【摘要】：【研究背景】在口腔頜面外科和整形外科領(lǐng)域,腫瘤切除、創(chuàng)傷、感染、先天性萎縮均可導(dǎo)致皮下脂肪層喪失及大體積軟組織缺損。軟組織缺損不僅影響正常組織功能,還嚴(yán)重影響患者美觀和心理狀態(tài),因此,理想的可移植的具有生理功能的脂肪組織在頜面外科及整形外科領(lǐng)域有非常大的需求。當(dāng)前,軟組織缺損的修復(fù)重建包括自體組織移植,人工合成假體植入等方法,但存在易吸收、供區(qū)缺損、手術(shù)復(fù)雜以及假體生物相容性不足的問(wèn)題。因此,整形重建外科一直在尋求能夠克服上述問(wèn)題的方法。近年來(lái)隨著再生醫(yī)學(xué)及組織工程技術(shù)快速發(fā)展,組織工程方法構(gòu)建大體積脂肪取得了可喜的進(jìn)展。然而,由于脂肪組織是高度血管化和高代謝活性的組織,而血運(yùn)重建是組織再生的基礎(chǔ),要構(gòu)建組織工程化脂肪組織,尤其是大體積的脂肪組織,必須保證移植物內(nèi)部盡早獲得營(yíng)養(yǎng)和氧氣的供給。血管化不足成為制約構(gòu)建大體積組織工程脂肪的瓶頸問(wèn)題。然而,我們對(duì)血管化機(jī)制的認(rèn)識(shí)仍然不足,為解決血管化的難題,需要從明確血管化的機(jī)制入手。既往的脂肪組織工程研究大多聚焦于脂肪間充質(zhì)干細(xì)胞/脂肪前體細(xì)胞,內(nèi)皮祖細(xì)胞/內(nèi)皮細(xì)胞,以及影響它們?cè)鲋�、分化的�?xì)胞因子篩選或支架設(shè)計(jì);而對(duì)脂肪和血管生成中的其他類(lèi)型細(xì)胞,如巨噬細(xì)胞,關(guān)注較少。近年來(lái)隨著對(duì)巨噬細(xì)胞在組織修復(fù)和再生中的重要性的認(rèn)識(shí)加深,人們認(rèn)識(shí)到巨噬細(xì)胞的功能不僅僅是一種參與非特異性免疫和特異性免疫的的吞噬細(xì)胞,在固有免疫應(yīng)答中發(fā)揮重要作用,其在組織器官的發(fā)育、內(nèi)穩(wěn)態(tài)的維持、多種組織器官損傷的修復(fù)和再生等生理和病理過(guò)程中的作用也受到越來(lái)越多的關(guān)注。近年來(lái),有學(xué)者發(fā)現(xiàn)巨噬細(xì)胞參與了組織工程脂肪構(gòu)建中的血管生成和脂肪再生。然而,巨噬細(xì)胞是一種具有高度異質(zhì)性和可塑性的細(xì)胞,在不同的局部微環(huán)境下,巨噬細(xì)胞可極化為不同的表型,分泌多種不同的細(xì)胞因子。在脂肪再生和脂肪組織工程領(lǐng)域不同的巨噬細(xì)胞表型及其在脂肪再生中的作用,尚無(wú)文獻(xiàn)報(bào)告。綜上,本課題擬構(gòu)建血管化組織工程脂肪組織,在此基礎(chǔ)上研究血管生成和脂肪生成中巨噬細(xì)胞的分布及表型特點(diǎn),并深入探討巨噬細(xì)胞及其不同表型在血管化組織工程脂肪構(gòu)建中的作用,為揭示脂肪再生的機(jī)制以及為構(gòu)建符合臨床要求的血管化組織工程脂肪提供理論基礎(chǔ)和實(shí)驗(yàn)依據(jù)�！狙芯磕康摹拷⒋笫笾窘M織工程模型,通過(guò)對(duì)模型的改良和優(yōu)化,探索血管化脂肪再生的合適條件。研究組織工程脂肪構(gòu)建中巨噬細(xì)胞分布及表型變化,分析組織工程室內(nèi)多種抗炎和促炎細(xì)胞因子的微環(huán)境;明確巨噬細(xì)胞對(duì)組織工程室內(nèi)血管生成和脂肪生成及微環(huán)境的影響,對(duì)巨噬細(xì)胞及表型調(diào)控在組織工程脂肪構(gòu)建中的作用進(jìn)行了初步探索。【研究方法】1組織工程室脂肪再生模型的構(gòu)建利用中空的硅膠管作為組織工程室模型,植入大鼠腹股溝,硅膠管內(nèi)注入FGF-2緩釋的Matrigel凝膠支架,比較軸型血管蒂+骨蠟封口組、無(wú)血管蒂+脂肪瓣封口組、軸型血管蒂+脂肪墊封口組三種不同的血管化組織工程脂肪構(gòu)建方法脂肪再生的差異。2組織工程室脂肪再生過(guò)程中的巨噬細(xì)胞表型轉(zhuǎn)化研究利用實(shí)驗(yàn)一構(gòu)建的大鼠脂肪組織工程室模型,在不同時(shí)間點(diǎn)取材,分析組織工程室血管生成和脂肪再生情況,通過(guò)免疫組化和免疫熒光技術(shù)分析再生過(guò)程中巨噬細(xì)胞數(shù)量及表型的變化,并通過(guò)ELISA法對(duì)組織工程室內(nèi)促炎和抗炎細(xì)胞因子微環(huán)境進(jìn)行分析。3早期巨噬細(xì)胞清除對(duì)組織工程室脂肪再生的影響利用大鼠脂肪組織工程室模型,采用脂質(zhì)體介導(dǎo)的巨噬細(xì)胞自殺技術(shù),分析早期巨噬細(xì)胞清除對(duì)組織工程室內(nèi)血管生成和脂肪再生的影響,通過(guò)免疫組化和免疫熒光技術(shù)分析組織工程室內(nèi)內(nèi)皮細(xì)胞、中性粒細(xì)胞、巨噬細(xì)胞的分布,以及巨噬細(xì)胞的表型情況。并通過(guò)ELISA法分析早期巨噬細(xì)胞清除對(duì)組織工程室內(nèi)促炎和抗炎細(xì)胞因子微環(huán)境的影響�！緦�(shí)驗(yàn)結(jié)果】三個(gè)組6周取材時(shí)血管蒂通暢,軸型血管蒂+脂肪墊封口組組織工程室內(nèi)容物的平均重量和體積最大,血管蒂周?chē)梢?jiàn)大量的成熟脂肪組織,無(wú)軸型血管蒂+脂肪墊封口組脂肪生成相對(duì)較少,而軸型血管蒂+骨蠟封口組新生組織量最少,主要為纖維結(jié)締組織,幾乎看不見(jiàn)脂肪細(xì)胞。組織工程室植入后第3天,大量的炎細(xì)胞浸潤(rùn),內(nèi)皮細(xì)胞進(jìn)入Matrigel凝膠,呈現(xiàn)出血外觀,植入后第7天,Matrigel開(kāi)始部分降解,并被新生結(jié)締組織和毛細(xì)血管替代。植入后第14天,Matrigel大部分降解,Matrigel凝膠被新生結(jié)締組織和新生血管替代,未見(jiàn)明顯的脂肪生成。植入后第42天,Matrigel完全降解,可見(jiàn)大量的成熟脂肪組織,周?chē)梢?jiàn)結(jié)締組織包膜。Lectin血管內(nèi)皮染色顯示,血管密度明顯增加,在2周時(shí)達(dá)到峰值,隨后相對(duì)穩(wěn)定。CD68染色顯示,第3天即可見(jiàn)明顯巨噬細(xì)胞浸潤(rùn),巨噬細(xì)胞密度在第7天到達(dá)峰值,隨后顯著降低。在不同時(shí)間點(diǎn),巨噬細(xì)胞均有M1和M2兩種表型。M1巨噬細(xì)胞比例第3天最后,隨后逐漸下降,M2巨噬細(xì)胞比例有持續(xù)增高的趨勢(shì),而M2/M1比值從7-42天整個(gè)血管生成脂肪再生階段持續(xù)增加。ELISA檢測(cè)組織工程室內(nèi)不同時(shí)間點(diǎn)促炎和抗炎細(xì)胞因子的分泌水平,促炎細(xì)胞因子IL-1β、TNF-α和IL-6整體呈下降趨勢(shì),抗炎細(xì)胞因子IL-4、IL-10和TGF-β整體呈上升趨勢(shì)。