摘要
背景:目前临床治疗瘢痕疙瘩效果较差、常易复发。瘢痕疙瘩的发病机制仍不完全清楚,而关于成纤维细胞增殖及凋亡的研究为研究的热点。目的:分析瘢痕疙瘩组织中Livin、Smac、Caspase-3的表达的相关性,初步探讨3种因子在瘢痕疙瘩组织发病机制中的作用。方法:采用RT-PCR和免疫组织化学分别检测Livin、Smac、Caspase-3的mR NA和蛋白在20例瘢痕疙瘩组织和20例正常皮肤组织中的表达,并进行相关性分析结果与结论:瘢痕疙瘩组织中Livin的m RNA表达水平和蛋白的阳性表达率显著高于正常皮肤组织(P<0.05),瘢痕疙瘩组织中Smac和Caspase-3的mR NA表达水平和蛋白的阳性表达率低于正常皮肤组织(P<0.05)。瘢痕疙瘩组织中Livin和Smac、Caspase-3蛋白的表达呈负关联。结果提示Livin基因高表达可能抑制了Smac、Caspase-3基因表达从而导致了瘢痕疙瘩成纤维细胞增殖和凋亡的失衡,最终导致了瘢痕疙瘩的形成。
BACKGROUND: Currently, there is no effective treatment for keloids that often recur. Its pathogenesis is still entirely unclear, and fibroblast proliferation and apoptosis have become a research hotspot. OBJECTIVE: To investigate the expression of Livin, Smac and Caspase-3 in keloids and to analyze their relationship so as to preliminarily explore the significance of Livin, Smac and Caspase-3 in the pathogenesis of keloids. METHODS: RT-PCR and immunohistochemical methods were used to detect the mR NA and protein expressions of Livin, Smac and Caspase-3 in keloids(n=20) and normal skin tissues(n=20). RESULTS AND CONCLUSION: Compared with the normal skin tissue, the m RNA and protein positive expressions of Livin were significantly higher in keloids(P〈0.05), while the m RNA and protein positive expressions of Smac and Caspase-3 were lower in keloids(P〈0.05). There was a negative association between Livin and Smac, Caspase-3 protein expression in keloids. These findings indicate that the high mR NA expression of Livin may cause the imbalance between proliferation and apoptosis of fibroblasts by inhibiting the m RNA expression of Smac and Caspase-3, and eventually lead to the formation of keloid.
出处
《中国组织工程研究》
CAS
北大核心
2016年第11期1558-1563,共6页
Chinese Journal of Tissue Engineering Research
基金
徐州市科技局社会发展-临床医学研究项目(XM13B088)~~