Format

Send to

Choose Destination
Exp Ther Med. 2017 Oct;14(4):3880-3886. doi: 10.3892/etm.2017.4956. Epub 2017 Aug 17.

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

Author information

1
Department of Clinical Laboratory, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510630, P.R. China.
2
Department of Clinical Laboratory, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510120, P.R. China.
3
Department of Infectious Diseases, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510150, P.R. China.
4
Department of Infectious Diseases, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510630, P.R. China.
5
Vaccine Research Institute, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510630, P.R. China.

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.

KEYWORDS:

hepatic fibrosis; hepatic stellate cells; integrin αvβ6; interleukin-32γ

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center