本文關(guān)鍵詞：胰島素樣生長(zhǎng)因子2及受體參與角膜上皮細(xì)胞生長(zhǎng)和創(chuàng)傷修復(fù)的研究　出處：《山東大學(xué)》2016年博士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 角膜損傷 胰島素樣生長(zhǎng)因子2 角膜修復(fù) mTOR/STAT3

【摘要】：背景角膜上皮細(xì)胞層是眼球抵御外界有害致病因素侵犯的第一道屏障,在受到創(chuàng)傷后可以快速修復(fù)愈合,當(dāng)愈合延遲時(shí),會(huì)造成視力下降,嚴(yán)重時(shí)導(dǎo)致失明。目前部分臨床及動(dòng)物實(shí)驗(yàn)報(bào)道角膜上皮本身存在一定的自我更新及修復(fù)能力,但角膜損傷后發(fā)揮主要作用的并非角膜上皮而是來(lái)自于角膜緣的細(xì)胞組織,該組織中含有角膜緣干細(xì)胞(LSC),角膜緣干細(xì)胞可以通過(guò)細(xì)胞增殖、分化及遷移來(lái)修復(fù)損傷的角膜組織。有報(bào)道稱角膜緣干細(xì)胞缺失時(shí)角膜的修復(fù)功能會(huì)受到限制,且角膜修復(fù)功能還與角膜結(jié)膜化、新生血管生成、慢性炎癥刺激及持續(xù)性的角膜上皮損害等因素有密切關(guān)系,在上述因素等持續(xù)存在,角膜最終不能夠修復(fù)時(shí)可產(chǎn)生嚴(yán)重的后果即失明,同時(shí)研究表明,我們可通過(guò)移植角膜緣組織及角膜緣干細(xì)胞進(jìn)行角膜損傷的治療,這提示了角膜緣干細(xì)胞組織在創(chuàng)傷角膜修復(fù)過(guò)程中發(fā)揮著重要作用。在角膜損傷后,角膜緣干細(xì)胞即開始增殖,并分化為過(guò)渡性細(xì)胞,這種細(xì)胞可遷移至損傷部位,誘導(dǎo)細(xì)胞表達(dá)角膜上皮細(xì)胞標(biāo)記進(jìn)而促進(jìn)角膜損傷的修復(fù)。然而角膜上皮細(xì)胞與角膜緣干細(xì)胞組織之間相互作用的分子通路及機(jī)制目前尚不清楚。Jia等報(bào)道角膜機(jī)械或化學(xué)損傷后細(xì)胞中負(fù)責(zé)生長(zhǎng)及分化的因子基因表達(dá)明顯增強(qiáng),包括轉(zhuǎn)化生長(zhǎng)因子α (TGF-α)、轉(zhuǎn)化生長(zhǎng)因子β (TGF-β)、表皮生長(zhǎng)因子(EGF)、肝素樣生長(zhǎng)因子(HGF)、成纖維細(xì)胞生長(zhǎng)因子β (FGF-β)等,這些因子均可由角膜上皮細(xì)胞生成,它們參與調(diào)節(jié)細(xì)胞的增殖與生長(zhǎng)。此外,胰島素樣生長(zhǎng)因子2(IGF-2)也被證實(shí)能夠促使角蛋白細(xì)胞增殖,并使黏附連接蛋白N鈣黏附素的生成增加,.使細(xì)胞外基質(zhì)增加,從而促使角蛋白膠原的生成。胰島素樣生長(zhǎng)因子信號(hào)通路已被證實(shí)與細(xì)胞增殖及分化相關(guān),在細(xì)胞及器官水平的生長(zhǎng)調(diào)節(jié)中起重要作用,IGF及以上所述其他細(xì)胞調(diào)節(jié)因子與角膜緣干細(xì)胞的增殖、分化及遷移的發(fā)生有關(guān)。胰島素樣生長(zhǎng)因子家族(IGFs))是由兩種低分子多肽(IGF-1、IGF-2)、兩類特異性受體及六種結(jié)合蛋白組成。人體內(nèi)許多組織都可以合成、分泌胰島素樣生長(zhǎng)因子,但循環(huán)中的IGF則主要是由肝臟分泌的。胰島素樣生長(zhǎng)因子家族的生物學(xué)功能是通過(guò)與特異性的靶細(xì)胞表面的胰島素樣生長(zhǎng)因子受體結(jié)合而實(shí)現(xiàn)的。已發(fā)現(xiàn)有兩種結(jié)構(gòu)完全不同的IGF受體：IGF-1受體和IGF-2受體(即甘露糖-6磷酸受體)分別又稱1型受體和2型受體。正常情況下,IGF與其結(jié)合蛋白的親和力大于或近似等于與其受體的結(jié)合,加之高親和力受體低表達(dá),使少量游離IGF與大量IGF/IGFBP復(fù)合物處于平衡狀態(tài)。IGFs的合成與分泌受血液中生長(zhǎng)激素水平的控制,循環(huán)中IGFs對(duì)生長(zhǎng)激素的分泌具有負(fù)反饋調(diào)節(jié)作用,從而形成了一個(gè)生長(zhǎng)激素—胰島素樣生長(zhǎng)因子軸,其對(duì)機(jī)體組織的分化、增殖及物質(zhì)代謝具有重要的調(diào)節(jié)作用。以往研究表明,借助角膜上皮細(xì)胞表面的細(xì)胞表型標(biāo)記細(xì)胞角蛋白K3及K12或連接蛋白43可對(duì)角膜緣干細(xì)胞與角膜上皮細(xì)胞進(jìn)行區(qū)分,并且此類因子與角膜緣干細(xì)胞的增殖及分化亦相關(guān),且還有研究報(bào)道說(shuō),角膜上皮細(xì)胞培養(yǎng)液的上層部分可促使多種干細(xì)胞包括毛囊干細(xì)胞、間充質(zhì)干細(xì)胞及胚胎干細(xì)胞等,分化為攜帶角膜上皮細(xì)胞標(biāo)記K12的細(xì)胞,但相關(guān)的分子機(jī)制仍不清楚。目的角膜創(chuàng)傷修復(fù)的過(guò)程通常包括細(xì)胞的激活、增殖、分化,細(xì)胞因子的釋放,細(xì)胞外基質(zhì)的合成與重塑等,都是由多種細(xì)胞因子在時(shí)間和空間上高度協(xié)調(diào)而完成的。明確角膜損傷修復(fù)過(guò)程中關(guān)鍵的調(diào)控分子及其作用機(jī)制,對(duì)于角膜損傷后減少瘢痕形成、促進(jìn)角膜愈合具有重要意義。本研究中我們利用小鼠角膜機(jī)械損傷模型對(duì)損傷后角膜上皮細(xì)胞與角膜緣干細(xì)胞間的相互作用分子機(jī)制進(jìn)行初步探究。方法構(gòu)建小鼠單側(cè)眼角膜機(jī)械損傷模型,對(duì)側(cè)角膜為對(duì)照組,不同時(shí)間點(diǎn)采集小鼠雙側(cè)角膜中央及角膜緣組織,進(jìn)行細(xì)胞培養(yǎng)并基因檢測(cè)EGF、FGF-b、KGF、HGF、TGF-b1、IGF-1及IGF-2等細(xì)胞因子不同程度的反應(yīng)性改變,探究這些細(xì)胞因子對(duì)角膜緣干細(xì)胞分化及成纖維細(xì)胞轉(zhuǎn)化的影響,并探討mTOR/STAT3信號(hào)通路在IGF-2調(diào)控角膜上皮細(xì)胞增殖分化過(guò)程中的作用。