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作 者:徐红涛[1] 王旻晨[2] 杨亚安[2] 王晓春[2] 焦磊[2] 吴开云[2]
机构地区:[1]盐城卫生职业技术学院,盐城224006 [2]苏州大学医学院解剖学教研室,苏州215123
出 处:《解剖学杂志》2009年第2期162-165,共4页Chinese Journal of Anatomy
基 金:苏州大学创新团队项目(9034602);苏州大学医学发展基金资助项目(EE134519)
摘 要:目的:通过内皮素-1作用于大鼠血管平滑肌细胞(VSMC)及对内皮素-1受体信号的阻断,探讨内皮素-1对VSMC表型转化和增殖的影响及机制。方法:取大鼠主动脉贴块培养VSMC,用内皮素-1及其受体阻断剂BQ123分别作用于一般培养的VSMC和血清饥饿培养的VSMC。用BrdU标记细胞增殖;RT-PCR检测高血压相关基因-1(HRG-1)和SM22α表达变化。结果:内皮素-1作用后VSMC增殖显著增多,HRG-1和SM22αmRNA在一般培养和饥饿培养的VSMC中表达均明显减少;而加入阻断剂BQ123后增殖细胞大大减少,HRG-1和SM22αmRNA表达明显上调。结论:内皮素-1有促进VSMC增殖作用并可使VSMC从收缩型向合成型转化,并且内皮素-1对VSMC的作用是不可逆的;受体信号途径是内皮素-1对VSMC表型转化和增殖作用的机制之一。Objective: To investigate the effect of endothelin-1 (ET-1) on the proliferation and phenotypic transformation of vascular smooth muscle cells (VSMC) and the mechanisms underlying this effect. Methods: VSMC were isolated from the rat abdominal aorta. VSMC cultured in both serum-containing or in a serum-free medium were treated with ET-1, ET-1 receptor agonist (BQ123) and various combinations of these factors. VSMC proliferation was determined by bromodeoxyuridine (BrdU) assays. The mRNA expression levels of HRG-1 and SM22α were determined by reverse transcription-polymerase chain reaction (RT-PCR). Results: The proliferous .cells labeled by BrdU of cultured with ET-1 were increased and the mRNA expression of HRG-1 and SM22α was decreased. While the VSMC were cultured into the culture medium containing ET-1 receptor agonist (BQ123), the proliferous cells labeled by BrdU were obviously decreased and the mRNA expression of HRG-1 and SM22α was significantly increased. Conclusion: ET- 1 can notably promote the proliferation of VSMC and nonreversibly change the VSMC from contractile to synthetic phenotype, which may be related to receptor signaling pathway.
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