Hepatitis B virus X protein decreases nephrin expression and induces podocyte apoptosis via activating STAT3
Hepatitis B virus X protein decreases nephrin expression and induces podocyte apoptosis via activating STAT3
复制标题
乙型肝炎病毒X蛋白通过激活STAT3降低去氧肾上腺素表达并诱导足细胞凋亡
DOI：
10.3892/etm.2019.7453
复制
发表时间：
2019-05-01
影响因子：
2.7
通讯作者：
Suo, Yan-Hong
中科院分区：
文献类型：
--
作者：
Lei, Xiao-Yan;Chen, Xing-Xing;Suo, Yan-Hong
B型肝炎病毒X蛋白（HBx）的基因包含HBV基因组中最小的开放阅读框，并且该蛋白产物可以激活各种细胞信号传导途径并调节细胞凋亡等作用。然而，在不同的细胞类型和不同的外部条件下，其作用机制不同。在本研究中，HBx对小鼠足细胞克隆5（MPC 5）细胞的活力和凋亡的影响进行了研究。用pEX质粒转染HBx基因，实时定量PCR和western blot检测转染效率和相关蛋白表达。转染后48 h，HBx表达最高。HBx转染组nephrin蛋白表达低于空白组和阴性对照组。HBx基因转染后，足细胞活力受到抑制，细胞凋亡率增加，信号转导和转录激活因子3（STAT 3）和磷酸化STAT 3的表达与对照组相比增加。本研究提示STAT 3的激活可能参与了HBV注射致肾损伤的发病机制。因此，STAT 3是治疗HBV-GN的潜在分子靶点。
The gene for hepatitis B virus X protein (HBx) comprises the smallest open reading frame in the HBV genome, and the protein product can activate various cell signaling pathways and regulate apoptosis, among other effects. However, in different cell types and under different external conditions, its mechanism of action differs. In the present study, the effect of HBx on the viability and apoptosis of mouse podocyte clone 5 (MPC5) cells was investigated. The cells were transfected with the HBx gene using pEX plasmid, and real-time quantitative PCR and western blot analysis were used to test the transfection efficiency and assess related protein expression. The highest expression of HBx occurred at 48 h after MPC5 cells were transfected with HBx. The expression of nephrin protein in the HBx transfection group was lower than that in blank and negative control groups. Following transfection of the HBx gene, podocyte viability was suppressed, while the rate of cell apoptosis was increased; moreover, the expression of signal transducer and activator of transcription 3 (STAT3) and phospho-STAT3 was increased compared with in the control groups. The present study suggests that STAT3 activation may be involved in the pathogenic mechanism of renal injuries caused by HBV injection. Thus STAT3 is a potential molecular target in the treatment of HBV-GN.