結(jié)果1.角膜上皮損傷后,小鼠眨眼加劇,有畏光的現(xiàn)象,角膜上有不規(guī)則的斑塊狀結(jié)構(gòu)；對(duì)損傷角膜組織行蘇木精-伊紅(HE)染色后顯示,針尖破壞角膜上皮層,而基質(zhì)層未受損,提示我們所采用的角膜機(jī)械損傷模型方法可行性良好。2.中央角膜損傷后(0、3、6、12及24h)采集受損側(cè)小鼠角膜組織,實(shí)時(shí)PCR檢測(cè)相關(guān)細(xì)胞因子的基因表達(dá),損傷后3h及6h EGF、FGF-b、KGF、HGF、TGF-b1、IGF-1及IGF-2的基因表達(dá)水平升高,IGF-2因子的水平損傷后3h最高,并且顯著高于其他各種檢測(cè)的細(xì)胞因子(p0.05)3.角膜損傷后角膜緣干細(xì)胞組織較角膜上皮細(xì)胞中兩種受體的基因表達(dá)水平顯著增加,3h后其表達(dá)差異均具有統(tǒng)計(jì)學(xué)意義(p0.05)。4.IGF-2對(duì)角膜上皮細(xì)胞的增殖有促進(jìn)作用,并且隨著培養(yǎng)時(shí)間延長(zhǎng),IGF-2干預(yù)組的增殖能力與對(duì)照組比較有明顯的區(qū)別。從24h開始,IGF-2干預(yù)組的角膜上皮細(xì)胞遷移能力明顯高于對(duì)照組,48h更為明顯。通過(guò)對(duì)細(xì)胞骨架進(jìn)行染色觀察,發(fā)現(xiàn)IGF-2組較對(duì)照組有更強(qiáng)的粘附率。5.胰島素樣生長(zhǎng)因子2(IGF-2)在角膜損傷后迅速大量表達(dá),同時(shí)促使角膜緣細(xì)胞IGF2受體的表達(dá)增加并誘導(dǎo)角膜緣干細(xì)胞分化為帶有K12標(biāo)記的角膜上皮細(xì)胞。6.免疫熒光染色分析顯示受損角膜組織細(xì)胞中α-平滑肌肌動(dòng)蛋白水平顯著增加,提示可能存在成纖維細(xì)胞向肌成纖維細(xì)胞的轉(zhuǎn)化。7.檢測(cè)磷酸化mTOR與磷酸化STAT3蛋白表達(dá)的變化,發(fā)現(xiàn)p-mTOR與p-STAT3蛋白的表達(dá)均隨IGF-2濃度的增加而增多。8.使用IGF-2后,檢測(cè)EGF、FGF-b、KGF、HGF及TGF-bl等細(xì)胞因子損傷相關(guān)蛋白的表達(dá)變化,發(fā)現(xiàn)這幾個(gè)細(xì)胞因子在受到IGF-2刺激后,其蛋白表達(dá)水平均較對(duì)照組有顯著的升高,但當(dāng)同時(shí)再給予mTOR/STAT3信號(hào)通路抑制劑RAPA50 μmol/L后,發(fā)現(xiàn)上述幾個(gè)細(xì)胞因子的蛋白表達(dá)被明顯抑制。結(jié)論1.小鼠單側(cè)眼角膜機(jī)械損傷模型具有可重復(fù)性,角膜上皮能完全修復(fù),模型制作成功,可用于對(duì)角膜上皮損傷修復(fù)過(guò)程的研究。2.角膜機(jī)械損傷后角膜上皮中IGF-2因子表達(dá)明顯上調(diào),角膜緣組織中IGF-2受體表達(dá)增加,其共同作用促使角膜緣干細(xì)胞向角膜上皮細(xì)胞轉(zhuǎn)化,同時(shí)在成纖維細(xì)胞向肌成纖維細(xì)胞的轉(zhuǎn)化中起一定的作用,對(duì)角膜損傷修復(fù)有促進(jìn)作用。3.在體外培養(yǎng)狀態(tài)下,特異性的阻斷mTOR/STAT3信號(hào)通路可以阻斷IGF-2對(duì)角膜上皮細(xì)胞的修復(fù)作用,IGF-2對(duì)角膜上皮細(xì)胞修復(fù)的這種效應(yīng)可能是通過(guò)激活mTOR/STAT3信號(hào)通路而發(fā)揮作用。
[Abstract]:The background of the corneal epithelium is the first barrier against external harmful pathogenic factors of eye trauma in the invasion, can quickly repair and healing, when healing delay, cause vision loss, leading to severe blindness. At present some animal experiments and clinical reports on the cornea skin itself has a self renewal and repair ability, but the cornea after the injury does not play a major role in corneal epithelium but from the limbal tissue, the tissue contained limbal stem cells (LSC), corneal limbal stem cells through cell proliferation, differentiation and migration to repair the damage of corneal tissue. Reports of corneal limbal stem cell deficiency when the corneal repair function will be limit, and also with the function of cornea and conjunctiva cornea repair, angiogenesis, inflammation and chronic persistent corneal epithelial damage and other factors are closely related, in the Such factors continue to exist, and ultimately can not repair the cornea can have serious