Cirrhosis is a world wide, bad prognosis liver disease and characterized by excessive collagen deposition and liver function damage. In our previous work, p90RSK is observed significantly up-regulated in association with elevated collagen type I levels in rat liver fibrosis. But detail mechanism of this phenomenon is still unknown.
Now, there has a research article to be published on May 7, 2009 in the World Journal of Gastroenterology addresses this question. The research team led by Professor Zhu from Department of Gastroenterology, Jinling Hospital observed the mechanism between p90RSK and collagen type I in vivo and in vitro.
In fibrotic liver tissue, p90RSK was over-expressed and located in activated HSC, which had a significant positive correlation with collagen type I levels. In HSC-T6 cells transfected with RNAi targeted to p90RSK, the expression of collagen type I was down regulated according with that of p90RSK. However, collagen type I promoter activity was not alternated with up-regulation or down-regulation of p90RSK expression. Otherwise, p90RSK RNAi inhibited the proliferation of HSC significantly. These results indicate that P90RSK was a critical element in activation of HSC, which is primarily responsible for excessive collagen expression via the initiation of HSC proliferation during liver fibrosis.
Lacking of the knowledge about pathological proceeding of liver fibrosis results in the lack of effective method to prevent and treat liver fibrosis. These results prefer a new view of p90RSK on liver fibrosis, and thus may provide a new therapeutic target to liver fibrosis.