本文選題：子宮內(nèi)膜異位癥 + Twist��； 參考：《浙江大學(xué)》2017年博士論文

【摘要】：子宮內(nèi)膜異位癥(endometriosis,EMs)是指具有生長功能的子宮內(nèi)膜組織(腺體和間質(zhì))出現(xiàn)在子宮腔被覆內(nèi)膜及宮體肌層以外的其他部位。它是育齡婦女的常見病,以25～45歲婦女多見,發(fā)病率高達(dá)10%-15%,近年有明顯上升趨勢,它所引起的慢性盆腔疼痛、痛經(jīng)和不孕嚴(yán)重影響了婦女健康和生活質(zhì)量。自1860年Von Rokitansky首先描述子宮內(nèi)膜異位癥以來,本病發(fā)病機(jī)制至今仍未完全闡明。雖然Sampson等提出的經(jīng)血逆流學(xué)說被廣為接受,但經(jīng)血逆流在生育期婦女中非常普遍,發(fā)生率高達(dá)76%～90%,而EMs的發(fā)病率卻僅占10%～15%,說明經(jīng)血逆流可能只是誘因,而異位子宮內(nèi)膜的遷移和侵襲能力以及對卵巢等盆腔器官和腹膜的粘附、浸潤等生物學(xué)行為,才可能是其發(fā)病的關(guān)鍵。近年來,有文獻(xiàn)報(bào)道證實(shí)了表觀遺傳學(xué)為子宮內(nèi)膜異位癥發(fā)病的重要機(jī)制之一,基因甲基化是表觀遺傳學(xué)的一個(gè)重要組成部分。Twist是新近發(fā)現(xiàn)的凋亡抑制蛋白,作為基因組中的高度保守序列,在胚胎發(fā)育和人類疾病發(fā)展過程中普遍存在著甲基化。該基因的功能包括參與上皮-間質(zhì)轉(zhuǎn)化促進(jìn)細(xì)胞遷移侵襲、抗細(xì)胞凋亡、促進(jìn)腫瘤血管生成和導(dǎo)致染色體不穩(wěn)定等。一般來說基因甲基化可使基因表達(dá)沉默,而去甲基化則可使其表達(dá)增加。但迄今為止,Twist基因啟動(dòng)子的甲基化狀態(tài)與子宮內(nèi)膜異位癥的關(guān)系國內(nèi)外尚未見報(bào)道。Twist可通過抑制E-cadherin和誘導(dǎo)N-cadherin來調(diào)節(jié)上皮-間質(zhì)轉(zhuǎn)化(epithelial-mesenchymal transition,EMT),是上皮細(xì)胞獲得遷移能力并侵犯到其他部位的有效方式,在腫瘤的發(fā)生及浸潤過程中扮演了重要角色,同時(shí)也可能是具有惡性生物學(xué)特征的EMs重要發(fā)病機(jī)制之一。本研究的目的是檢測和比較Twist、E-cadherin和N-cadherin在卵巢型異位內(nèi)膜及其在位子宮內(nèi)膜、非EMs者子宮內(nèi)膜組織和細(xì)胞中的表達(dá)差異,研究Twist對EMs在位內(nèi)膜間質(zhì)細(xì)胞遷移和侵襲能力的影響,研究三種不同組織中Twist甲基化狀態(tài)的差異,探討Twist異常甲基化所介導(dǎo)的細(xì)胞遷移和侵襲在EMs發(fā)病機(jī)制中可能的作用,同時(shí)為EMs靶向藥物治療和復(fù)發(fā)的預(yù)防提供新的思路。第一部分 Twist、N-cadherin和E-cadherin在不同子宮內(nèi)膜組織中的表達(dá)差異目的:在翻譯和轉(zhuǎn)錄水平上,研究Twist、N-cadherin和E-cadherin在卵巢型異位內(nèi)膜、EMs在位內(nèi)膜和非EMs子宮內(nèi)膜組織中的表達(dá)差異。方法:用Western blot和免疫組織化學(xué)法檢測Twist、N-cadherin和E-cadherin蛋白,比較卵巢型異位內(nèi)膜、在位內(nèi)膜與非EMs子宮內(nèi)膜組織三種蛋白的表達(dá)和定位情況;用定量RT-PCR檢測并比較三組組織中Twist、N-cadherin和E-cadherin的mRNA表達(dá)情況。結(jié)果:1.免疫組化結(jié)果顯示Twist、N-cadherin和E-cadherin在子宮內(nèi)膜腺上皮和間質(zhì)細(xì)胞均有表達(dá),Twist和N-cadherin的表達(dá):卵巢型異位內(nèi)膜在位內(nèi)膜非EMs子宮內(nèi)膜,E-cadherin則相反,組間差異均有顯著性(P0.05)。Spearman分析表明N-cadherin和Twist呈正相關(guān),E-cadherin與Twist呈負(fù)相關(guān)。2.Western blot提示Twist和N-cadherin蛋白表達(dá)量由高到低排列順序?yàn)?卵巢型異位內(nèi)膜在位內(nèi)膜非EMs子宮內(nèi)膜,且差異有顯著性(P0.05)。E-cadherin蛋白的表達(dá):非EMs子宮內(nèi)膜EM在位內(nèi)膜卵巢型異位內(nèi)膜,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。3.RT-PCR顯示Twist和N-cadherinmRNA表達(dá)量在卵巢型異位內(nèi)膜和在位內(nèi)膜的表達(dá)較非EMs子宮內(nèi)膜明顯升高(P0.05);E-cadherin mRNA表達(dá)在非EMs子宮內(nèi)膜中表徶最高,組間差異有顯著性。結(jié)論:Twist與EMs的發(fā)病有關(guān),可能通過介導(dǎo)上皮間質(zhì)轉(zhuǎn)化參與EMs的發(fā)病。第二部分 高表達(dá)的Twist促進(jìn)子宮內(nèi)膜間質(zhì)細(xì)胞遷移和侵襲能力目的:探討Twist對在位子宮內(nèi)膜間質(zhì)細(xì)胞遷移和侵襲能力的影響。方法:原代培養(yǎng)子宮內(nèi)膜間質(zhì)細(xì)胞,構(gòu)建質(zhì)粒過表達(dá)載體(cmv-mcs-3flag-sv40-Neom-Twist)并穩(wěn)定轉(zhuǎn)染至在位子宮內(nèi)膜間質(zhì)細(xì)胞,使其過表達(dá)Twist;用Western blot檢測轉(zhuǎn)染前后在位子宮內(nèi)膜間質(zhì)細(xì)胞的Twist、N-cadherin、E-cadherin蛋白表達(dá)情況;用RT-PCR檢測比較轉(zhuǎn)染前后在位子宮內(nèi)膜間質(zhì)細(xì)胞Twist、N-cadherin、E-cadherin的mRNA表達(dá)情況;Transwell法檢測子宮內(nèi)膜間質(zhì)細(xì)胞遷移和侵襲能力的改變。免疫熒光法檢測卵巢型異位內(nèi)膜、在位子宮內(nèi)膜和非EMs子宮內(nèi)膜的間質(zhì)細(xì)胞形態(tài)和三種蛋白的表達(dá)差異以及在細(xì)胞內(nèi)的定位情況。結(jié)果:1.