本文選題：干細(xì)胞 + 隧道納米管��； 參考：《第三軍醫(yī)大學(xué)》2017年碩士論文

【摘要】：研究背景和目的視網(wǎng)膜變性類疾病包括:視網(wǎng)膜色素變性疾病、黃斑變性疾病、Stargardt病、視錐視桿細(xì)胞發(fā)育不良等疾病。此類疾病的共同特點(diǎn)在于視網(wǎng)膜的關(guān)鍵細(xì)胞(包括感光細(xì)胞、視網(wǎng)膜色素上皮細(xì)胞)的變性、凋亡和壞死,從而導(dǎo)致患者的視功能不可逆的喪失。由于變性和凋亡的感光細(xì)胞或視網(wǎng)膜色素上皮(retinal pigment epithelial,RPE)細(xì)胞不能夠進(jìn)行自我再生,該類疾病目前尚無有效的治療方法。RPE是單層的色素上皮細(xì)胞,位于視網(wǎng)膜神經(jīng)上皮層與脈絡(luò)膜之間,其主要功能包括:構(gòu)成視網(wǎng)膜外屏障、吞噬感光細(xì)胞的外節(jié)、黑色素能吸收可見光起遮光暗房作用、分泌多種生長因子、細(xì)胞因子和神經(jīng)營養(yǎng)因子以及抗氧化作用等。RPE細(xì)胞在發(fā)揮其正常生理功能的同時(shí),隨之產(chǎn)生了大量的活性氧類物質(zhì)(reactive oxygen species,ROS)。線粒體是細(xì)胞內(nèi)ROS清除的關(guān)鍵細(xì)胞器,也是細(xì)胞內(nèi)最先最易受到氧化損傷的部位。有研究顯示RPE細(xì)胞線粒體的功能障礙與AMD等視網(wǎng)膜變性類疾病、糖尿病視網(wǎng)膜病變等疾病的發(fā)生、發(fā)病機(jī)制等有著密切的聯(lián)系。移植健康的視網(wǎng)膜細(xì)胞或者健康的視網(wǎng)膜組織,已成為目前最具有前景的治療策略。干細(xì)胞移植治療視網(wǎng)膜變性類疾病的主要治療機(jī)制包括:細(xì)胞替代效應(yīng)(cell replacement effect)、營養(yǎng)支持效應(yīng)(by stander effect)、移植區(qū)微環(huán)境免疫調(diào)控(immune-regulatory effect)作用等。干細(xì)胞來源的RPE細(xì)胞移植是目前治療濕性AMD等致盲性眼病頗具前景的治療手段。Rustom等研究人員在體外培養(yǎng)大鼠嗜鉻細(xì)胞瘤細(xì)胞(PC12細(xì)胞)時(shí),發(fā)現(xiàn)兩個(gè)相鄰但未直接接觸的細(xì)胞之間可以通過建立一個(gè)直的細(xì)長的管道進(jìn)行連接,將其命名為隧道納米管(tunneling nanotubes,TNT)。并且發(fā)現(xiàn)該結(jié)構(gòu)可以作為細(xì)胞間物質(zhì)相互交換、信息相互交流的通道。近來有研究顯示間充質(zhì)干細(xì)胞能夠通過線粒體交換改善受者細(xì)胞的功能。本研究的主要目的是探索干細(xì)胞及人胚胎干細(xì)胞來源的視網(wǎng)膜色素上皮細(xì)胞(human embryonic stem cell-derived retinal pigment epithelium,h ESC-RPE)能否與原代分離的遺傳性視網(wǎng)膜色素變性模型的皇家外科學(xué)院大鼠(Royal college of surgeons rat,RCS rat)的RPE細(xì)胞間形成TNT結(jié)構(gòu)、可否進(jìn)行線粒體轉(zhuǎn)運(yùn)、線粒體轉(zhuǎn)運(yùn)方向以及線粒體轉(zhuǎn)運(yùn)后對(duì)RCS大鼠RPE細(xì)胞的ROS水平、細(xì)胞增殖能力和細(xì)胞凋亡水平的影響。初步研究能否通過線粒體轉(zhuǎn)運(yùn)機(jī)制參與干細(xì)胞治療視網(wǎng)膜變性疾病。方法:第一部分:小鼠神經(jīng)干細(xì)胞與RCS大鼠RPE細(xì)胞的線粒體轉(zhuǎn)運(yùn)及其對(duì)RPE細(xì)胞功能影響的研究1.分別用含有線粒體特異標(biāo)記物Mitotracker-red及Mitotracker-green的培養(yǎng)液標(biāo)記RCS大鼠原代分離的RPE細(xì)胞(RCS-RPE)與小鼠神經(jīng)干細(xì)胞(mouse neural stem cells,m NSC)后,將其按照1:1的比例等量直接共培養(yǎng)24 h后,于激光掃描共聚焦顯微鏡下觀察mNSC與RCS-RPE細(xì)胞之間TNT的形成及線粒體轉(zhuǎn)運(yùn)。2.將RCS-RPE細(xì)胞與已轉(zhuǎn)染綠色熒光蛋白(green fluorescent protein,GFP)病毒的mNSC 1:1等量直接共培養(yǎng)48h,然后行流式細(xì)胞分選,分選出GFP陰性的RCS-RPE細(xì)胞。3.收集分選出的RCS-RPE細(xì)胞,與單獨(dú)培養(yǎng)的RCS-RPE細(xì)胞,采用流式細(xì)胞術(shù)檢測細(xì)胞ROS水平、細(xì)胞周期及細(xì)胞凋亡水平。第二部分:正常與損傷的人RPE細(xì)胞系(ARPE-19細(xì)胞)間線粒體轉(zhuǎn)運(yùn)及其對(duì)損傷ARPE-19細(xì)胞功能影響的研究1.分別用含有線粒體特異性標(biāo)記物Mitotracker-red及Mitotracker-green的培養(yǎng)液標(biāo)記正常ARPE-19細(xì)胞和用碘酸鈉(NaIO3)預(yù)先處理24h的ARPE-19細(xì)胞,1:1等量直接共培養(yǎng)24 h后,于激光掃描共聚焦顯微鏡下觀察TNT的形成以及線粒體轉(zhuǎn)運(yùn)現(xiàn)象。2.將200ug/ml Na IO3預(yù)處理24h的ARPE-19細(xì)胞與轉(zhuǎn)染GFP病毒的ARPE-19細(xì)胞等量直接共培養(yǎng)24h,然后進(jìn)行流式細(xì)胞分選,分選出未帶GFP的ARPE-19細(xì)胞。