| Objective: SLC39A7(Solute carrier family 39 Member 7,ZIP7)is a member of the SLC39 A family,which locates in the Golgi apparatus and endoplasmic reticulum.It plays a key role in maintaining intracellular zinc balance and regulating cell growth and differentiation pathways,including HER2,EGFR,Src and IGF1 R signaling pathways.ZIP7,as a multifunctional protein,regulates a wide range of cellular processes,including endoplasmic reticulum stress during development and adult homeostasis.It has been found that ZIP7 plays an important role in maintaining intestinal epithelial homeostasis and dermal development by regulating endoplasmic reticulum function.However,the role in liver fibrosis has not been reported.This study explored the expression and role of SLC39A7 in liver fibrosis,and preliminarily studied the possible molecular mechanism of SLC39A7 regulating liver fibrosis,providing a new therapeutic target and research direction for future clinical treatment and experimental research of liver fibrosis.Methods:(1)The expression of SLC39A7 in cirrhotic tissues was evaluated by immunohistochemistry(IHC);(2)A mouse model of liver fibrosis induced by CCl4 was established,and the liver tissue of the mice was collected,and the expression of SLC39A7 in the liver tissue of the fibrosis model mice was detected by Western blot;(3)Specific si RNA was used to knock down the expression of SLC39A7 in human hepatic stellate cells LX2,and then Western blot assay was performed to evaluate the effect of SLC39A7 knockdown on hepatic fibrosis of LX2.Results:(1)The content of SLC39A7 in normal human tissues was significantly higher than that in cirrhotic human tissues;(2)Western blot assay was performed on hepatic fibrosis model mice,and it was found that the content of SLC39A7 in liver tissue of normal mice was significantly higher than that of hepatic fibrosis model mice.(3)Cell experiments showed that the expression of liver fibrosis related moleculesα-SMA and Colla1 increased significantly after SLC39A7 knockdown,indicating that the degree of liver fibrosis was deepened.Conclusions:(1)The expression level of SLC39A7 in human liver cirrhosis and mouse fibrosis liver tissue decreased;(2)Deletion of SLC39A7 aggravated liver fibrosis in LX2 cells. |
