本文選題：EGR1 + 肌腱干細(xì)胞�。� 參考：《第三軍醫(yī)大學(xué)》2017年博士論文

【摘要】：腱-骨愈合(tendon-bone healing)是運(yùn)動(dòng)醫(yī)學(xué)與骨科面臨的主要科學(xué)問(wèn)題之一。肩袖止點(diǎn)斷裂后局部應(yīng)用生物學(xué)制劑(如細(xì)胞成分,細(xì)胞外基質(zhì)或各種生長(zhǎng)因子)可有效增加手術(shù)修復(fù)的成功率,改善修復(fù)術(shù)后的長(zhǎng)期療效。然而,生物力學(xué)結(jié)果表明,生物學(xué)制劑并不能真正提高肩袖修補(bǔ)的生物力學(xué)。如何更好地解決腱-骨愈合問(wèn)題,成為運(yùn)動(dòng)醫(yī)學(xué)面臨的熱點(diǎn)、難點(diǎn)。以往的研究表明,生長(zhǎng)因子如骨形態(tài)發(fā)生蛋白2、7(BMP-2、BMP-7),轉(zhuǎn)化生長(zhǎng)因子β1和β3(TGF-β1、TGF-β3),堿性成纖維細(xì)胞生長(zhǎng)因子(FGF)等有效提高動(dòng)物模型中腱-骨愈合的治愈率。由于過(guò)分強(qiáng)調(diào)骨側(cè)“被動(dòng)”愈合,修復(fù)后生物力學(xué)強(qiáng)度并未見(jiàn)明顯增加,應(yīng)用此類因子提高手術(shù)成功率的結(jié)論存在質(zhì)疑。最近的研究表明,早期生長(zhǎng)反應(yīng)因子(early growth response-1,Egr1)參與了肌腱分化。EGR1不僅促進(jìn)胚胎時(shí)期四肢肌腱細(xì)胞的分化,并且能誘導(dǎo)肌腱形成標(biāo)志物Scleraxis(SCX)的表達(dá)和肌腱膠原的形成。體內(nèi)研究進(jìn)一步證實(shí),過(guò)表達(dá)Egr1的間充值干細(xì)胞(mesenchymal stem cells,MSCs)對(duì)損傷跟腱有明顯的修復(fù)作用。前期課題組大量研究發(fā)現(xiàn),肌腱干細(xì)胞(tendon stem cells,TSCs)是修復(fù)肌腱損傷最有效的前體細(xì)胞之一。如何刺激TSCs向肌腱方向分化,進(jìn)而促進(jìn)腱側(cè)“主動(dòng)”愈合成為本課題主要重點(diǎn)。本部分?jǐn)M觀察EGR1誘導(dǎo)TSC細(xì)胞向肌腱分化的作用。本研究擬從EGR1對(duì)TSCs分化作用的影響,觀察影響TSCs成肌腱分化的信號(hào)通路,最后將EGR1導(dǎo)入TSCs,觀察EGR1-TSCs對(duì)腱-骨愈合影響的表現(xiàn)。第一部分EGR1對(duì)TSCs多向分化影響的初步觀察本部分?jǐn)M觀察EGR1對(duì)TSCs的多向分化能力的觀察,對(duì)比成肌腱分化與病理性分化的差異。一、實(shí)驗(yàn)方法雙酶切法將EGR1 c DNA編碼序列從pCMV-EGR1切除,回收后并進(jìn)一步克隆至pcDNA3.1+載體上,獲得pCDNA-EGR1。細(xì)胞轉(zhuǎn)染pCDNA-EGR1或載體(對(duì)照)單獨(dú)使用Lipofectamine 2000轉(zhuǎn)染試劑。G418(800μg/ml)篩選穩(wěn)定轉(zhuǎn)染細(xì)胞。TSCs與pCDNA-EGR1轉(zhuǎn)染TSCs(EGR1-TSCS)進(jìn)行向肌腱方向培養(yǎng)培養(yǎng),細(xì)胞接種于含有DMEM的6孔板中。采用免疫熒光染色和熒光定量PCR檢測(cè),對(duì)分化相關(guān)的基因SCX、TNMD、TNC、Col I表達(dá)的檢測(cè)。二、實(shí)驗(yàn)結(jié)果免疫熒光染色顯示:過(guò)表達(dá)EGR1的TSCs可以表達(dá)較高水平的肌腱標(biāo)記物SCX、TNMD與TNC,表明EGR1基因影響這些細(xì)胞腱性分化相關(guān)基因的轉(zhuǎn)錄水平。細(xì)胞特殊染色顯示,過(guò)表達(dá)EGR1的TSCs誘導(dǎo)分化抑制成脂肪分化、成骨分化、成軟骨分化。此外,PPARγ、Runx2、Sox9基因轉(zhuǎn)錄水平下降,表明EGR1下調(diào)非腱性分化(成脂、成骨、成軟骨等)相關(guān)基因的轉(zhuǎn)錄。三、小結(jié)1.將EGR1轉(zhuǎn)染至TSCs后,獲得過(guò)表達(dá)EGR1的穩(wěn)定TSCs細(xì)胞株。2.從蛋白表達(dá)、基因轉(zhuǎn)錄水平檢測(cè)顯示,EGR1促進(jìn)TSCs向成肌腱方向分化。3.EGR1特異性促進(jìn)TSCs向成肌腱分化,同時(shí)抑制TSCs向脂肪細(xì)胞、成骨細(xì)胞、軟骨細(xì)胞方向分化。第二部分EGR1對(duì)TSCs向成肌腱方向分化的通路研究本部分在第一部分研究基礎(chǔ)上進(jìn)一步研究EGR1影響TSCs成肌腱分化的信號(hào)通路。一、實(shí)驗(yàn)方法在成肌腱分化研究過(guò)程中,分析BMP12/Smad1/5/8通路蛋白的產(chǎn)量,兩組在不同時(shí)間點(diǎn)收集細(xì)胞。用BCA蛋白濃度測(cè)定試劑盒測(cè)定總蛋白濃度與等量的蛋白質(zhì),通過(guò)SDS-聚丙烯酰胺凝膠電泳。然后將蛋白轉(zhuǎn)移到聚偏氟乙烯膜,依次用第一和第二抗體阻斷。使用LICOR Odyssey成像儀觀察結(jié)果。二、實(shí)驗(yàn)結(jié)果在EGR1-TSCs組,BMP12基因m RNA和蛋白水平和p-Smad1/5/8蛋白水平相似,逐漸增加并呈時(shí)間依賴性過(guò)表達(dá),并促進(jìn)向成肌腱分化,但在TSCs組中并不明顯。肌腱分化中Smad1蛋白水平總量沒(méi)有增加。EGR1-TSCS組肌腱相關(guān)基因的表達(dá),SCX、TNMD、TNC、Col I呈時(shí)間依賴性逐漸增加。三、小結(jié)1.BMP12能誘導(dǎo)TSC向成肌腱分化,并得出最優(yōu)劑量及最優(yōu)持續(xù)時(shí)間。2.BMP12與BMPRI型受體結(jié)合后激活Smad表達(dá),EGR1通過(guò)BMP12/Smad1/5/8信號(hào)通路促進(jìn)TSCs向成肌腱分化。