3.收集分選出的ARPE-19細(xì)胞、200ug/ml Na IO3預(yù)處理并單獨(dú)培養(yǎng)24h的ARPE-19細(xì)胞、200ug/ml Na IO3預(yù)處理并Transwell小室與正常ARPE-19細(xì)胞間接共培養(yǎng)的ARPE-19細(xì)胞,采用流式細(xì)胞術(shù)檢測細(xì)胞ROS水平、細(xì)胞周期及細(xì)胞凋亡水平。第三部分:hESC-RPE細(xì)胞與ARPE-19細(xì)胞及RCS-RPE細(xì)胞間TNT的形成及線粒體轉(zhuǎn)運(yùn)方向的初步研究1.分別用含有線粒體特異性標(biāo)記物Mitotracker-red及Mitotracker-green的培養(yǎng)液標(biāo)記hESC-RPE與正常ARPE-19細(xì)胞,將其按照1:1比例等量直接共培養(yǎng)24 h后,于激光掃描共聚焦顯微鏡下觀察TNT的形成及線粒體轉(zhuǎn)運(yùn)情況。2.分別用含有線粒體特異標(biāo)記物Mitotracker-red及Mitotracker-green的培養(yǎng)液標(biāo)記hESC-RPE與200ug/ml Na IO3預(yù)處理24h的ARPE-19細(xì)胞,按照1:1比例等量直接共培養(yǎng)24 h后,于激光掃描共聚焦顯微鏡下觀察TNT的形成及線粒體轉(zhuǎn)運(yùn)現(xiàn)象。3.分別用含有線粒體特異標(biāo)記物Mitotracker-red及Mitotracker-green的培養(yǎng)液標(biāo)記hESC-RPE與2000ug/mlNaIO3預(yù)處理的ARPE-19細(xì)胞,1:1等量直接共培養(yǎng)24 h后,于激光掃描共聚焦顯微鏡下觀察TNT的形成及線粒體轉(zhuǎn)運(yùn)的現(xiàn)象。4.分別用含有線粒體特異標(biāo)記物Mitotracker-red及Mitotracker-green的培養(yǎng)液標(biāo)記h ESC-RPE與RCS-RPE,1:1等量直接共培養(yǎng)24 h后,于激光掃描共聚焦顯微鏡下觀察TNT的形成及線粒體轉(zhuǎn)運(yùn)的情況。結(jié)果:第一部分:小鼠神經(jīng)干細(xì)胞與RCS-RPE細(xì)胞的線粒體轉(zhuǎn)運(yùn)及其對(duì)RPE細(xì)胞功能影響的研究1.通過激光掃描共聚焦顯微鏡觀察,mNSC與RCS-RPE細(xì)胞之間可見TNT的形成,并且可觀察到mNSC將自身線粒體轉(zhuǎn)運(yùn)到RCS-RPE細(xì)胞中。2.體外m NSC與RCS-RPE細(xì)胞直接共培養(yǎng)體系下,直接共培養(yǎng)組相比單獨(dú)培養(yǎng)組RPE細(xì)胞的ROS水平有所降低、細(xì)胞增殖能力提高、凋亡水平降低,差異均具有統(tǒng)計(jì)學(xué)意義。說明干細(xì)胞能夠通過線粒體轉(zhuǎn)運(yùn)的機(jī)制,改善RCS-RPE細(xì)胞的增殖、凋亡功能。第二部分:正常與損傷的人RPE細(xì)胞系(ARPE-19細(xì)胞)間線粒體轉(zhuǎn)運(yùn)及其對(duì)損傷ARPE-19細(xì)胞功能影響的研究1.正常ARPE-19細(xì)胞與損傷的ARPE-19細(xì)胞之間,可以借助激光掃描共聚焦顯微鏡觀察到其間TNT的形成,線粒體從正常ARPE-19細(xì)胞向損傷的ARPE-19細(xì)胞轉(zhuǎn)運(yùn)。2.損傷的ARPE-19細(xì)胞與正常ARPE-19細(xì)胞直接共培養(yǎng)后,ROS水平較單獨(dú)培養(yǎng)組及Transwell小室間接共培養(yǎng)組均明顯降低;增殖能力較單獨(dú)培養(yǎng)組有所增加,胞凋亡水平較單獨(dú)培養(yǎng)組有所降低,差異具有統(tǒng)計(jì)學(xué)意義。表明正常的RPE細(xì)胞可以向損傷的RPE細(xì)胞轉(zhuǎn)運(yùn)線粒體,以挽救損傷RPE細(xì)胞的功能。第三部分:hESC-RPE細(xì)胞與人RPE細(xì)胞系(ARPE-19細(xì)胞)及RCS大鼠RPE細(xì)胞間TNT的形成及線粒體轉(zhuǎn)運(yùn)方向的初步研究1.通過激光掃描共聚焦顯微鏡觀察到正常ARPE-19細(xì)胞與hESC-RPE細(xì)胞間可以形成TNT,并且線粒體從正常ARPE-19細(xì)胞向h ESC-RPE細(xì)胞方向轉(zhuǎn)運(yùn)。2.借助激光掃描共聚焦顯微鏡觀察到200ug/ml Na IO3預(yù)處理的ARPE-19細(xì)胞與h ESC-RPE細(xì)胞間可以觀察到TNT形成,線粒體從200ug/ml Na IO3預(yù)處理的ARPE-19細(xì)胞向hESC-RPE細(xì)胞方向轉(zhuǎn)運(yùn)。3.借助激光掃描共聚焦顯微鏡觀察到2000ug/ml NaIO3預(yù)處理的ARPE-19細(xì)胞與h ESC-RPE細(xì)胞間可以觀察到TNT形成,線粒體從2000ug/mlNaIO3預(yù)處理的ARPE-19細(xì)胞向hESC-RPE細(xì)胞方向轉(zhuǎn)運(yùn)。4.通過激光掃描共聚焦顯微鏡可以觀察到h ESC-RPE細(xì)胞與RCS大鼠RPE細(xì)胞間TNT形成,線粒體從RCS大鼠RPE細(xì)胞向hESC-RPE細(xì)胞方向轉(zhuǎn)運(yùn)。結(jié)論:1.神經(jīng)干細(xì)胞能夠通過線粒體轉(zhuǎn)運(yùn)的機(jī)制,改善視網(wǎng)膜變性大鼠RPE細(xì)胞的增殖、凋亡功能。2.正常ARPE-19細(xì)胞可通過向受損ARPE-19細(xì)胞轉(zhuǎn)運(yùn)線粒體的機(jī)制,挽救氧化損傷的RPE細(xì)胞的ROS水平、細(xì)胞增殖、凋亡功能。3.hESC-RPE細(xì)胞可與正常及損傷的ARPE-19細(xì)胞間形成TNT結(jié)構(gòu)。h ESC-RPE細(xì)胞可與視網(wǎng)膜變性大鼠RPE細(xì)胞之間形成TNT結(jié)構(gòu)。線粒體從正常的ARPE-19細(xì)胞、損傷的ARPE-19細(xì)胞、視網(wǎng)膜變性大鼠RCS-RPE細(xì)胞向h ESC-RPE細(xì)胞方向轉(zhuǎn)運(yùn)。我們推測可能是由于線粒體從成熟程度較高的向線粒體成熟程度相對(duì)較低的細(xì)胞方向轉(zhuǎn)運(yùn)有關(guān)。
