中文摘要：

我们的以前的研究证明了那个 podocyte 数字显著地与联系的肝炎 B 病毒(HBV ) 在孩子的 glomeruli 被减少 glomerulonephritis。在这研究，我们试图探索 HBx 蛋白质的外长的表示是否能直接在 vitro 禁止 podocyte 增长，并且在房间周期规定调查它的角色。HBx 基因通过基于侵入人体气管粘膜的病菌的向量被交付进有教养的老鼠 podocytes。房间形态学被评估， Wright-Giemsa 染色。细胞生长和增长被 3-(4,5-dimethylthiazol-2-yl ) 测量 -2,5-diphenyltetrazolium 溴化物(MTT ) 和 5,6-carboxyfluorescein diacetate， succinimidyl 酉旨(CFSE ) 基于增长试金。房间周期阶段被房间周期的流动 cytometry，和表示分析规章的蛋白质被西方的污点分析检验。象双、多重的 micronuclei 一样的异常原子变化，反映有丝分裂的大祸，在 5 天以后在 podocytes 积累了，这被发现感染以后。MTT 试金证明感染 Ad.HBx 的 podocytes 在白天 4 点比控制更慢慢地成长了感染以后并且此后。而且，基于 CFSE 的增长试金也证明表示 HBx podocytes 的增长显著地比控制的被禁止在 3 天感染以后，并且差别在白天 5 点变得更明显感染以后。房间周期分析证明 HBx 的 transfection 导致了 cyclin B1 和 CDK 禁止者 p21 表示和 G ₂/M 阶段的重要起来规定 cyclin 的拘捕，和细微下面规定表情。这些结果证明 HBx 的那外长的表情可能通过房间周期规定限制 podocytes 的 proliferative 能力，因此建议那 HBx 可以在联系 HBV 的 glomerulonephritis 在 podocyte 损害起一个作用。

英文摘要：

Our previous studies have shown that podocyte number is significantly decreased in glomeruli of children with hepa- titis B virus （HBV）-associated glomerulonephritis. In this study, we aimed to explore whether exogenous expression of HBx protein could directly inhibit podocyte proliferation in vitro, and to investigate its role in cell cycle regulation. HBx gene was delivered into cultured mouse podocytes through an adenovirus-based vector. Cell morphology was evaluated with Wright-Giemsa staining. Cell growth and proliferation were measured by 3-（4,5-dimethylthiazol-2-yl）- 2,5-diphenyltetrazolium bromide （MTT） and 5,6-carboxy- fluorescein diacetate, succinimidyl ester （CFSE）-based pro- liferation assays. Cell cycle phase was analyzed by flow cytometry, and the expression of cell cycle regulatory pro- teins was examined by western blot analysis. It was found that the aberrant nuclear changes like double and multiple micronuclei, which reflect mitotic catastrophe, accumulated in podocytes after 5 days post-infection. MTT assay showed that Ad.HBx-infected podocytes grew much more slowly than controls at day 4 post-infection and thereafter. Furthermore, CFSE-based proliferation assay also showed that the prolifer- ation of HBx-expressing podocytes was significantly inhibited than that of controls at 3-day post-infection, and that the dif- ference became much more obvious at day 5 post-infection. Cell cycle analysis showed that the transfection of HBx resulted in significant up-regulation of both cyclin B1 and CDK-inhibitor p21 expression and G2/M phase arrest, and slight down-regulation of cyclin A expression. These results demonstrated that exogenous expression of HBx might limit the proliferative capacity of podocytes through cell cycle regu- lation, thus suggesting that HBx may play a role in podocyte injuries in HBV-associated glomerulonephritis.