| [Objective]:1. To observe the expression of cyclin D1, p27 and p57 in HBV-IgAN, and explore their roles in the progress of HBV-IgAN.2. To investigate the effect of human HBV-DNA positive serum on cell proliferation, cell apoptosis and the expression of p27 mRNA, cyclin D1mRNA of mouse podocyte, and explore their clinical value in HBV-GN.[Methods]:1. The protein expression of cyclin D1, p27 and p57 in renal biopsy specimens were determined by immunohistochemistry, tested by semi-quantitative method. The relationship among the expression of cyclin D1, p27 and p57 and the clinicopathologic data was analyzed.2. The mouse podocyte was cultured in the presence of the human serum of healthy person, the HBV-DNA positive serum from patients with HBV (without kidney diease) and HBV-GN. The proliferation measurement of each group was determined by MTT, the apoptosis by Annexin, and the mRNA of p27mRNA and cyclinD1mRNA by RT-PCR.[Results]:1. The expression of p27 down-regulated and cyclin D1 up-regulated as glomerular lesions and mesangium proliferation grew worse in HBV-IgAN and pIgAN. The expression of p57 was highest in the podocyte of normal control group, compared with which, the degree II of pIgAN group was not significantly affected, but the degree II of HBV-IgAN group down-regulated significantly(P<0.05), and the degree II~III groups either in pIgAN or HBV-IgAN expressed lowest. The expression of p27 and p57 decreased and cyclin D1 increased significantly in the case of saccule adhesion and glomerular sclerosis, and p57 was expressed significantly lower in crescent formation while p27 and cyclin D1 were not significantly changed. In pIgAN, the expression of p27 decreased and cyclin D1 increased in the NS group, compared with the albuminuria with hematuria and hematuria group. In HBV-IgAN, p57 expressed significantly lower in the NS group than albuminuria with hematuria group, and in pIgAN it expressed significantly higher in the hematuria group than albuminuria with hematuria group. The down-regulation of p57 occured when albuminuria >1.0g/24h, compared with that≤1.0g/24h.2. Human HBV-DNA positive serum could stimulate podocytes proliferation. Compared with the normal control group, HBV-DNA <10~3copy/ml of HBV-GN group performed no significantly distinction, while HBV-DNA 10~4 and10~6copy/ml of HBV-GN group and HBV-DNA 10~6copy/ml without glomerular diseases group significantly proliferated, and the last 3 groups has no significantly difference. We observed no discernible effect on the apoptosis of podocytes cultured in Human HBV-DNA positive serum. Compared with the normal control group, the Human HBV positive serum had no significant effect on the expression of cyclin D1 mRNA of podocytes, but the p27mRNA was significantly down-regulated.[Conclusion]:1. The down-regulation of p57 which can be observed in the early stage of HBV-IgAN is inconspicuous in pIgAN. The damage of podocyte may be important in the process of the early HBV-IgAN.2. P27 and cyclinD1 may play key parts in the process on HBV-IgAN and pIgAN. The down-regulation of p27 and up-regulation of cyclinD1 may synergistically affect glomerular mesangium proliferation, saccule adhesion and glomerular sclerosis.3. P57 may play an important role in the damage of the podocyte. The down-regulation of p57 could cause albuminuria, promote the formation of saccule adhesion, glomerular sclerosis and crescent.4. Human HBV-DNA positive serum can stimulate mouse podocyte to proliferate, but has no significantly effect on its apoptosis and the expression of cyclin D1mRNA. The proliferation of podocyte may be attributable to the down-regulation of the expression of p27. |
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