consequences that blindness, and research shows that we can treat by the transplantation of limbal and corneal limbal corneal injury, suggesting that the limbal stem cells play an important role in corneal trauma repair process after corneal injury. That limbal stem cells begin to proliferate, and differentiate into transitional cells, these cells can migrate to sites of damage and induce expression of corneal epithelial cell markers and promote corneal wound healing. However, corneal epithelial cells and corneal limbal stem cells and the molecular pathway of the interaction mechanism between tissues is unclear factor gene.Jia reports of corneal mechanical or chemical injury in cells responsible for growth and differentiation was significantly enhanced, including transforming growth factor alpha (TGF- alpha), transforming growth factor (Zi T GF- beta), epidermal growth factor (EGF), heparin like growth factor (HGF), fibroblast growth factor beta (FGF- beta), these factors can be generated by corneal epithelial cells, they are involved in the regulation of cell proliferation and growth. In addition, insulin-like growth factor 2 (IGF-2) has also been shown to promote keratin cell proliferation, adhesion and connection to generate N cadherin protein increased. The increase of extracellular matrix, which prompted the formation of keratin collagen. Insulin-like growth factor signaling pathway has been demonstrated to be associated with cell proliferation and differentiation in cell and organ level growth regulation plays an important role in IGF, and other cells above regulatory factor and limbal stem cell proliferation, differentiation and migration associated insulin-like growth factor family (IGFs)) is composed of two kinds of low molecular peptides (IGF-1, IGF-2), two types and six kinds of specific receptor binding protein White. Many organizations in the human body can synthesis, secretion of insulin-like growth factor, but the cycle of IGF is mainly secreted by the liver. The biological function of insulin-like growth factor family is through the surface and the specific target cells of insulin-like growth factor receptor binding and has been found to have two. The structure of different IGF receptors: IGF-1 receptors and IGF-2 receptors (i.e. -6 phosphate mannose receptor) were also called type 1 receptor and type 2 receptor. Under normal circumstances, the IGF binding protein affinity is greater than or equal to the approximate binding to its receptor, coupled with the high affinity receptor of low expression, so that a small amount of free IGF and a large number of IGF/IGFBP composite the thing is in equilibrium state of synthesis and secretion of.IGFs by controlling the level of growth hormone in blood circulation in IGFs has a negative feedback effect