Survivin基因在病理性瘢痕中的表达及与c-myc、p27～（kip1）蛋白表达的关系

发布时间：2018-01-01 14:33

本文关键词：Survivin基因在病理性瘢痕中的表达及与c-myc、p27～（kip1）蛋白表达的关系　出处：《郑州大学》2005年硕士论文　论文类型：学位论文

更多相关文章： 病理性瘢痕 癌基因 Survivin c-myc p27

【摘要】：病理性瘢痕(pathologic scar)是由创伤、感染和烧伤等引起,以成纤维细胞(fibroblast)的过度增生和以胶原等大量细胞外基质(extracellular matrix,ECM)的过度沉积为特征的人类真皮区特有的纤维代谢性疾病,其主要包括增生性瘢痕(hypertrophic scar,HS)和瘢痕疙瘩(keloid,K),临床表现为感觉异常、瘤样增生并伴有不同程度的功能障碍。病理性瘢痕的病因和发病机制尚未明了。近年来,随着现代细胞生物学和分子生物学在瘢痕领域的深入研究,从而进一步认识了病理性瘢痕的生物学基础,即修复细胞(主要是成纤维细胞)的大量增殖与凋亡抑制、细胞外基质中胶原合成与降解失衡、部分细胞因子的大量产生及其三者之间的密切关系。病理性瘢痕成纤维细胞的生物学行为是探索其发病机制的重点,而参与调控成纤维细胞增殖凋亡及胶原代谢的基因被相继克隆及其功能亦被逐渐阐明,因此研究原癌基因、抑癌基因和细胞凋亡基因等与病理性瘢痕发生发展的相关性具有重要意义。凋亡抑制基因Survivin可以抑制细胞凋亡、促进细胞增殖并参与血管形成。其可直接抑制终末效应蛋白Caspase 3和Caspase 7,阻断细胞的凋亡过程。原癌基因c-myc与细胞分裂、增殖、分化、凋亡有密切关系。c-myc的激活可能参与了成纤维细胞的增殖甚至表型的转化、或胶原合成与降解及细胞因子的调控过程。抑癌基因p27可抑制cyclinE—CDK2和cyclinD-CDK4等激酶复合物活性,而cyclinE-CDK2是细胞通过G_1/S限制点的关键,因此可抑制细胞增殖,从而控制细胞周期进程。可见,Survivin、c-myc、p27基因与成纤维细胞的增殖/凋亡调控有关,但其在病理性瘢痕组织中的表达、意义及相互关系尚不清楚。本课题利用原位杂交技术和免疫组化染色技术,探讨Survivin mRNA、c-myc蛋白、p27~(kip1)
[Abstract]:Pathologic scar is caused by trauma, infection, and burn. Hyperproliferation of fibroblast and extracellular matrix with a large amount of extracellular matrix such as collagen. Ecm) is characterized by hypertrophic scar, which is characterized by hypertrophic scar in human dermis. The clinical manifestations of HSV and keloido keloidae are abnormal sensation, tumor-like hyperplasia with different degrees of dysfunction. The etiology and pathogenesis of pathological scar have not been understood in recent years. With the deep research of modern cell biology and molecular biology in the field of scar, the biological basis of pathological scar has been further understood. That is, the proliferation and apoptosis inhibition of repair cells (mainly fibroblasts) and the imbalance of collagen synthesis and degradation in extracellular matrix. The production of some cytokines and their close relationship. The biological behavior of pathological scar fibroblasts is the key to explore its pathogenesis. The genes involved in the regulation of fibroblast proliferation, apoptosis and collagen metabolism have been cloned one after another and their functions have been gradually clarified. Therefore, proto-oncogenes have been studied. The relationship between tumor suppressor gene and apoptosis gene and pathological scar development is of great significance. Apoptosis suppressor gene Survivin can inhibit cell apoptosis. Promote cell proliferation and participate in angiogenesis, which can directly inhibit the terminal effector proteins Caspase 3 and Caspase 7. Proto-oncogene c-myc is closely related to cell division, proliferation, differentiation and apoptosis. The activation of c-myc may be involved in the proliferation and even phenotype transformation of fibroblasts. Tumor suppressor gene p27 can inhibit the activity of kinase complexes such as cyclinE-CDK2 and cyclinD-CDK4. CyclinE-CDK2 is the key for cells to pass through the 1 / S restriction point, so it can inhibit cell proliferation and thus control cell cycle progression. It can be seen that survivin c-myc can be seen. P27 gene is related to proliferation / apoptosis regulation of fibroblasts, but its expression, significance and correlation in pathological scar tissues are not clear. In this study, in situ hybridization and immunohistochemical staining were used. Study on Survivin mRNA-c-myc protein p27 and kip1
【学位授予单位】：郑州大学
【学位级别】：硕士
【学位授予年份】：2005
【分类号】：R363

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