AKT regulates IL-1 beta-induced proliferation and activation of hepatic stellate cellsopen access
- Authors
- Yoon, Yongdae; Hwang, Soonjae; Saima, Fatema Tuj; Kim, Moon Young; Baik, Soon Koo; Eom, Young Woo
- Issue Date
- Mar-2023
- Publisher
- TECH SCIENCE PRESS
- Keywords
- Hepatic stellate cell; Interleukin-1(3; AKT; Cell proliferation; Fibrosis
- Citation
- BIOCELL, v.47, no.3, pp.669 - 676
- Journal Title
- BIOCELL
- Volume
- 47
- Number
- 3
- Start Page
- 669
- End Page
- 676
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/87796
- DOI
- 10.32604/biocell.2023.025365
- ISSN
- 0327-9545
- Abstract
- Background: Activated hepatic stellate cells (HSCs) are closely involved in the initiation, perpetuation, and resolution of liver fibrosis. Pro-inflammatory cytokine levels are positively correlated with the transition from liver injury to fibrogenesis and contribute to HSC pathophysiology in liver fibrosis.Methods: In this study, we investigated the effect of the pro-inflammatory cytokine interleukin (IL)-1(3 on the proliferation and signaling pathways involved in fibrogenesis in LX-2 cells, an HSC cell line, using western blotting and cell proliferation assays.Results: IL-1(3 increased the proliferation rate and a-smooth muscle actin (SMA) expression of LX-2 cells in a dose-dependent manner. Within 1 h after IL-1(3 treatment, c-Jun N-terminal kinase (JNK), p38, and nuclear factor-KB (NF-KB) signaling was activated in LX-2 cells. Subsequently, protein kinase B (AKT) phosphorylation and an increase in aSMA expression were observed in LX-2 cells. Each inhibitor of JNK, p38, or NF-KB decreased cell proliferation, AKT phosphorylation, and a-SMA expression in IL-1(3-treated LX-2 cells. Conclusion: These results indicate that JNK, p38, and NF-KB signals converge at AKT phosphorylation, leading to LX-2 activation by IL-1(3. Therefore, the AKT signaling pathway can be used as a target for alleviating liver fibrosis by the inflammatory cytokine IL-1(3.
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