巨噬細(xì)胞清除組4天后組織工程室內(nèi)巨噬細(xì)胞密度較對(duì)照組顯著降低,14天后巨噬細(xì)胞密度恢復(fù)正常。進(jìn)一步分析巨噬細(xì)胞表型,發(fā)現(xiàn)第14天巨噬細(xì)胞清除組M1巨噬細(xì)胞所占比例顯著高于對(duì)照組,M2巨噬細(xì)胞比例以及M2/M1比值顯著低于對(duì)照組。在第4、14和42天,巨噬細(xì)胞清除組中性粒細(xì)胞密度顯著高于對(duì)照組。ELISA結(jié)果顯示,第14天時(shí),促炎細(xì)胞因子IL-1β、TNF-α和IL-6的分泌水平氯膦酸二鈉組顯著高于脂質(zhì)體組。而抗炎細(xì)胞因子IL-4、IL-10和TGF-β的分泌水平氯膦酸二鈉組顯著低于脂質(zhì)體對(duì)照組。【結(jié)論】利用組織工程室模型和血管化體內(nèi)預(yù)構(gòu)技術(shù),可實(shí)現(xiàn)血管化脂肪組織再生。組織工程室為組織再生提供了空間,血管蒂的引入,生物支架材料的植入以及與自體脂肪組織接觸,構(gòu)建了成血管和成脂的微環(huán)境,有利于血管生成和脂肪再生。巨噬細(xì)胞參與了組織工程室中血管生成和脂肪再生的全過(guò)程;在血管生成和脂肪再生的過(guò)程中,巨噬細(xì)胞經(jīng)歷了從炎癥期的促炎M1表型向增殖期的抗炎M2表型的轉(zhuǎn)換,小室微環(huán)境也從炎癥期的促炎狀態(tài)向增殖期的抗炎狀態(tài)轉(zhuǎn)換。通過(guò)脂質(zhì)體介導(dǎo)的巨噬細(xì)胞清除技術(shù),證實(shí)巨噬細(xì)胞在組織工程室的早期血管化和脂肪再生中發(fā)揮關(guān)鍵作用。脂質(zhì)體包裹的氯膦酸二鈉能高效清除組織工程室內(nèi)的巨噬細(xì)胞,但這種清除作用在兩周后消失;早期巨噬細(xì)胞清除會(huì)導(dǎo)致組織工程室內(nèi)的血管化顯著延遲,中性粒細(xì)胞持續(xù)浸潤(rùn),小室微環(huán)境處于持續(xù)的炎癥狀態(tài);早期巨噬細(xì)胞清除導(dǎo)致巨噬細(xì)胞增殖期從M1向M2表型轉(zhuǎn)換障礙。提示巨噬細(xì)胞表型調(diào)控,而不是巨噬細(xì)胞數(shù)量,是決定組織工程室內(nèi)脂肪再生的關(guān)鍵因素。本研究為大體積組織工程脂肪構(gòu)建提供了新的思路。在組織工程支架的設(shè)計(jì)理念上,使設(shè)計(jì)的生物支架植入體內(nèi)后有利于巨噬細(xì)胞向M2表型轉(zhuǎn)換,或通過(guò)導(dǎo)入外源性的細(xì)胞因子或細(xì)胞的方法,誘導(dǎo)巨噬細(xì)胞向M2表型轉(zhuǎn)換,使局部微環(huán)境從促炎狀態(tài)向抗炎狀態(tài)轉(zhuǎn)變,這可能是未來(lái)血管化組織工程脂肪構(gòu)建的重要策略之一。
[Abstract]:[background] in the field of oral and maxillofacial surgery and orthopedics, tumor resection, trauma, infection, and congenital atrophy can lead to subcutaneous fat layer loss and large volume soft tissue defect. Soft tissue defects not only affect normal tissue function, but also seriously affect the patient's aesthetic and mental state. Therefore, the ideal transplantation has physiological function. There is a great demand for adipose tissue in maxillofacial surgery and orthopedics. At present, the repair and reconstruction of soft tissue defects include autologous tissue transplantation, artificial prosthesis implantation and other methods, but there are problems of easy absorption, donor defect, complex operation, and imbiocompatibility of prosthesis. Therefore, plastic and reconstruction surgery has been seeking ability. In recent years, with the rapid development of regenerative medicine and tissue engineering technology, great progress has been made in the construction of mass fat by tissue engineering. However, as adipose tissue is highly vascularized and highly metabolized, revascularization is the basis of regenerative tissue, and the construction of tissue engineered fat is to be constructed. Tissue, especially large volume adipose tissue, must ensure the early access to nutrition and oxygen supply in the graft. Insufficient vascularization is a bottleneck to constraining the construction of mass tissue engineering fat. However, our understanding of the vascularization mechanism is still insufficient. In order to solve the problem of hemangiarization, the mechanism of vascularization should be defined. Hand. Previous adipose tissue engineering studies mostly focus on adipose mesenchymal stem cells / adipose progenitor cells, endothelial progenitor cells / endothelial cells, and cell factor screening or scaffold design that affect their