摘要
目的观察血管紧张素Ⅱ（angiotensinⅡ，AngⅡ）对增生性瘢痕成纤维细胞磷脂酰肌醇．3激酶／蛋白激酶B（phosphoinositide 3-kinase／Akt，P13K／Akt）信号通路的影响。方法体外培养人增生性瘢痕成纤维细胞，用免疫荧光组织化学染色检测细胞AngⅡ受体AT，和AT：的表达。以P13k活性测定法和Western Blotting法检测细胞P13K的活性和Akt的磷酸化。结果免疫荧光组织化学染色结果显示培养的增生性瘢痕成纤维细胞同表达AT1和AT2受体。AngⅡ（10 ^-9-10^-7mol／L）刺激可增加细胞Akt的磷酸化和P13K的活性。AT2受体拮抗剂PDl233191可显著增强AngⅡ诱导的细胞Akt磷酸化和P13K活性增加（P〈0．05）；AT1受体拮抗剂Valsartan可显著抑制AngⅡ诱导的细胞Akt磷酸化和P13K活性增加（P〈0．05）。结论AngⅡ通过其受体AT1和AT2可调控增生性瘢痕成纤维细胞Akt磷酸化和PI3K的活性。
Objective To study the effect of angiotensin Ⅱon phosphoinositide-3 kinase/Akt cascade in cultured fibroblasts derived from patients with hypertrophic scars. Methods The expression of AT1 and AT2 receptor was detected by immunofluorescence staining. Cultured human skin fibroblasts were treated with Ang Ⅱ （10-9 _ 10-7 mol/L） , with or without an AT1 receptor blocker, valsartan or an AT2 receptor antagonist, PD123319. The phosphorylation of Akt was detected by western blotting, and PI3K activity was measured by Assay of PI3-K activity. Results Immunofluorescence staining showed that cultured fibroblasts derived from hypretrophic scars expressed both AT1 and AT2 receptors. Ang Ⅱincreased Akt phosphorylation and PI3K activity in cultured hypertrophic Scar fibroblasts in a dose-and time-dependent manner. Additionally, Ang Ⅱ -induced Akt phosphorylation was blocked by wortmannin, a PI3-K inhibitor. This Ang Ⅱ -activated PI3-K/Akt cascade was significantly inhibited by valsartan, an ATl receptor specific blocker（ P 〈 0. 05 ） , whereas enhanced by PD123319, an AT2 receptor antagonist（ P 〈 0. 05）. Conclusion These results indicate that Ang II receptors regulates PI3-K/Akt cascade of hypertrophic scars fibroblasts via AT1 and AT2.
出处
《中华整形外科杂志》
CAS
CSCD
北大核心
2010年第1期57-60,共4页
Chinese Journal of Plastic Surgery
基金
国家重点基础研究发展规划基金（2005CB522603）,国家自然科学基金（30772257）,全军医学科学研究十一五计划科技攻关基金（08G027）