[Abstract]:Background and objective retina degeneration diseases include diseases such as retinitis pigmentosa, macular degeneration, Stargardt disease, cone optic dysplasia, and other diseases. The common characteristics of such diseases are the degeneration, apoptosis and necrosis of the key cells of the retina (including photoreceptors, retinoid epithelial cells), resulting in the disease. An irreversible loss of visual function. Due to degeneration and apoptosis of photoreceptor cells or retinal pigment epithelium (retinal pigment epithelial, RPE) cells are not capable of self regeneration. There is no effective treatment for this kind of disease at present,.RPE is a single layer of pigment epithelial cells, located between the retinal neuroepithelial layer and the choroid membrane, which is mainly located between the retina and the choroid. The functions include: the outer barrier of the retina, which engulf the outer segments of the photoreceptor cells, and the melanin can absorb visible light from the dark room, secrete a variety of growth factors, and.RPE cells, such as cytokine and neurotrophic factor, as well as the antioxidant activity, produce a large number of active oxygen substances (reactive). Oxygen species, ROS). Mitochondria are the key organelles of intracellular ROS scavenging and the first site of the most vulnerable oxidative damage in cells. Studies have shown that the dysfunction of mitochondria in RPE cells is closely related to the pathogenesis of retinal degeneration diseases such as AMD and other diseases such as diabetic retinopathy, and the pathogenesis of the disease. Retinal cells or healthy retinal tissues have become the most promising therapeutic strategies. The main mechanisms of treatment for retinal degeneration diseases by stem cell transplantation include cell replacement effect (cell replacement effect), nutritional support effect (by stander effect), and microenvironmental immunoregulation in transplant areas (immune-regulatory Effect) function and so on. Stem cell derived RPE cell transplantation is a promising treatment for blind eye diseases such as wet AMD,.Rustom and other researchers in the culture of pheochromocytoma cells (PC12 cells) in vitro, and found that two adjacent but not direct contact cells can be established by establishing a straight and slender pipe. It is called tunneling nanotubes (TNT). It is found