Abstract: Objective To investigate the changes and mechanism of golgi protein 73 (gp73) in mouse with liver fibrosis. Methods The model of hepatic fibrosis was developed by intraperitoneal injection of CCl₄ in C57BL6/J mice. Serum level of gp73 was determined by ELISA. The expression of gp73 in liver tissues was detected by immuno-histochemical staining. Hepatic stellate cell (HSC) was isolated by density gradient centrifugation and gp73 expression was detected. The expression of insulin like growth factor 2 mRNA binding protein 3 (IGF2BP3) in liver tissues was detected by immuno-histochemical staining. Next, IGF2BP3 over-expression and knock down plasmids were transfected, and the changes of GOLM1, which encodes gp73, were detected by RT-PCR. Furthermore, the expression of gp73 in hepatic stellate cells of fibrotic IGF2BP3 knockout mice was detected by flow cytometry. Results A higere expression of gp73 protein increased in serum(P＜0.01), liver (P＜0.05) and primary hepatic stellatecells (P＜0.001) in the fibrotic mice model was found as compared to the control animals. Along with that, the protein level of IGF2BP3 in the liver was also increased (P＜0.05). After over-expressing or knocking down IGF2BP3 by transient transfection, the mRNA expression of GOLM1 was also up-regulated (P＜0.001) and down-regulated (P＜0.01). Respectively, compared with the wide type group, the expression of gp73 was decreased in the hepatic stellate cells of fibrotic IGF2BP3 conditional knockout mice (P＜0.01). Conclusions In the CCl₄ induced liver fibrosis mice, the protein level of gp73 protein in hepatic stellate cells is increased, and RNA binding protein IGF2BP3 is a potential regulatory factor to promote its expression.

Key words: hepatic fibrosis, gp73, IGF2BP3