成功轉(zhuǎn)染Twist至在位子宮內(nèi)膜間質(zhì)細(xì)胞引起過表達(dá)后,Western blot和RT-PCR檢測發(fā)現(xiàn)N-cadherin在蛋白和mRNA水平表達(dá)增加,E-cadherin蛋白和mRNA表達(dá)則下降,轉(zhuǎn)染前后差異有統(tǒng)計(jì)學(xué)意義。2.Transwell法檢測發(fā)現(xiàn),在位子宮內(nèi)膜間質(zhì)細(xì)胞轉(zhuǎn)染Twist后細(xì)胞遷移和侵襲能力均明顯增加,差異有顯著性。3.免疫熒光檢測發(fā)現(xiàn)三組子宮內(nèi)膜間質(zhì)細(xì)胞均表達(dá)Twist、N-cadherin和E-cadherin,Twist和N-cadherin在卵巢型內(nèi)膜細(xì)胞表達(dá)最明顯,E-cadherin在非EMs子宮內(nèi)膜細(xì)胞表徶最明顯,異位子宮內(nèi)膜間質(zhì)細(xì)胞表型更為多態(tài)性。結(jié)論:Twist過表達(dá)后在位子宮內(nèi)膜間質(zhì)細(xì)胞遷移和侵襲能力增加,同時(shí)上調(diào)N-cadherin的蛋白和mRNA表達(dá),下調(diào)E-cadherin的蛋白和mRNA表達(dá),提示Twist引起EMs發(fā)病的機(jī)理可能與上皮間質(zhì)轉(zhuǎn)化引起的遷移和侵襲能力增加有關(guān)。第三部分 Twist基因啟動(dòng)子甲基化在不同子宮內(nèi)膜組織中的差異目的:探討卵巢型異位內(nèi)膜、在位內(nèi)膜和非EMs子宮內(nèi)膜組織Twist基因啟動(dòng)子甲基化狀態(tài)的差異。方法:設(shè)計(jì)Twist基因啟動(dòng)子CpG島的6對引物后,采用焦磷酸測序法的甲基化特異性PCR(MSP),檢測三組內(nèi)膜組織中啟動(dòng)子甲基化水平的差異。結(jié)果:Twist基因啟動(dòng)子在卵巢型異位內(nèi)膜和在位子宮內(nèi)膜的某些區(qū)域呈低甲基化狀態(tài)。結(jié)論:推測卵巢型異位內(nèi)膜和在位子宮內(nèi)膜組織Twist基因啟動(dòng)子的區(qū)域性低甲基化狀態(tài),可引起Twist蛋白過表達(dá),從而可能直接導(dǎo)致EMs的發(fā)病。
[Abstract]:Endometriosis (endometriosis, EMs) refers to the appearance of endometrium with growth function (glands and stroma) in other parts of the endometrium outside the endometrium and the intrauterine layer. It is a common disease of women of childbearing age. It is a common disease of women of childbearing age. The incidence of the 25~45 year old women is more common and the incidence is up to 10%-15%. Pelvic pain, dysmenorrhea and infertility seriously affect the health and quality of life of women. Since the first description of endometriosis in Von Rokitansky in 1860, the pathogenesis of this disease has still not been fully elucidated. Although the theory of blood reflux proposed by Sampson is widely accepted, the blood reverse flow is very common among women in the childbearing period, and the incidence is high. From 76% to 90%, the incidence of EMs is only 10% to 15%, indicating that the transmigration and invasion of the ectopic endometrium, as well as the adhesion to the pelvic organs and peritoneum of the ovary, and the infiltration of the peritoneum, may be the key to the disease. In recent years, the literature has reported that epigenetics is in the uterus. One of the important mechanisms of the pathogenesis of membrane heterotopic, gene methylation is an important part of epigenetics,.Twist is a newly discovered inhibitor of apoptosis. As a highly conservative sequence in the genome, methylation exists in the development of embryo and human disease. The function of this gene includes participation in epithelial mesenchymal transition. It promotes cell migration and invasion, anti apoptosis, promotes tumor angiogenesis and causes chromosomal instability. Generally, gene methylation can make gene expression silent, while demethylation can increase its expression. However, the relationship between the methylation status of the Twist gene promoter and endometriosis has not yet been reported to the home and abroad. .Twist can regulate epithelial mesenchymal transition (epithelial-mesenchymal transition, EMT) by inhibiting E-cadherin