3.EGR1-TSCs向成肌腱分化過(guò)程中,EGR1對(duì)BMP12、Smad1/5/8調(diào)節(jié)呈時(shí)間依賴性。第三部分過(guò)表達(dá)EGR1的TSCs對(duì)兔肩袖慢性損傷的影響本部分建立兔肩袖慢性損傷模型,將EGR1-TSCs植入腱-骨界面,觀察對(duì)腱-骨愈合的影響。一、實(shí)驗(yàn)方法將24只成年新西蘭大白兔的雙側(cè)岡上肌腱切斷,右側(cè)為實(shí)驗(yàn)組,左側(cè)假手術(shù)組。6周后行肩袖陳舊性損傷修補(bǔ)術(shù)。TSCs與EGR1-TSCS混合纖維蛋白膠中植入肩袖界面間。將實(shí)驗(yàn)用兔分為三組:1組(R),修復(fù)手術(shù);2組(TSCs),修補(bǔ)+植入含TSCs的纖維蛋白膠;3組(EGR1-TSCS),修復(fù)+植入含EGR1-TSCS的纖維蛋白膠。修復(fù)手術(shù)8周后處死所有兔。組織學(xué)分析和免疫組化檢測(cè)評(píng)估之間的差異。二、實(shí)驗(yàn)結(jié)果術(shù)后8周,TSCs組呈平行的纖維組織,可見(jiàn)沿應(yīng)力方向少量的Sharpey纖維;在EGR1-TSC組,膠原纖維排列更為有序,止點(diǎn)處Sharpey纖維較TSC組更明顯。三、小結(jié)1.通過(guò)建立穩(wěn)定的兔肩袖慢性損傷模型,為腱-骨愈合提供了良好的動(dòng)物模型。2.在兔肩袖慢性損傷模型中,腱-骨界面應(yīng)用含有EGR1-TSCs的纖維凝膠可有效促進(jìn)腱-骨愈合。
[Abstract]:Tendon bone healing (tendon-bone healing) is one of the major scientific problems in sports medicine and Department of orthopedics. The local application of biological agents (such as cell composition, extracellular matrix or various growth factors) after the rotator cuff break can effectively increase the success rate of surgical repair and improve the long-term effect after the repair. However, the biomechanical results show that Biological agents do not really improve the biomechanics of rotator cuff repair. How to better solve the problem of tendon bone healing has become a hot and difficult problem in sports medicine. Previous studies have shown that growth factors such as bone morphogenetic protein 2,7 (BMP-2, BMP-7), transforming growth factor beta 1 and beta 3 (TGF- beta 1, TGF- beta 3), basic fibroblast growth factors FGF and so on effectively improve the healing rate of tendon bone healing in animal models. Due to the excessive emphasis on the "passive" healing of the bone side, the biomechanical strength after repair has not been significantly increased, and the conclusion of the application of such factors to improve the success rate of the operation is questioned. Recent studies have shown that the early growth response factor (early growth response-1, Egr1) participated in the study. Tendon differentiation.EGR1 not only promotes the differentiation of tendon cells in the embryonic period, but also induces the expression of Scleraxis (SCX) and the formation of tendon collagen in the tendon formation markers. In vivo studies have further confirmed that the revalued stem cells (mesenchymal stem cells, MSCs) over expressed Egr1 have obvious repair effect on the injured Achilles tendon. A large number of studies have found that tendon stem cells (TSCs) is one of the most effective precursor cells for the repair of tendon injury. How to stimulate the direction differentiation of TSCs to the tendons and promote the "active" healing of the tendon side has become the main focus of this topic. This part is to observe the effect of EGR1 induced TSC cells to the differentiation of