proliferation and differentiation; and less attention has been paid to other types of cells in fat and angiogenesis, such as macrophages. The understanding of the importance of cells in tissue repair and regeneration has deepened. People realize that the function of macrophages is not only a phagocyte that participates in non specific immunity and specific immunity. It plays an important role in the inherent immune response, the development of the tissues and organs, the maintenance of internal homeostasis, and the repair of a variety of tissues and organs. In recent years, some scholars have found that macrophages are involved in angiogenesis and fat regeneration in tissue engineering fat construction. However, macrophages are highly heterogeneous and plastic cells, and macrophages can be found in different local microenvironments. Polarization is a different phenotype and secretes a variety of different cytokines. There is no literature report on the different phenotype of macrophage and its role in adipose regeneration in the field of adipose regeneration and adipose tissue engineering. To sum up, this topic intends to construct vascularized tissue engineering adipose tissue, on this basis, to study the giant macrophages in angiogenesis and adipose formation. The distribution and phenotypic characteristics of cells and the role of macrophages and their different phenotypes in the construction of vascular tissue engineering fat are discussed in order to reveal the mechanism of fat regeneration and to provide theoretical and experimental basis for the construction of vascularized tissue engineering fat, which is in accordance with the clinical requirements. Through the improvement and optimization of the model, the appropriate conditions for the regeneration of vascularized fat are explored. The distribution and phenotypic changes of macrophages in the construction of tissue engineering fat are studied, and the microenvironment of various anti-inflammatory and proinflammatory cytokines in the tissue engineering room is analyzed, and the angiogenesis, adipose formation and microring of the macrophages in the tissue engineering are clearly defined. The effect of macrophage and phenotypic regulation in the construction of tissue engineering fat was preliminarily explored. [Methods] the construction of 1 tissue engineering room fat regeneration model was constructed using hollow silicone tube as a tissue engineering room model, implanted in rat groin and implanted with FGF-2 sustained-release Matrigel gel stent in silica gel tube. Axial type vascular pedicle + bone wax seal group, no vascular pedicle + fat flap seal group, three different vascular tissue engineering fat construction methods of adipose tissue engineering in the group of adipose tissue engineering fat regeneration in.2 tissue engineering room The changes in the number and phenotype of macrophages in the process of regeneration were analyzed by immunohistochemistry and immunofluorescence, and the microenvironment of proinflammatory and anti-inflammatory cytokines in the tissue engineering room was analyzed by ELISA method, and the early.3 macrophage