姜文智2006-07-262018-07-112006-07-262018-07-112004http://ntur.lib.ntu.edu.tw//handle/246246/23665This study was designed to investigate the effect of YC-1 upon the proliferation of rat mesangial cells and its underlying mechanism. YC-1 inhibited cell proliferation and DNA synthesis in a dose and time-dependent manner. Flow-cytometry cell-cycle studies revealed that YC-1 prevented the entry of cells from G1 into S phase. The expression of cyclin D1 and the kinase activity of cyclin D1/CDK 4 were lower within YC-1-treated cells, revealed by Western blotting, Northern blotting and kinase assays. YC-1 did not increase the intracellular cGMP concentration in mesangial cells. Inhibitors of sGC, PKG, or PKA also did not reverse the inhibitory effect elicited by YC-1, while co-treatment with p38 MAPK inhibitor could partially reversed the suppressive effect. Conclusion: YC-1 inhibited proliferation and induced cell-cycle arrest by the reduction of cyclin D1 synthesis and cyclin D1/CDK4 kinase activity. This effect acts partially through p38 MAPK signal transduction activation and is independent of cGMP-signaling pathways.application/pdf10541916 bytesapplication/pdfzh-TW國立臺灣大學醫學院內科YC-1mesangial cellscyclin D1proliferationp38 mitogen-activated protein kinasereporthttp://ntur.lib.ntu.edu.tw/bitstream/246246/23665/1/922314B002363.pdf