HBx modulates apoptosis by activating JAK2/STAT3 signaling pathway in human renal proximal tubular epithelial cells
10.3969/j.issn.1000-4718.2014.08.020
- VernacularTitle:乙肝病毒X蛋白通过激活JAK2／STAT3信号通路调节肾小管上皮细胞凋亡
- Author:
Ping HE
;
Dan LI
;
Detian LI
;
Guohe FENG
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Hepatitis B virus X protein;
JAK2/STAT3 signal pathway;
HK-2 cells;
AG490
- From:
Chinese Journal of Pathophysiology
2014;(8):1451-1460
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the correlation of hepatitis B virus X protein (HBx) with renal tubular epithelialcell apoptosis in hepatitis B virus-associated glomerulonephritis (HBVGN) and the possible signaling mechanism. METHODS: The activation of JAK2/STAT3 signal pathway and the expression of apoptosis -related proteins in humankindey proximal tubular epithelial cells (HK-2 cells) were determined by Western blotting after transfection with HBx eukaryoticexpression vector.The cell proliferation was observed by CCK-8 assay.The cell apoptosis was analyzed by the imagingof HO33342 staining, transmission electron microscopy and flow cytometry with Annexin V /PI double staining.RESULTS:After transfection of the target gene HBx, the expression levels of both p-JAK2 and p-STAT3 were significantly increased.At the same time, the cell proliferation was obviously inhibited, and the apoptotic rate was increased.After incubationwith AG490, the JAK2/STAT3 signal pathway was partially blocked, and the cell apoptosis induced by HBx was reduced. CONCLUSION: HBx up-regulates the activation of JAK2/STAT3 signal pathway to induce renal tubular epithelialcell apoptosis, which is possibly involved in the pathogenic mechanism that HBV directly damages nephridial tissue .
