https://scholars.lib.ntu.edu.tw/handle/123456789/189491
標題: | Yc-1-Inhibited Proliferation of Rat Mesangial Cells through Suppression of Cyclin D1—Independent of Cgmp Pathway and Partially Reversed by P38 Mapk Inhibitor | 作者: | HSIEH, BOR-SHEN TSAI, TUN-JEN CHEN, YUNG-MING 林水龍 |
關鍵字: | p38 mitogen-activated protein kinase;Proliferation;Cyclin D1;Mesangial cells;YC-1 | 公開日期: | 2005 | 卷: | v.517 | 期: | n.1-2 | 起(迄)頁: | 1-10 | 來源出版物: | EUROPEAN JOURNAL OF PHARMACOLOGY | 摘要: | This study was designed to investigate the effect of 1- benzyl-3-(5′- hydroxymethyl-2′-furyl) indazole (YC-1), a guanylate cyclase activator, 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/cyclin-dependent kinase ( 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 soluble guanylate cyclase, protein kinase G, or protein kinase A also did not reverse the inhibitory effect elicited by YC-1, while co-treatment with p 38 mitogen -activated protein kinase (MAPK) inhibitor could partially reverse the suppressive effect. YC-1 inhibited proliferation of mesangial cells 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. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/93082 |
顯示於: | 醫學系 |
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