MESANGIAL CELL PROLIFERATION INDUCED BY TNF-α IS DETERMINED BY LEVELS OF CYCLIN-KINASE INHIBITOR P27

来源 :Journal of Shanghai Second Medical University | 被引量 : 0次 | 上传用户:myeclipse75
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Objective To investigate the role of cyclin-kinase inhibitor p27 on proliferation of mesangialcell(MC) induced by tumor necrosis factor α(TNF-α). Methods The p27 protein of MC lysate was detected with western blotting analysis. The degree of MC proliferation was estimated through [3H]thymidine incorporation. The effect of reducing p27 expression on MC proliferation was analysed with p27 antisense oligodeoxynucleotide (ODN). Results TNF- α(200000U/L) decreased p27 level to (0.6±0.1) from (1.1±0.1) of MC lysate cultured in serum free DM EM for 24h (P <0.01) and increased [3H] thymidine incorporation to (2060±112) from (685±53) cpm/well(P <0. 01). p27 antisense ODN transfection decreased p27 level of MC stimulated by TNF-αfor 24h [(0.3±0.1) vs (0. 6±0. 1) , P < 0. 01 ] and increased [3H] thymidine incorporation [ (2420±130) vs (2060±112) cpm/well, P <0. 05]. Conclusion The decline of p27 protein maybe play an important role in MC proliferation induced by TNF-α. Objective To investigate the role of cyclin-kinase inhibitor p27 on proliferation of mesangial cells (MC) induced by tumor necrosis factor α (TNF-α). Methods The p27 protein of MC lysate was detected with western blotting analysis. The degree of MC proliferation was The effect of reducing p27 expression on MC proliferation was analyzed with p27 antisense oligodeoxynucleotide (ODN). Results TNF- [alpha] (200000U / L) decreased p27 level to (0.6 ± 0.1) from (1.1 ± 0.1 ) of MC lysate cultured in serum free DM EM for 24h (P <0.01) and increased [3H] thymidine incorporation to (2060 ± 112) from (685 ± 53) cpm / transfection decreased p27 level of MC stimulated by TNF-αfor 24h [(0.3 ± 0.1) vs (0.6 ± 0.1, P <0.01] and increased [3H] thymidine incorporation [(2420 ± 130) vs 2060 ± 112) cpm / well, P <0.05]. Conclusion The decline of p27 protein maybe play an important role in MC proliferation induced by TNF-α.
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