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  本文關(guān)鍵詞：Survivin基因在病理性瘢痕中的表達(dá)及與c-myc、p27～（kip1）蛋白表達(dá)的關(guān)系　出處：《鄭州大學(xué)》2005年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 病理性瘢痕 癌基因 Survivin c-myc p27

【摘要】：病理性瘢痕(pathologic scar)是由創(chuàng)傷、感染和燒傷等引起,以成纖維細(xì)胞(fibroblast)的過度增生和以膠原等大量細(xì)胞外基質(zhì)(extracellular matrix,ECM)的過度沉積為特征的人類真皮區(qū)特有的纖維代謝性疾病,其主要包括增生性瘢痕(hypertrophic scar,HS)和瘢痕疙瘩(keloid,K),臨床表現(xiàn)為感覺異常、瘤樣增生并伴有不同程度的功能障礙。病理性瘢痕的病因和發(fā)病機(jī)制尚未明了。近年來,隨著現(xiàn)代細(xì)胞生物學(xué)和分子生物學(xué)在瘢痕領(lǐng)域的深入研究,從而進(jìn)一步認(rèn)識了病理性瘢痕的生物學(xué)基礎(chǔ),即修復(fù)細(xì)胞(主要是成纖維細(xì)胞)的大量增殖與凋亡抑制、細(xì)胞外基質(zhì)中膠原合成與降解失衡、部分細(xì)胞因子的大量產(chǎn)生及其三者之間的密切關(guān)系。病理性瘢痕成纖維細(xì)胞的生物學(xué)行為是探索其發(fā)病機(jī)制的重點,而參與調(diào)控成纖維細(xì)胞增殖凋亡及膠原代謝的基因被相繼克隆及其功能亦被逐漸闡明,因此研究原癌基因、抑癌基因和細(xì)胞凋亡基因等與病理性瘢痕發(fā)生發(fā)展的相關(guān)性具有重要意義。 凋亡抑制基因Survivin可以抑制細(xì)胞凋亡、促進(jìn)細(xì)胞增殖并參與血管形成。其可直接抑制終末效應(yīng)蛋白Caspase 3和Caspase 7,阻斷細(xì)胞的凋亡過程。原癌基因c-myc與細(xì)胞分裂、增殖、分化、凋亡有密切關(guān)系。c-myc的激活可能參與了成纖維細(xì)胞的增殖甚至表型的轉(zhuǎn)化、或膠原合成與降解及細(xì)胞因子的調(diào)控過程。抑癌基因p27可抑制cyclinE—CDK2和cyclinD-CDK4等激酶復(fù)合物活性,而cyclinE-CDK2是細(xì)胞通過G_1/S限制點的關(guān)鍵,因此可抑制細(xì)胞增殖,從而控制細(xì)胞周期進(jìn)程�？梢�,Survivin、c-myc、p27基因與成纖維細(xì)胞的增殖/凋亡調(diào)控有關(guān),但其在病理性瘢痕組織中的表達(dá)、意義及相互關(guān)系尚不清楚。本課題利用原位雜交技術(shù)和免疫組化染色技術(shù),探討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
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2005
【分類號】：R363

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本文編號：1364933