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