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Regulation of MAPK in glucose/angiotensin Ⅱ-induced proliferation of vascular smooth muscle cells
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- Author:
- No author available
- Journal Title:
- JOURNAL OF THE FOURTH MILITARY MEDICAL UNIVERSITY
- Issue:
- 22
- DOI:
- 10.3321/j.issn:1000-2790.2006.22.004
- Key Word:
- 丝裂原活化蛋白激酶(MAPK);细胞外信号调节MAP激酶类(ERKs);血管紧张素Ⅱ(AngⅡ);高糖;肌,平滑,血管/细胞学;增殖反应
Abstract： 目的: 研究丝裂原活化蛋白激酶(MAPK)信号途径在葡萄糖(GS)和/或血管紧张素Ⅱ(AngⅡ)介导大鼠动脉平滑肌细胞促增殖中的作用及其可能的调控机制. 方法: 实验以平滑肌细胞蛋白合成速率和蛋白含量为平滑肌细胞增殖的指标,以平滑肌细胞3H-亮氨酸掺入率表示细胞蛋白质合成速率,通过3H-胸苷(3H-TdR)反映平滑肌细胞DNA的代谢及细胞增殖情况;并通过给予PD098059及高浓度葡萄糖(HG)预处理,观察它们对细胞蛋白合成、DNA代谢及细胞增殖的影响. 结果: ① AngⅡ(10-7 mol/L)处理平滑肌细胞,3H-胸苷掺入率明显增高;HG (25×10-3 mol/L)处理平滑肌细胞,3H-胸苷掺入率明显增高;AngⅡ+HG处理平滑肌细胞3H-胸苷掺入率显著增高. ② AngⅡ增加3H-胸苷掺入的作用可明显被PD098059所抑制;AngⅡ+HG增高3H-胸苷掺入的作用也可被PD098059所抑制. ③ AngⅡ(10-7 mol/L)处理平滑肌细胞,3H-亮氨酸掺入率明显增高;HG (25×10-3 mol/L)处理平滑肌细胞,3H-亮氨酸掺入率增加;AngⅡ+HG处理平滑肌细胞3H-亮氨酸掺入率显著增加. ④ AngⅡ增加3H-亮氨酸掺入的作用可部分被PD098059所抑制;AngⅡ+HG增加3H-亮氨酸掺入的作用可显著被PD098059所抑制. 结论: 应用MAPK的特异性抑制剂PD098059抑制血管平滑肌细胞的增殖,证明MAPK激活在GS和/或AngⅡ导致平滑肌细胞增殖反应中有重要作用.
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