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Effects of 1,25(OH)2D3 on proliferation and expression of PCNA of human glomerular mesangial cells / 天津医药
Tianjin Medical Journal ; (12): 17-19,20, 2015.
Artículo en Chino | WPRIM | ID: wpr-601840
ABSTRACT
Objective To investigate the effects of 1,25-dihydroxyvitamin D3 [1,25 (OH)2D3] on PCNA expression and cell proliferation in human glomerular mesangial cells. Methods The cultured human mesangial cells, which was subcul?tured 3-8 generations, were randomly divided into four groups normal control group (plus the DMEM medium containing 5%fetal bovine serum), proliferation in the control group (EGF group, plus 10μg/L of EGF), general intervention group [VD group, plus 10-8 mol/L of 1,25(OH)2D3], proliferation in the intervention group [EGF+VD group, plus 10μg/L EGF and 10-8 mol/L 1,25(OH)2D3] for treatment of 48 h. The cell cycle was detected by flow cytometry,and the expression of PCNA was detected by Western blot assay in four groups. Results (1) Compared with normal control group, G1 phase cells were signifi?cantly reduced, S, G2/M phase cells were increased and PI index was higher in EGF group. And G1 phase cells were signifi?cantly increased, S and G2/M phase cells were significantly decreased, and PI index was lower in VD group. Compared with the EGF group, G1 phase cells were significantly increased in VD group and EGF+VD group, and S, G2/M phase cells de?creased, PI index was lower. (2) Compared with normal control group, the expression of PCNA was higher in EGF group, and lower in VD group. Compared with EGF group, the expression of PCNA was lower in VD group and EGF+VD group. Conclu?sion 1,25 (OH) 2D3 inhibits the proliferation of human glomerular mesangial cells by arresting cell cycle and inhibiting the expression of PCNA protein.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Tianjin Medical Journal Año: 2015 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Tianjin Medical Journal Año: 2015 Tipo del documento: Artículo