mTOR pathway.
- Source :
- Journal of Gastroenterology & Hepatology; Jul2024, Vol. 39 Issue 7, p1422-1430, 9p
- Publication Year :
- 2024
-
Abstract
- Background and Aim: The role of C6ORF120 in promoting CCL4‐induced hepatic fibrosis and its possible mechanisms were explored in C6orf120 knockout rats (C6orf120−/−) and LX‐2 cells (a type of human hepatic stellate cell line). Methods: In vivo experiments, wild‐type and C6orf120−/− rats were used to investigate the function of C6ORF120. In the in vitro experiments, C6ORF120 recombinant protein (rC6ORF120) at a concentration of 200 ng/mL was used to stimulate LX‐2 cells. Sirius Red staining, Masson staining, western blotting, polymerase chain reaction, immunohistochemistry, and immunofluorescence were used to explore fibrosis‐associated factors. Results: C6orf120−/− rats showed mild fibrosis and liver injury in the CCL4‐induced liver fibrosis model. Furthermore, RNA‐seq revealed that C6orf120−/− rats had less extracellular matrix deposition and activated stellate cells. Consistent with the in vivo, the rC6ORF120 induced LX‐2 cell activation. Moreover, mechanistic studies revealed that the p‐PI3K/PI3K, p‐Akt/Akt, and p‐mTOR/mTOR levels were significantly elevated and LY294002 (a PI3K/Akt/mTOR typical pathway inhibitor) reversed the function of C6ORF120 in activating LX‐2 cells. Conclusion: C6ORF120 could activate hepatic stellate cells and promote hepatic fibrosis via the PI3K/Akt/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 08159319
- Volume :
- 39
- Issue :
- 7
- Database :
- Complementary Index
- Journal :
- Journal of Gastroenterology & Hepatology
- Publication Type :
- Academic Journal
- Accession number :
- 178427901
- Full Text :
- https://doi.org/10.1111/jgh.16538