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IL-32γ promotes integrin αvβ6 expression through the activation of NF-κB in HSCs.


ABSTRACT: Hepatic stellate cell (HSC) activation is important in the pathogenesis of liver fibrosis. However, the molecular mechanism of HSC activation is not completely understood. In the present study, it was demonstrated that interleukin-32γ (IL-32γ) is capable of enhancing intefgrin αvβ6 expression by inducing integrin αvβ6 promoter activity in a dose-dependent manner in HSCs. Furthermore, it was determined that nuclear factor κB (NF-κB) activation is required for IL-32γ-induced integrin αvβ6 expression. Increased integrin αvβ6 expression is then able to activate HSCs. These results indicate that NF-κB activation is required for IL-32γ to induce integrin αvβ6 expression and consequently promote HSC activation. Therefore, IL-32γ activates HSCs and therefore may be associated with hepatic fibrogenesis. These results may enable the development of novel effective strategies to treat hepatic fibrosis.

SUBMITTER: Liu H 

PROVIDER: S-EPMC5639283 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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IL-32γ promotes integrin αvβ6 expression through the activation of NF-κB in HSCs.

Liu Hongcan H   Pan Xingfei X   Cao Hong H   Shu Xin X   Sun Haixia H   Lu Jianxi J   Liang Jiayin J   Zhang Ka K   Zhu Fengqin F   Li Gang G   Zhang Qi Q  

Experimental and therapeutic medicine 20170817 4


Hepatic stellate cell (HSC) activation is important in the pathogenesis of liver fibrosis. However, the molecular mechanism of HSC activation is not completely understood. In the present study, it was demonstrated that interleukin-32γ (IL-32γ) is capable of enhancing intefgrin αvβ6 expression by inducing integrin αvβ6 promoter activity in a dose-dependent manner in HSCs. Furthermore, it was determined that nuclear factor κB (NF-κB) activation is required for IL-32γ-induced integrin αvβ6 expressi  ...[more]

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