the tendon to the tendon. This study is to be taken from EGR1 pairs. The effect of TSCs differentiation, observing the signal pathway affecting the differentiation of TSCs tendon, and finally introducing EGR1 into TSCs to observe the effect of EGR1-TSCs on the healing of tendon bone. The first part of the preliminary observation on the effect of EGR1 on the multidirectional differentiation of TSCs, this part is to observe the observation of the multidirectional differentiation energy of EGR1 to TSCs, and to contrast the differentiation and pathological differentiation of the tendon. First, the EGR1 C DNA coding sequence was removed from pCMV-EGR1 by double enzyme digestion method, and then recovered and cloned to pcDNA3.1+ vector, and pCDNA-EGR1. cells were transfected to pCDNA-EGR1 or carrier (control) to use Lipofectamine 2000 transfection reagent.G418 (800 mu g/ ml) to screen the stable transfection cell.TSCs and transfection GR1-TSCS) was cultured in the direction of tendon, and the cells were inoculated in the 6 orifice plate containing DMEM. Immunofluorescence staining and fluorescence quantitative PCR detection were used to detect the expression of SCX, TNMD, TNC, Col I related genes. Two, the experimental results of immunofluorescence staining showed that the TSCs of overexpressed EGR1 could express the higher level of tendon markers SCX, TNM D and TNC show that EGR1 genes affect the transcriptional level of the genes related to the differentiation of these cells. Cell specific staining shows that the TSCs induced differentiation of overexpressed EGR1 can inhibit adipose differentiation, osteogenesis and chondrodifferentiation. In addition, the transcriptional level of PPAR gamma, Runx2, Sox9 gene decreases, indicating that EGR1 downplays non Achilles differentiation (lipid, osteogenesis, cartilage, etc.) The transcription of related genes. Three, after transfection of EGR1 to TSCs, the stable TSCs cell line.2. expressing EGR1 was obtained from the protein expression, and the gene transcriptional level detection showed that EGR1 promoted TSCs to differentiate.3.EGR1 specificity from TSCs into tendons to promote the differentiation of TSCs into tendon, and inhibit TSCs to adipocytes, osteoblasts and chondrocytes. Second part of the pathway of EGR1 to the direction differentiation of TSCs into the tendons of the tendon. This part further studies the signal pathway that EGR1 affects the differentiation of TSCs tendon in the first part of the study. One, the experimental method analyses the production of BMP12/Smad1/5/8 pathway protein in the process of tendon differentiation, and the two groups collect cells at different time points. CA protein concentration assay kit was used to determine the total protein concentration and equal amount of protein by SDS- polyacrylamide gel