Novel protein C6ORF120 promotes liver fibrosis by activating hepatic stellate cells through the PI3K/Akt/mTOR pathway
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View abstract on PubMed
Summary
This summary is machine-generated.C6ORF120 promotes liver fibrosis by activating hepatic stellate cells. This occurs through the PI3K/Akt/mTOR signaling pathway, as shown in knockout rats and cell models.
Area Of Science
- Hepatology
- Molecular Biology
- Cell Biology
Background
- Hepatic fibrosis is a significant health concern.
- C6ORF120's role in liver fibrosis is not well understood.
Purpose Of The Study
- To investigate the role of C6ORF120 in carbon tetrachloride (CCL4)-induced hepatic fibrosis.
- To elucidate the underlying molecular mechanisms involving hepatic stellate cell activation.
Main Methods
- Utilized C6orf120 knockout rats (C6orf120<sup>-/-</sup>) and LX-2 human hepatic stellate cells.
- Administered CCL4 to induce liver fibrosis in vivo.
- Stimulated LX-2 cells with recombinant C6ORF120 (rC6ORF120) in vitro.
- Employed Sirius Red, Masson staining, western blotting, PCR, immunohistochemistry, and immunofluorescence.
Main Results
- C6orf120<sup>-/-</sup> rats exhibited reduced fibrosis and liver injury.
- RNA-seq analysis showed decreased extracellular matrix deposition and stellate cell activation in knockout rats.
- rC6ORF120 stimulated LX-2 cell activation, mirroring in vivo findings.
- Mechanistic studies identified elevated p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR levels.
- LY294002, a PI3K/Akt/mTOR inhibitor, reversed C6ORF120-induced LX-2 cell activation.
Conclusions
- C6ORF120 activates hepatic stellate cells.
- C6ORF120 promotes hepatic fibrosis.
- The PI3K/Akt/mTOR signaling pathway mediates C6ORF120's pro-fibrotic effects.
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