Mechanism of interleukin-1β-induced proliferation in rat hepatic stellate cells from different levels of signal transduction.

Autor: Yaping, Zhang, Ying, Wang, Luqin, Di, Ning, Tang, Xuemei, Ai, Xixian, Yao
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Zdroj: APMIS; May2014, Vol. 122 Issue 5, p392-398, 7p
Abstrakt: Hepatic stellate cells ( HSCs) are the major producers of collagen in the liver. Their conversion from resting cells to proliferative, contractile, and activated cells is a critical step leading to liver fibrosis that is characterized by the deposition of excessive extracellular matrix. Interleukin-1 ( IL-1) may play a role in maintaining HSC in a proliferative state that is responsible for hepatic fibrogenesis. The aim of this study was to study the roles of the IL-1 type I receptor ( IL-1R1), c-Jun N-terminal kinase ( JNK), and activation protein-1 ( AP-1) in IL-1β-mediated proliferation in rat HSCs. We showed that IL-1β can upregulate proliferation in rat HSCs; however, inhibition of the JNK pathway could inhibit HSCs proliferation. Furthermore, IL-1β activated IL-1R1 expression, the JNK signaling pathway, and AP-1 activity in a time-dependent manner in rat HSCs. These data demonstrate that IL-1β could promote the proliferation of rat HSCs and that the IL-1R1, JNK, and AP-1 pathways were involved in this process. In summary, IL-1β-induced proliferation is possibly mediated by the IL-1R1, JNK, and AP-1 pathways in rat HSCs. Therefore, drugs that block these pathways may inhibit the proliferation of HSCs and suppress liver fibrosis. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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