that the structure can be used as a channel for intercellular exchange and exchange of information. Recently, studies have shown that mesenchymal stem cells can improve the power of the recipient cells through mitochondrial exchange. The main purpose of this study is to explore stem cells and human beings. Can the embryonic stem cell derived retinal pigment epithelial cells (human embryonic stem cell-derived retinal pigment epithelium, H ESC-RPE) form a structure between the Royal Academy of surgery (Royal College of) cells of the hereditary retinal pigment degeneration model isolated from the original generation Body transport, mitochondrial transport direction and the effect of mitochondrial transport on the level of ROS, cell proliferation and apoptosis of RPE cells in RCS rats. Preliminary study whether or not through mitochondrial transport mechanism to participate in stem cell treatment of retinal degeneration disease. Methods: the first part: mouse neural stem cells and RCS rat RPE cells The study of body transport and its effect on the function of RPE cells 1., respectively, to mark the primary isolated RPE cells (RCS-RPE) of RCS rats and the mouse neural stem cells (mouse neural stem cells, m NSC) with the culture solution containing the mitochondrial specific markers Mitotracker-red and Mitotracker-green, respectively, and then directly co culture them according to the proportion of the mouse neural stem cells and m NSC. The formation of TNT and mitochondrial transport between mNSC and RCS-RPE cells were observed by laser scanning confocal microscopy..2. was directly co cultured with RCS-RPE cells and mNSC 1:1 equal to green fluorescent protein, GFP virus, and then separated by flow cytometry. RCS-RPE cells and isolated RCS-RPE cells, using flow cytometry to detect cell ROS level, cell cycle and cell apoptosis level. Second part: mitochondrial transport between normal and injured human RPE cell line (ARPE-19 cell) and Study on the function response to damage of ARPE-19 cells, respectively, contain mitochondrial specific marker M Itotracker-red and Mitotracker-green culture medium labeled normal ARPE-19 cells and 24h ARPE-19 cells treated with sodium iodate (NaIO3). 1:1 equal quantities were directly co cultured for 24 h, and the formation of TNT and mitochondrial transport were observed under the laser scanning confocal microscope..2. 