Zhonghua zheng xing wai ke za zhi = Zhonghua zhengxing waike zazhi = Chinese journal of plastic surgery · 2010
[The effect of angiotensin II on phosphoinositide-3 kinase/Akt cascade in cultured fibroblasts derived from patients with hypertrophic scars].
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Liu Hong-wei, Cheng Biao, Wu Heng-jun, Gu Yong-feng, Chen Xuan, Chen Zhi-gang, Liu Wen-zhong
Аннотация
OBJECTIVE: To study the effect of angiotensin II on 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 hypertrophic scars expressed both AT1 and AT2 receptors. Ang II increased 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 AT1 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.
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 hypertrophic scars expressed both AT1 and AT2 receptors. Ang II increased 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 AT1 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.