@Article{biocell.2023.025365,
AUTHOR = {YONGDAE YOON, SOONJAE HWANG, FATEMA TUJ SAIMA, MOON YOUNG KIM, SOON KOO BAIK, YOUNG WOO EOM},
TITLE = {AKT regulates IL-1β-induced proliferation and activation of hepatic stellate cells},
JOURNAL = {BIOCELL},
VOLUME = {47},
YEAR = {2023},
NUMBER = {3},
PAGES = {669--676},
URL = {http://www.techscience.com/biocell/v47n3/51085},
ISSN = {1667-5746},
ABSTRACT = {<b>Background:</b> 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. <b>Methods:</b> In this study, we investigated
the effect of the pro-inflammatory cytokine interleukin (IL)-1β on the proliferation and signaling pathways involved
in fibrogenesis in LX-2 cells, an HSC cell line, using western blotting and cell proliferation assays. <b>Results:</b> IL-1β
increased the proliferation rate and α-smooth muscle actin (SMA) expression of LX-2 cells in a dose-dependent
manner. Within 1 h after IL-1β treatment, c-Jun N-terminal kinase (JNK), p38, and nuclear factor-κB (NF-κB)
signaling was activated in LX-2 cells. Subsequently, protein kinase B (AKT) phosphorylation and an increase in α-
SMA expression were observed in LX-2 cells. Each inhibitor of JNK, p38, or NF-κB decreased cell proliferation, AKT
phosphorylation, and α-SMA expression in IL-1β-treated LX-2 cells. <b>Conclusion: </b>These results indicate that JNK,
p38, and NF-κB signals converge at AKT phosphorylation, leading to LX-2 activation by IL-1β. Therefore, the AKT
signaling pathway can be used as a target for alleviating liver fibrosis by the inflammatory cytokine IL-1β.},
DOI = {10.32604/biocell.2023.025365}
}