200ug/ml Na pretreated and transfected. The ARPE-19 cells of the virus were directly co cultured with 24h, then the flow cytometry was carried out to separate the ARPE-19 cells from the ARPE-19 cells without GFP, and the 200ug/ml Na IO3 pretreated and individually cultured for ARPE-19 cells of 24h. Cell, cell ROS, cell cycle and apoptosis level were detected by flow cytometry. Third part: the formation of TNT between hESC-RPE cells and ARPE-19 cells and RCS-RPE cells and the preliminary study on the direction of mitochondrial transport, 1. respectively labeled hESC-RPE with the culture solution containing mitochondrial specific markers, Mitotracker-red and Mitotracker-green, respectively The normal ARPE-19 cells were directly co cultured for 24 h according to the proportion of 1:1, and the formation of TNT and the mitochondrial transport were observed under the laser scanning confocal microscope..2. was used to mark hESC-RPE and 200ug/ml Na IO3 pretreatment 24h, respectively, with the medium containing mitochondrial specific markers Mitotracker-red and Mitotracker-green. After a direct co culture of 24 h according to the proportion of 1:1, the formation of TNT and the mitochondrial transport were observed under the laser scanning confocal microscope..3. was labeled with hESC-RPE and 2000ug/mlNaIO3 with the culture solution containing the mitochondrial specific markers Mitotracker-red and Mitotracker-green respectively. The 1:1 equal amount was directly co cultured with 24. After h, the formation of TNT and mitochondrial transport were observed under the laser scanning confocal microscope..4. was marked with H ESC-RPE and RCS-RPE with mitochondria specific markers Mitotracker-red and Mitotracker-green respectively. The 1:1 equivalent was directly co cultured with 24 h, and the formation and mitochondria of TNT were observed under the laser scanning confocal microscope. Results: Part 1: the first part: mitochondrial transport of mouse neural stem cells and RCS-RPE cells and the effect of RCS-RPE cells on the function of RPE cells. 1. the formation of TNT was observed between mNSC and RCS-RPE cells by laser scanning confocal microscopy, and mNSC could be observed to transport its own mitochondria to.2. in vitro m NSC in RCS-RPE cells. Compared with the direct co culture system of RCS-RPE cells, the ROS level of RPE cells in the direct co culture group was lower than that in the single culture group. The cell proliferation ability and the apoptosis level were reduced. The difference was statistically significant. The second part: the stem cells could improve the proliferation and apoptosis function of RCS-RPE cells through the mitochondrial transport mechanism. Mitochondrial transport between the RPE cell line (ARPE-19 cell) and the damaged human RPE cell line (ARPE-19 cell) and its effect on the function of damaged ARPE-19 cells; between normal ARPE-19 cells and