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. 2014 May;122(5):392-8.
doi: 10.1111/apm.12155. Epub 2013 Aug 29.

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

Zhang Yaping  1 , Wang Ying, Di Luqin, Tang Ning, Ai Xuemei, Yao Xixian
Affiliations

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

Zhang Yaping et al. APMIS. 2014 May.

Abstract

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.

Keywords: IL-1 type I receptor; Proliferation; activation protein-1; c-Jun N-terminal kinase; interleukin-1β.

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