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尾加压素Ⅱ对自发性高血压大鼠血管外膜成纤维细胞增殖活性及细胞外信号调节激酶1/2磷酸化的影响 被引量:2

Effect of Urotensin Ⅱ on Proliferative Potential and Phosphorylation of Extracellular Signal-regulated Kinase 1/2 of Adventitial Fibroblasts from Spontaneously Hypertensive Rat
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摘要 目的研究尾加压素Ⅱ(UⅡ)对自发性高血压大鼠(SHR)血管外膜成纤维细胞增殖活性的影响,并进一步探讨其可能涉及的信号转导通路。方法用胸腺嘧啶掺入法(3H-TdR)观察UⅡ诱导的SHR大鼠血管外膜成纤维细胞的增殖活性,及UⅡ受体拮抗剂Urantide、细胞外信号调节激酶1/2(ERK1/2)特异性的抑制剂PD98059对UⅡ诱导SHR大鼠血管外膜成纤维细胞增殖活性的影响;用免疫印迹技术观察UⅡ诱导后ERK1/2的磷酸化,及Urantide、PD98059对ERK1/2磷酸化的影响。结果UⅡ可以剂量依赖性地诱导SHR大鼠血管外膜成纤维细胞的增殖活性,且这一作用可以完全及部分被Urantide、PD98059抑制;UⅡ可以时间依赖性地诱导血管外膜成纤维细胞ERK1/2的磷酸化,且这一作用可以完全被Urantide、PD98059抑制。结论UⅡ可以诱导SHR大鼠血管外膜成纤维细胞的增殖活性,且该过程部分由ERK1/2信号通路所介导。 Objective To study the effect of urotensin Ⅱ ( U Ⅱ ) on the proliferative potential of adventitial fibroblasts (AFs) from spontaneously hypertensive rat (SHR) and to determine whether extracellular signal-regulated kinase 1/2 (ERK1/2) pathway is involved in this progress. Methods 3 ^H-thymidine incorporation test was used to estimate the U Ⅱ -induced proliferative potential of AFs from SHR and the influence of Urantide ( U Ⅱ receptor antagonist) and PD98059 ( ERK1/2 inhibitor). Western blotting was used to test the U Ⅱ -induced ERK1/2 phosphorylation as well as the effect of Urantide and PD98059 on U Ⅱ -induced ERK1/2 phosphorylation. Results U Ⅱ increased the proliferative potential of AFs from SHR in a dose-dependent way. Urantide and PD98059 wholly or partly inhibited U Ⅱ -induced proliferation of SHR-AFs. In SHR-AFs, U Ⅱ induced the phosphorylation of ERK1/2 in a time-dependent way, which was completely inhibited by Urantide and PD98059. Conclusion U Ⅱ can increase the proliferative potential of AFs from SHR and ERK1/2 pathway is partly involved in this progress.
出处 《中国医学科学院学报》 CAS CSCD 北大核心 2006年第6期776-780,共5页 Acta Academiae Medicinae Sinicae
关键词 尾加压素Ⅱ 成纤维细胞 增殖 细胞外信号调节激酶1/2 urotensin Ⅱ fibroblasts proliferation extracellular signal-regulated kinase 1/2
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参考文献10

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共引文献5

同被引文献23

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