| Summary: | 碩士 === 國立成功大學 === 生物科技研究所碩博士班 === 92 === Liver disease is a severe problem in Taiwan. Recently Huang et al. reported that Delta-like protein (DLK1) was demonstrated to decrease significantly in the progression of liver fibrosis in biliary atresia. It is suggested that DLK1 maybe involve in the pathogenesis of liver fibrosis. However, the molecular mechanism underlying the implication is still unknown. This study was aimed to investigate effects of DLK1 on liver cells during wound healing .We hypothesize that DLK1 maybe involve in the progression of liver injury by promoting liver regeneration and affecting activation of HSCs.
In liver regeneration, we produced recombinant DLK1 protein containing the extracellular domain of human DLK1 (DLK-EC). The results show that DLK-EC can promote proliferation and migration of hepatocytes, the major liver cells. It is suggested DLK-EC can promote hepatocyte recruitment. Adding DLK-EC to the culture medium can promote proliferation and migration of endothelial cells and fibroblasts. These results support that DLK-EC has functions during liver regeneration.
In activation of HSCs, we added recombinant DLK-EC protein into HSCs cell culture. Experimental results show DLK-EC promotes proliferation and migration of freshly isolated HSCs and inhibits the proliferation, migration and smooth muscle α-actin expression of perpetual activated HSCs.
The results of the study support that DLK1 is implicated with liver regeneration and inhibition of fibrogenesis.
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