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机构地区:[1]山东大学齐鲁医院儿科,济南250012 [2]山东大学齐鲁医院低温医学研究室,济南250012
出 处:《山东大学学报(医学版)》2011年第12期13-17,共5页Journal of Shandong University:Health Sciences
摘 要:目的研究尾加压素Ⅱ(UⅡ)对大鼠肺动脉平滑肌细胞(PASMC)增殖及细胞外信号调节激酶1/2(ERK1/2)蛋白磷酸化的影响,探讨肺动脉高压肺血管重塑的可能机制。方法采用消化法培养大鼠PASMC,WST-8测定不同浓度UⅡ诱导的大鼠PASMC的增殖活性及ERK1/2特异性抑制剂PD98059对UⅡ诱导的大鼠PASMC增殖活性的影响。Western blot法检测不同浓度UⅡ诱导的PASMC胞内ERK1/2蛋白磷酸化水平及PD98059对UⅡ诱导的ERK1/2蛋白磷酸化的抑制作用。结果 UⅡ在一定浓度范围(10-9~10-7mol/L)能浓度依赖性提高大鼠PASMC的增殖活性,并且能促进细胞内ERK1/2蛋白磷酸化。PD98059可阻断UⅡ诱导的PASMC增殖及PASMC胞内ERK1/2蛋白磷酸化。结论 UⅡ可促进大鼠PASMC增殖,ERK1/2通过磷酸化在其中发挥重要作用。Objective To investigate effects of urotensinⅡ(UⅡ) on proliferation of pulmonary artery smooth muscle cells(PASMCs) and phosphorylation level of extracellular signal-regulated kinase 1/2(ERK1/2),and to explore mechanisms responsible for the progression of vascular remodeling.Methods WST-8 was used to estimate UⅡ-induced proliferation of PASMCs.Western blot was carried out to determine the phosphorylation level of ERK1/2 and the effect of the ERK kinase inhibitor PD98059.Results UⅡ(10-9-10-7mol/L) could significantly stimulate the proliferation of PASMCs and phosphorylation level of ERK1/2 in does-dependent manners.The proliferation of PASMCs and phosphorylation of ERK1/2 were inhibited by PD98059.Conclusion UⅡ can induce proliferation of PASMCs,and activation of the ERK pathway plays a critical role in the process.
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