and inducing N-cadherin. It is an effective way for epithelial cells to obtain migration and invasion to other parts. It plays an important role in the process of tumor development and invasion, and may also have malignant biological characteristics. The purpose of this study is to detect and compare the differences in the expression of Twist, E-cadherin and N-cadherin in the ovarian endometrium and its eutopic endometrium, in the endometrium and in the non EMs endometrium, and to study the effect of Twist on the migration and invasion of the eutopic interstitial cells of the endometrium in EMs, and the study of three different tissues. The difference in Twist methylation status, to explore the possible role of Twist abnormal methylation mediated cell migration and invasion in the pathogenesis of EMs, and to provide new ideas for the prevention of EMs targeting drug therapy and recurrence. Part I, Twist, N-cadherin and E-cadherin expression differences in different endometrium tissues: in translation and At transcriptional level, the differences in expression of Twist, N-cadherin and E-cadherin in ovarian ectopic endometrium, EMs eutopic endometrium and non EMs endometrium were studied. Methods: Western blot and immunohistochemistry were used to detect Twist, N-cadherin and E-cadherin proteins, ovarian endometrium, eutopic endometrium and non EMs endometrium, three species. The expression and localization of protein were detected by quantitative RT-PCR and the mRNA expression of Twist, N-cadherin and E-cadherin in the three groups was compared. Results: 1. immunohistochemical results showed that Twist, N-cadherin and E-cadherin were expressed in the endometrium and interstitial cells of the endometrium, and the expression of Twist and N-cadherin: ovarian ectopic endometrium in the position of the endometrium The membrane was not EMs endometrium, and E-cadherin was opposite, and there was a significant difference between the groups (P0.05).Spearman analysis showed that N-cadherin and Twist were positively correlated, E-cadherin and Twist showed a negative correlation of.2.Western blot suggesting Twist and N-cadherin protein expression from high to low order: the ectopic endometrium in the ovum type endometrium was not the endometrial endometrium, and the difference was poor. The expression of P0.05.E-cadherin protein: the non EMs endometrium EM eutopic endometrium endometrium, the difference was statistically significant (P0.05).3.RT-PCR showed that the expression of Twist and N-cadherinmRNA in the ovarian endometrium and the eutopic endometrium was significantly higher than that of the non EMs endometrium (P0.05); E-cadherin mRNA was expressed in non ovarian endometrium. Conclusion: Twist is associated with the pathogenesis of EMs and may be involved in the pathogenesis of EMs by mediating epithelial transformation. The second part of high expression Twist promotes the migration and invasion of endometrial stromal cells: To explore the ability of Twist to migrate and invasiveness of endometrial