on the secretion of growth hormone, thus forming a student Growth hormone - insulin-like growth factor axis, the body tissue differentiation, plays an important role in the regulation of proliferation and metabolism. Previous studies showed that the cell phenotypic markers of cell surface corneal epithelial cells and keratin K3 K12 or connexin 43 of limbal stem cells and corneal epithelial cells were distinguished, and such factors and limbal stem cell proliferation and differentiation are related, and there are reports that the upper part of corneal epithelial cell culture solution can promote a variety of stem cells including hair follicle stem cells, mesenchymal stem cells and embryonic stem cells, differentiate into corneal epithelial cells with labeled K12 cells, but the molecular mechanism the purpose of the process is still not clear. Corneal wound repair usually include cell activation, proliferation, differentiation, cytokine release, extracellular matrix synthesis and remodeling, are made of a variety of cells Factor in time and space are highly coordinated and completed. Clear corneal injury and its mechanism of key regulatory molecules in the repair process, to reduce the scar formation after corneal injury, which is of great significance to the corneal healing. In this study, we use the model of corneal mechanical damage on mice interaction molecular mechanism between cells of corneal epithelial cells and corneal limbal stem injury study. Methods corneal mechanical injury model of mice unilateral construction, contralateral cornea as control group were collected at different time points of bilateral central cornea and limbus tissue, cell culture and gene detection of EGF, FGF-b, KGF, HGF, TGF-b1, IGF-1 and IGF-2 cytokine responses in different degrees change into these cytokines of limbal stem cell differentiation and the effects of fibroblast transformation, and to explore the mTOR/STAT3 signaling pathway in the regulation of IGF-2. Membrane epithelial cell proliferation and differentiation process. Results of the 1. corneal epithelium after injury, mice have the phenomenon of increased blink, photophobia, a plaque like structure of irregular cornea; damage to corneal tissue by hematoxylin eosin (HE) staining showed that the needle destruction of corneal epithelium. The stromal layer is not damaged, the feasibility that corneal mechanical injury model we adopt the method of good.2. central cornea after injury (0,3,6,12 and 24h) acquisition damaged corneal tissue side of mice, expression was detected by real-time PCR cytokines related genes, 6h and 3h after injury EGF, FGF-b, KGF, HGF, TGF-b1, IGF-1 and IGF-2 gene expression level increased, the level of the damage factor IGF-2 after 3H is the highest, and was significantly higher than