黏着斑激酶在增生性瘢痕中的作用研究  

Experimental Study of Mechanism of Focal Adhesion Kinase in Hypertrophic Scar

作　　者：何征宇[1] 侯晓宾[1] 范志宏[1] 

机构地区：[1]上海第二医科大学仁济医院整形外科,上海200127

出　　处：《上海第二医科大学学报》2005年第5期463-466,共4页Acta Universitatis Medicinalis Secondae Shanghai

基　　金：国家自然科学基金(30000176)资助项目.

摘　　要：目的探讨黏着斑激酶(FAK)在整合素与TGFβ受体介导的瘢痕增生和挛缩过程中的作用。方法取10例增生性瘢痕标本进行成纤维细胞原代培养,通过荧光定量PCR法(FQ-PCR),测定经FAK抗体阻断后培养的瘢痕成纤维细胞中整合素β1、TGF-β受体Ⅰ(TGF-βRⅠ)以及α平滑肌肌动蛋白(αSMA)mRNA表达量的变化。结果经FAK抗体阻断后培养的成纤维细胞整合素β1、TGFβRⅠ以及αSMA的基因拷贝数均较阴性对照组明显下降(P<0.05)。结论FAK可能是整合素和TGF-βR两条信号传导途径的交汇点,调节整合素、TGF-βR、αSMA的基因表达和蛋白合成,在瘢痕增生和挛缩过程中具有重要作用。Objective To study the mechanism of focal adhesion kinase(FAK) in hypertrophic scar. Methods Fibroblasts from 10 samples of human hypertrophic scars were cultured. FQ-PCR assay was applied to detect the mRNA expression of integrin β 1, TGF-βRⅠ and α-SMA in the fibroblasts of hypertrophic scar after FAK antibody blocking. Results mRNA of integrin β 1, TGF-βRⅠ and α-SMA expressions in fibroblasts were obviously lower after FAK antibody blocking than those of control groups (P<0.05). Conclusion FAK is the key point of signal transmission pathway mediated by integrins and TGF-βR, which regulate gene expression and protein synthesis of integrin β 1, TGF-βR Ⅰ and α-SMA. It may play an important role in the proliferation and contracture of hypertrophic scar.

关 键 词：增生性瘢痕 黏着斑激酶 作用研究 荧光定量PCR法 Α平滑肌肌动蛋白 瘢痕成纤维细胞 TGF-Β受体 mRNA表达量 TGF-βRⅠ 整合素β1 α-SMA 细胞原代培养 信号传导途径 瘢痕增生 基因拷贝数 FAK 受体介导 蛋白合成 基因表达 

分 类 号：R622[医药卫生—整形外科]