stromal cells. Methods: the primary endometrial stromal cells were cultured, the plasmid overexpression vector (cmv-mcs-3flag-sv40-Neom-Twist) was constructed and transfected to the eutopic endometrial stromal cells to overexpress Twist. The expression of Twist, N-cadherin, E-cadherin protein in the eutopic endometrium cells before and after transfection was detected by Western blot; and RT-PC was used in RT-PC. R was used to detect the mRNA expression of Twist, N-cadherin, E-cadherin in eutopic endometrial stromal cells before and after transfection. Transwell assay was used to detect the change of migration and invasion of endometrial stromal cells. Immunofluorescence was used to detect ectopic endometrium, the morphology of interstitial cells in the eutopic endometrium and non EMs endometrium and the table of three proteins Results: after 1. successful transfection of Twist to eutopic endometrial stromal cells, the expression of N-cadherin at the level of protein and mRNA increased, the expression of E-cadherin protein and mRNA decreased, and the difference between before and after transfection was statistically significant. The cell migration and invasion ability of endometrial stromal cells transfected with Twist were increased obviously. The difference was significant.3. immunofluorescence detection found that three groups of endometrial stromal cells expressed Twist, N-cadherin and E-cadherin, Twist and N-cadherin were most obvious in ovarian endometrial cells, E-cadherin in non EMs endometrium. The phenotype of ectopic endometrium was more polymorphic. Conclusion: after Twist overexpression, the migration and invasion ability of eutopic endometrial stromal cells increased, and the expression of protein and mRNA was up-regulated, the protein and mRNA expression of E-cadherin was down regulated, suggesting that the mechanism of Twist to cause the pathogenesis of EMs may be related to the transformation of epithelial mesenchymal transition. Increased migration and invasiveness. Third differences in the methylation of the Twist gene promoter in different endometrium purposes: To explore the difference in the methylation status of the Twist gene promoter in the ovarian ectopic endometrium, the eutopic endometrium and the non EMs endometrium. Methods: after the design of 6 pairs of primers in CpG island of the promoter of the Twist gene, The methylation specific PCR (MSP) of the pyrosequencing method was used to detect the difference in the level of promoter methylation in the three groups of endometrium. Results: the Twist gene promoter was methylation in some regions of the ovarian ectopic endometrium and in the eutopic endometrium. Conclusion: the Twist gene of the ovarian endometrium and the eutopic endometrium was presumed to be initiated. The regional hypomethylation of mover can cause over expression of Twist protein, which may directly lead to the pathogenesis of EMs.
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2017
【分類號】：R711.71

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