本文選題：nm23 + 增殖�。� 參考：《重慶醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:成功的胚胎著床依賴(lài)于有良好活性的胚泡和處于容受態(tài)的子宮二者間的相互作用,在這一過(guò)程中母體子宮內(nèi)膜涉及到一系列基因和信號(hào)通路的表達(dá)和變化。nm23是最早發(fā)現(xiàn)的抑制細(xì)胞遷移的基因,參與細(xì)胞各種生理過(guò)程,例如增殖、分化。為了探究nm23在胚胎著床中的調(diào)控作用,我們應(yīng)用免疫組織化學(xué)技術(shù)、Western Blot、RT-q PCR研究nm23基因在早孕小鼠模型,假孕小鼠模型的表達(dá)規(guī)律;檢測(cè)nm23基因在人的子宮內(nèi)膜組織及蛻膜組織中的表達(dá)模式;通過(guò)體內(nèi)和體外人工誘導(dǎo)蛻膜化研究nm23在基質(zhì)細(xì)胞蛻膜化過(guò)程中的調(diào)控作用;利用體外激素模型驗(yàn)證激素對(duì)nm23的調(diào)節(jié)作用;并借助基質(zhì)細(xì)胞體外功能試驗(yàn)進(jìn)一步探究PI3K-Akt-mTOR信號(hào)通路在nm23調(diào)控的蛻膜化過(guò)程中的作用。方法:(1)應(yīng)用免疫組織化學(xué)技術(shù),Western blot及RT-q PCR檢測(cè)nm23在早孕小鼠模型和假孕小鼠模型中的表達(dá)規(guī)律。(2)應(yīng)用免疫組織化學(xué)技術(shù)及Western blot檢測(cè)nm23在正常人子宮內(nèi)膜組織以及蛻膜組織中的表達(dá)規(guī)律。(3)通過(guò)體內(nèi)及體外人工誘導(dǎo)蛻膜化實(shí)驗(yàn),探討n(yōu)m23在子宮內(nèi)膜基質(zhì)細(xì)胞的蛻膜化的調(diào)控作用。(4)利用分離的原代小鼠子宮基質(zhì)細(xì)胞和人的子宮基質(zhì)細(xì)胞系建立體外激素模型探討激素對(duì)nm23是否有調(diào)節(jié)作用。(5)通過(guò)基質(zhì)細(xì)胞體外功能試驗(yàn)檢測(cè)nm23在蛻膜化過(guò)程中的潛在機(jī)制。結(jié)果:(1)nm23-m1在早孕小鼠模型中主要表達(dá)在蛻膜區(qū),其在假孕小鼠模型的表達(dá)模式與早孕小鼠模型相似。(2)在人的子宮組織表達(dá)模式中,相對(duì)于增生期和分泌期子宮內(nèi)膜組織,nm23-h1在蛻膜組織中呈高表達(dá)。(3)nm23-m1在體內(nèi)人工誘導(dǎo)蛻膜化組織表達(dá)升高,并且,si-nm23可以顯著降低基質(zhì)細(xì)胞的增殖和分化進(jìn)而來(lái)影響蛻膜化過(guò)程。(4)小鼠和人的基質(zhì)細(xì)胞激素模型證明雌激素和孕激素對(duì)nm23基因有調(diào)節(jié)作用。(5)PI3K-Akt-mTOR信號(hào)通路參與nm23調(diào)控的子宮內(nèi)膜基質(zhì)細(xì)胞蛻膜化過(guò)程。結(jié)論:nm23可通過(guò)PI3K-Akt-mTOR信號(hào)通路調(diào)節(jié)基質(zhì)細(xì)胞的蛻膜化過(guò)程。
[Abstract]:Objective: successful embryo implantation depends on the interaction between a well-active blastocyst and a receptive uterus. During this process, maternal endometrium is involved in a series of genes and signal pathway expression and changes. Nm23 is the first discovered gene to inhibit cell migration, involved in various physiological processes of cell, such as proliferation and differentiation. In order to investigate the regulation of nm23 in embryo implantation, we used immunohistochemical technique to study the expression of nm23 gene in mouse model of early pregnancy and pseudopregnant mouse model. The expression pattern of nm23 gene in human endometrial tissue and decidua tissue was detected, and the regulation of nm23 in decidualization of stromal cells was studied by in vivo and in vitro induced decidualization. In vitro hormone model was used to verify the regulatory effect of hormone on nm23, and the role of PI3K-Akt-mTOR signaling pathway in decidualization regulated by nm23 was further explored by stromal cell function test in vitro. Methods: (1) Immunohistochemical technique was used to detect the expression of nm23 in early pregnant mice and pseudopregnant mice. (2) Immunohistochemical technique and Western blot were used to detect the expression of nm23 in normal endometrium. (3) artificial induced decidualization in vivo and in vitro, To investigate the regulation of nm23 on decidualization of endometrial stromal cells. (4) to establish an in vitro hormone model using isolated primary mouse stromal cells and human stromal cell lines to investigate whether hormones can regulate nm23. The potential mechanism of nm23 in decidualization was detected by in vitro function test of stromal cells. Results: (1) the expression of nm23-m1 was mainly in decidual region in early pregnant mice, and the expression pattern in pseudopregnancy mice was similar to that in early pregnancy mice. (2) in human uterine tissues, the expression pattern of nm23-m1 was similar to that in early pregnancy mice. The expression of nm23-h1 in decidua tissue was higher than that in proliferative and secretory endometrium. (3) the expression of nm23-h1 was increased in decidualized tissue induced by nm23-m1 in vivo. In addition, PI3K-Akt-mTOR signaling pathway is involved in the regulation of nm23 gene. (4) the mouse and human stromal cell hormone models demonstrate that estrogen and progesterone can regulate nm23 gene. (5) PI3K-Akt-mTOR signaling pathway is involved in the regulation of nm23. Controlled decidualization of endometrial stromal cells. Conclusion:% nm23 can regulate the decidualization of stromal cells through PI3K-Akt-mTOR signaling pathway.
【學(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類(lèi)號(hào)】：R714

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