clearance group was analyzed by the method of immunohistochemistry and immunofluorescence. The effect of fat regeneration in the weaving room was used in the rat adipose tissue engineering room model. The effect of early macrophage clearance on the angiogenesis and fat regeneration in the tissue engineering was analyzed by liposome mediated macrophage suicide technique. The endothelial cells in the tissue engineering were analyzed by immunohistochemistry and immunofluorescence. The distribution of macrophages and the phenotype of macrophages. The effects of early macrophage clearance on the microenvironment of proinflammatory and anti-inflammatory cytokines in the tissue engineering room were analyzed by ELISA method. [experimental results] the blood vessels were patted when three groups were harvested for 6 weeks, and the average volume of tissue engineering in the axial type and fat pad seal group was average. The weight and volume were the largest, and a large number of mature adipose tissue were found around the pedicle. The adipose formation in the non axial vascular pedicle and the fat pad seal group was relatively less, while the axial type and the bone wax seal group had the least new tissue, mainly fibrous connective tissue and almost no adipocytes. A large number of inflammatory cells were immersed in the tissue engineering room third days after implantation. The endothelial cells entered Matrigel gel, showing the appearance of bleeding, seventh days after implantation, Matrigel began to degrade partially, and was replaced by new connective tissue and capillaries. Fourteenth days after implantation, most of Matrigel was degraded and Matrigel gel was replaced by new connective tissue and neovascularization, and no obvious adipose formation was found. Forty-second days after implantation, Matrigel Complete degradation, a large number of mature adipose tissue were visible, and the surrounding connective tissue enveloped.Lectin vascular endothelial staining showed that the blood vessel density increased significantly, reached the peak at 2 weeks, followed by relatively stable.CD68 staining, and the obvious macrophage infiltration was visible on the third day, the peak of macrophage density reached the peak at seventh days, then decreased significantly. At different time points, the proportion of macrophages with two phenotypes of M1 and M2 was third days last, then decreased gradually, and the proportion of M2 macrophages continued to increase, while the M2/M1 ratio continued to increase from the 7-42 days of 7-42 days of angiogenesis in the adipose regeneration stage to detect the proinflammatory and anti-inflammatory cytokines at different time points in the tissue engineering. Secretory level, proinflammatory cytokines IL-1 beta, TNF- alpha and IL-6 overall decreased, anti-inflammatory cytokines IL-4, IL-10 and TGF- beta overall increased. Macrophage density in the tissue engineering room was significantly lower than that of the control group after 4 days of macrophage clearance, and the density of macrophages returned to normal after 14 days. Further analysis of macrophage phenotypes was made. The