血清撤军对l型钙通道的贡献(CaV1.2)细胞内钙离子反应和人工培养的血管平滑肌细胞的趋化作用。

文章的细节

引用

复制到剪贴板

Patel可Clunn GF, Lymn JS,奥斯汀O,休斯广告

血清撤军对l型钙通道的贡献(CaV1.2)细胞内钙离子反应和人工培养的血管平滑肌细胞的趋化作用。

Br J杂志。2005年7月,145 (6):811 - 7。

PubMed ID

15880143 (在PubMed

]

文摘

血管平滑肌细胞(VSMC)趋化作用是动脉粥样硬化的基础和内膜的增生。增加细胞内钙离子[Ca2 +]我在趋化性是一个重要的信号,但l型钙通道的作用(CaV1.2)在这个反应在人类血管平滑肌细胞(hVSMC)还没有检查。隐静脉hVSMC从外植体生长的文化。支流hVSMC通道3研究了在文化中含15%胎牛血清(FCS)(随机循环)或血清剥夺后7天。平滑肌alpha-actin被免疫印迹和免疫荧光显微镜测量。[Ca2 +]我使用fura 2荧光测定。趋化性测量使用修改后的Boyden室技术和细胞对gelatin-coated板块也量化。的数量和亲和力dihydropyridine-binding网站评估使用[5-methyl-3H] PN 200 - 110绑定。在随机循环细胞钙通道激动剂,湾8644 K和100毫米氯化钾并不影响[Ca2 +]我。此外,[Ca2 +]我的上升引起的血小板源生长factor-BB (PDGF) CaV1.2拮抗剂的影响,氨氯地平与维拉帕米。 In randomly cycling cells amlodipine did not affect PDGF-induced migration. In serum-deprived cells, smooth muscle alpha-actin was increased and Bay K 8644a and 100 mM KCl increased [Ca2+]i. PDGF-induced rises in [Ca2+]i were also inhibited by amlodipine and verapamil. The ability of Bay K 8644a to increase [Ca2+]i and verapamil to inhibit PDGF-induced rises in [Ca2+]i was evident within 3 days after serum withdrawal. In serum-deprived hVSMC Bay K 8644a induced chemotaxis and amlodipine inhibited PDGF-induced migration. Cell attachment in the presence of PDGF was unaffected by amlodipine in either randomly cycling or serum-deprived hVSMC. Serum withdrawal was associated with a decrease in the maximum number of dihydropyridine-binding sites (B(max)) and a decrease in affinity (K(D)). Serum deprivation of hVSMC results in increased expression of smooth muscle alpha-actin, a marker of more differentiated status, and increased [Ca2+]i responses and chemotaxis mediated by CaV1.2. These observations may have important implications for understanding the therapeutic benefits of calcium channel antagonists in cardiovascular disease.

beplay体育安全吗DrugBank数据引用了这篇文章

药物靶点

药物	目标	类	生物	药理作用	行动
维拉帕米	压敏电阻器l型钙通道亚基alpha-1C	蛋白质	人类	是的	抑制剂	细节