injured ARPE-19 cells, the formation of TNT can be observed by laser scanning confocal microscope, and mitochondria transfer.2 from normal ARPE-19 cells to damaged ARPE-19 cells. After direct co culture of damaged ARPE-19 cells and normal ARPE-19 cells, the level of ROS was significantly lower than that in the single culture group and the indirect co culture group of the Transwell compartment, and the proliferation ability was higher than that in the single culture group, and the apoptosis level was lower than that in the single culture group. The difference had the significance of the overall planning. It showed that the normal RPE cells could be damaged to the injury. RPE cells transport mitochondria to save the function of damaged RPE cells. Third part: a preliminary study on the formation of TNT and the direction of mitochondrial transport between hESC-RPE cells and human RPE cell lines (ARPE-19 cells) and RPE cells in RCS rats. 1. by laser scanning confocal microscopy, a TNT ARPE-19 cell and hESC-RPE cells can be observed to form TNT. And mitochondria transfer from normal ARPE-19 cells to h ESC-RPE cell direction and.2. by laser scanning confocal microscope to observe that TNT formation can be observed between ARPE-19 cells pretreated by 200ug/ml Na IO3 and H ESC-RPE cells. Scanning confocal microscopy observed that TNT formation was observed between ARPE-19 cells pretreated with 2000ug/ml NaIO3 and H ESC-RPE cells. Mitochondria from ARPE-19 cells pretreated by 2000ug/mlNaIO3 were transported to hESC-RPE cells in the direction of.4. through laser scanning confocal microscopy. Mitochondria transfer from RCS rat RPE cells to hESC-RPE cells. Conclusion: 1. neural stem cells can improve the proliferation of RPE cells in retinal degeneration rats through the mechanism of mitochondrial transport. The apoptosis function.2. normal ARPE-19 cells can save the ROS of RPE cells damaged by oxidative damage by the mechanism of transporting the mitochondria to the damaged ARPE-19 cells. The level, cell proliferation and apoptosis function.3.hESC-RPE cells can form the TNT structure with the normal and damaged ARPE-19 cells. The.H ESC-RPE cells can form the TNT structure with the RPE cells of the retina denatured rats. Mitochondria from normal ARPE-19 cells, damaged ARPE-19 cells, retinal degeneration rat RCS-RPE cells turn to h ESC-RPE cells. We speculate that mitochondria may be related to the transport of mitochondria from relatively high maturity to relatively low degree of mitochondria maturation.
【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R774

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