proportion of M1 macrophages in the fourteenth days of macrophage clearance group was significantly higher than that in the control group. The proportion of M2 macrophages and the ratio of M2/M1 were significantly lower than that of the control group. In the 4,14 and 42 days, the neutrophils density in the macrophage clearance group was significantly higher than that of the control group.ELISA results, and the secretion of proinflammatory cytokines, IL-1 beta, TNF- A and IL-6 at fourteenth days. The level of level chlorphosphonic acid two sodium was significantly higher than that in the liposome group. The secretory level of anti inflammatory cytokine IL-4, IL-10 and TGF- beta was significantly lower than that in the liposome control group. [Conclusion] tissue engineering room model and vascularized preconditioning can be used to regenerate vascular fat group. Tissue engineering room is provided for tissue regeneration. Space, the introduction of vascular pedicle, implantation of scaffold materials and contact with autologous fat tissue, construction of vascular and lipid microenvironment, which is beneficial to angiogenesis and fat regeneration. Macrophages participate in the whole process of angiogenesis and fat regeneration in the tissue engineering room; in the process of angiogenesis and fat regeneration, macrophages Through the transformation of inflammatory M2 phenotype from proinflammatory M1 phenotype to proliferation stage, small chamber microenvironment also converts from inflammatory proinflammatory to proliferative stage to anti-inflammatory state. Through liposome mediated macrophage clearance technology, macrophages play a key role in early vascularization and fat regeneration in tissue engineering. The plastid encapsulated sodium chlorosonate two could efficiently remove macrophages in the tissue engineering room, but this scavenging effect disappeared after two weeks. Early macrophage clearance would lead to significant delayed vascularization in the tissue engineering room, continuous infiltration of neutrophils, and a sustained inflammatory condition in the microenvironment; early macrophage clearance resulted in giant macrophages. The phagocytosis phase transforms from M1 to M2 phenotype. It suggests that the macrophage phenotypic regulation, not the number of macrophages, is the key factor in determining the regeneration of fat in the tissue engineering. This study provides a new idea for the construction of mass tissue engineering fat. In the design concept of tissue engineering scaffold, the designed biological scaffold is implanted in the tissue engineering scaffold. In vivo, it is beneficial for the transformation of macrophages to M2 phenotypes, or by introducing exogenous cytokines or cells, inducing macrophages to convert to M2 phenotypes and change the local microenvironment from proinflammatory to anti-inflammatory state, which may be one of the important strategies for the construction of vascularized tissue engineering fat in the future.
【學(xué)位授予單位】：第四軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類(lèi)號(hào)】：R318.08

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