that of other kinds of cytokine detection (P0.05) 3. corneal limbal stem cells with two receptors of corneal epithelial cells in a tissue gene expression level increased 3 After h the expression differences were statistically significant (P0.05.4.IGF-2) on the proliferation of corneal epithelial cells has a role in promoting, and with the extension of the culture time, the proliferation of IGF-2 in the intervention group compared with the control group have significant difference. Starting from 24h, corneal epithelial cell migration ability of IGF-2 in the intervention group was significantly higher than the control group, 48h the staining is obvious. Through the cytoskeleton, found in IGF-2 group than in the control group has a stronger adhesion rate of.5. insulin-like growth factor 2 (IGF-2) quickly expressed in corneal limbal cells and induce the expression of IGF2 receptor increased and induce limbal stem cell differentiation into corneal epithelial cells.6. staining immunofluorescence with the mark of K12 analysis show that the damaged corneal tissue cells of alpha smooth muscle actin levels increased significantly, suggesting the transformation of fibroblasts fibroblasts to muscle. 7. expression detection of phosphorylated mTOR and phosphorylated STAT3 protein, expression of p-mTOR and p-STAT3 protein was increased with the concentration of IGF-2 and.8. increased after using IGF-2, FGF-b, KGF, EGF detection, the expression of HGF protein and cytokines such as TGF-bl damage, found that several cytokines in response to IGF-2 later, the expression level of the protein were higher than those in control group were significantly increased, but also when given the mTOR/STAT3 signaling pathway inhibitor RAPA50 mol/L, found that the expression of several cytokines protein was inhibited. Conclusion 1. mice with unilateral corneal mechanical injury model with repeatability, corneal epithelium can be fully restored, the success of the model that can be used for the upregulated expression of IGF-2 factor of.2. on the process of corneal wound healing of the cornea after mechanical injury of corneal epithelium, the expression of IGF-2 receptor increased the total limbal tissues The same effect to limbal stem cells into corneal epithelial cells, and in fibroblasts to muscle plays a certain role in transforming fiber cells, promote the role of.3. in vitro on corneal wound healing, the specificity of blocking the mTOR/STAT3 signaling pathway can inhibit the effect of IGF-2 on the repair of corneal epithelial cells, the effect of IGF-2 on the repair of corneal epithelial cells may play a role through the activation of the mTOR/STAT3 pathway.

【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類號(hào)】：R77

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