Hepatitis B Virus X Protein Upregulate The Expression Of CD59 And Crry In Mouse Podocytes

The aim of this study was to investigate the influence of HBx on the expression of CD59 and Crry in mouse podocytes. CD59 and Crry mRNA expression in podocytes were assayed by semiquantitative RT-PCR and the proteins of CD59 and Crry were tested by flow cytometry. MTT method was used to detect the effect of HBx on complement activation. And then, the effects of ERK1/2, P38MAPK and PI-3K pathway inhibitor on CD59 and Crry expression were respectively detected by flow cytometry. The results showed that CD59 and Crry proteins and their mRNA expression were found to be significantly upregulated in HBx transgenic podocytes. The increased CD59 and Crry expression could insensitize cells to complement-dependent lysis. Compared with ERK1/2 and PI-3K pathway inhibitor, P38MAPK pathway inhibitor could significantly reduce the upregulation of CD59 and Crry by HBx. These results demonstrate that HBx can insensitize podocytes to complement-dependent cytotoxicity (CDC) through upregulating CD59 and Crry by P38MAPK pathway, which may lead to less activation of complement system and facilitate latent HBV infection in podocytes, which can not easily be removed and play a role in development of HBV-GN.