Zhonghua zheng xing wai ke za zhi = Zhonghua zhengxing waike zazhi = Chinese journal of plastic surgery · 2007
[Role of angiotensin II receptors in proliferation of fibroblast derived from human hypertrophic scars].
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Liu Hong-wei, Cheng Biao, Yu Wen-Lin, Sun Rui-xia, Tang Jian-bing, Fu Xiao-bing
Аннотация
OBJECTIVE: The present study was undertaken to observe the expression of angiotensin II (Ang II) type 1 (AT1) and type 2 (AT2) receptors in human hypertrophic scars, and explore their role in the proliferation of fibroblasts in human hypertrophic scars.
METHODS: The expression of both ATL and AT2 receptors in fibroblasts of hypertrophic scars was detected with immunohistochemical staining. Radioligand receptor binding assay and RT-PCR were used to determined expression level of AT1 and AT2 receptors in cultured fibroblasts derived from hypertrophic scars. DNA synthesis was examined in cultured fibroblasts of hypertrophic scars by measuring [3H]-TdR incorporation into fibroblasts.
RESULTS: Positive staining signals of both AT1 and AT2 receptors were found in fibroblasts of hypertrophic scars. Expression level of AT1 and AT2 receptors were (10.69 +/- 2.15) fmol/10(6) cells, (4.9 +/- 1.05) fmol/10(6) cells respectively in cultured fibroblasts derived from hypertrophic scars. RT-PCR showed the similar results. In cultured fibroblasts, Ang II stimulation significantly increased DNA synthesis (P < 0.05 vs negative control), which was inhibited by valsartan, an AT1 receptor blocker, but augmented by PD123319, an AT2 receptor antagonist. Valsartan or PD123319 alone did not influence the proliferation of fibroblasts derived from hypertrophic scars.
CONCLUSIONS: Both AT1 and AT2 receptors were expressed in the fibroblasts of hypertrophic scars, and Ang II regulates DNA synthesis in hypertrophic scar fibroblasts through a negative cross-talk between AT1 and AT2 receptors, which might contribute, at least partly to formation and maturation of human hypertrophic scars. The present study provides new insight into pathogenesis of hypertrophic scars.
METHODS: The expression of both ATL and AT2 receptors in fibroblasts of hypertrophic scars was detected with immunohistochemical staining. Radioligand receptor binding assay and RT-PCR were used to determined expression level of AT1 and AT2 receptors in cultured fibroblasts derived from hypertrophic scars. DNA synthesis was examined in cultured fibroblasts of hypertrophic scars by measuring [3H]-TdR incorporation into fibroblasts.
RESULTS: Positive staining signals of both AT1 and AT2 receptors were found in fibroblasts of hypertrophic scars. Expression level of AT1 and AT2 receptors were (10.69 +/- 2.15) fmol/10(6) cells, (4.9 +/- 1.05) fmol/10(6) cells respectively in cultured fibroblasts derived from hypertrophic scars. RT-PCR showed the similar results. In cultured fibroblasts, Ang II stimulation significantly increased DNA synthesis (P < 0.05 vs negative control), which was inhibited by valsartan, an AT1 receptor blocker, but augmented by PD123319, an AT2 receptor antagonist. Valsartan or PD123319 alone did not influence the proliferation of fibroblasts derived from hypertrophic scars.
CONCLUSIONS: Both AT1 and AT2 receptors were expressed in the fibroblasts of hypertrophic scars, and Ang II regulates DNA synthesis in hypertrophic scar fibroblasts through a negative cross-talk between AT1 and AT2 receptors, which might contribute, at least partly to formation and maturation of human hypertrophic scars. The present study provides new insight into pathogenesis of hypertrophic scars.