Objective To investigate the role of α
3β
1 integrin and α/β-dystroglycan in protective effects of 1,25(OH)
2D
3 on podocytes in rats with adriamycin-induced nephropathy.
Methods Sprague-Dawley rats were randomly divided into three groups: control group (NC), nephropathy group (NE), and nephropathy+1,25(OH)
2D
3 group (ND). Rats in NE and ND group were injected intravenously with adriamycin (0.1 mg/10 g body weight) to induce nephropathy, and those in ND group were then subcutaneously treated with 1,25(OH)
2D
3 for 8 weeks. Urinary protein level, number of urine podocytes, foot process width and glomerulosclerotic index were determined. Nephrin and podocin mRNA and protein expressions were determined by RT-PCR and western blot, respectively. Podocyte density and expressions of α
3β
1 integrin and α/β-dystroglycan (DG) were analyzed by immunohistochemistry and western blot, respectively.
Results The increase in proteinuria, podocyturia and width of foot process in NE group were ameliorated after treatment with 1,25(OH)
2D
3 for 8 weeks. The glomerulosclerotic index was significantly decreased in ND group when compared with NE group. The podocyte density in ND group (10.3 ± 1.64 cells/glomerulus) was significantly higher than that in NE group (8.43 ± 1.75 cells/glomerulus) (p=0.008). 1,25(OH)
2D
3 treatment could significantly up-regulate the mRNA and protein expressions of nephrin and podocin, and the protein expressions of α
3β
1 integrin and α/β-DG.
Conclusion The expressions of nephrin, podocin, α
3β
1 integrin and α/β-DG were decreased in rats with nephropathy. However, 1,25(OH)
2D
3 treatment could significantly up-regulate the expressions of nephrin, podocin, α
3β
1 integrin and α/β-DG proteins which might suppress podocyte detachment and podocytopenia.
View full abstract