electrophoresis. Then the protein was transferred to polyvinylidene fluoride membrane, and the first and second antibodies were interrupted in turn. The results were observed by the LICOR Odyssey imager. Two, the experimental results were in the EGR1-TSCs group, the BMP12 gene m RNA and protein levels and p-. Smad1/5/8 protein levels were similar, gradually increased and showed time dependent overexpression, and promoted the differentiation of the tendon into the tendon, but it was not obvious in the TSCs group. The total amount of Smad1 protein in the tendon differentiation did not increase the expression of the gene related genes in the.EGR1-TSCS group. SCX, TNMD, TNC, Col I showed a gradual increase in time dependence. Three, nodules 1.BMP12 could induce TSC. The optimal dose and optimal duration of.2.BMP12 are combined with BMPRI receptor to activate Smad expression. EGR1 through BMP12/Smad1/5/8 signaling pathway promotes TSCs into tendon differentiation.3.EGR1-TSCs into tendon differentiation process, EGR1 is time dependent on BMP12, Smad1/5/8 regulation. The third part overexpresses EGR1 TSCs pairs. The chronic injury of the rotator cuff in rabbits was used to establish a chronic injury model of the rabbit's rotator cuff. EGR1-TSCs was implanted into the tendon bone interface and the effect of the tendon bone healing was observed. One, the experimental method was used to cut the bilateral supraspinatus tendon of 24 adult New Zealand white rabbits, the right was the experimental group, and the left rotator cuff old injury repair operation was performed after the left hand prosthesis group.6 weeks after the repair of.TSCs and the repair of the rotator cuff. EGR1-TSCS mixed fibrin glue was implanted into the rotator cuff interface. The experimental rabbits were divided into three groups: 1 groups (R), repair operation; 2 groups (TSCs), repair + implantation of fibrin glue containing TSCs; 3 groups (EGR1-TSCS), repair and implantation of fibrin glue containing EGR1-TSCS. All rabbits were killed after 8 weeks of repair. Histology analysis and immunohistochemical detection assessment Two, 8 weeks after the operation, group TSCs showed a parallel fibrous tissue, and a small amount of Sharpey fibers along the stress direction; in group EGR1-TSC, the collagen fibers were arranged more orderly, and the Sharpey fibers were more obvious at the stop point. Three, nodule 1., by establishing a stable chronic injury model of the rabbit rotator cuff, provided a good movement for the tendon bone healing. Object model.2. in rabbit chronic rotator cuff injury model, fibrous gel containing EGR1-TSCs can be used to promote tendon bone healing in tendon bone interface.
【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2017
【分類號(hào)】：R687

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