论文摘要
目的:揭示TβRI、Smad2、Smad3和Smad7等分子在瘢痕疙瘩形成中的可能作用,为利用TGF-β1及其下游因子预防和治疗瘢痕疙瘩提供正确的理论依据。 方法:运用免疫组化方法对瘢痕疙瘩、正常瘢痕及正常皮肤组织中TβRI、Smad2、Smad3和Smad7的表达进行分析;运用实时荧光定量PCR技术对TGF-β1作用前后瘢痕疙瘩、正常瘢痕、正常皮肤来源的成纤维细胞中Smad3基因的表达进行检测。 结果:瘢痕疙瘩中TβRI阳性率增高,Smad7阳性率降低,三种组织中Smad2、3表达无明显差异;TGF-β1作用后,三种组织成纤维细胞Smad3基因的表达都有下降。 结论:TβRI、Smad2、3和Smad7作为TGF-β1和靶基因之间的桥梁,在信号传导通路中发挥了关键的作用。TGF-β传导通路内部调节机制的异常可能是包括瘢痕疙瘩在内的各种纤维化疾病的根本原因。
论文目录
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