本文選題：血管平滑肌 + 胎肝激酶-1�。� 參考：《大連醫(yī)科大學(xué)》2007年碩士論文

【摘要】： 研究背景和目的 血管增殖失調(diào)是臨床常見的病理過程,如動(dòng)脈粥樣硬化、同種異體移植后血管重塑、支架內(nèi)再狹窄、經(jīng)皮球囊血管成形術(shù)等,探討血管平滑肌細(xì)胞(Vascular smooth muscle cells,VSMCs)的起源有助于增生性血管病的治療。以往認(rèn)為胚胎的VSMCs起源于神經(jīng)嵴和胚胎中胚層;新近發(fā)現(xiàn)VSMCs還可能起源于成體骨髓干細(xì)胞或祖細(xì)胞、外周血的單核細(xì)胞、骨骼肌的成體干細(xì)胞和內(nèi)皮細(xì)胞(Endothelium cells,ECs)等。Yamashita J等的體外研究證實(shí),胚胎干細(xì)胞來源的胎肝激酶-1(Fetal liver kinase-1,Flk-1),即血管內(nèi)皮生長因子受體-2陽性細(xì)胞在血管內(nèi)皮生長因子(Vascular endothelial growth factor,VEGF)作用下可分化為血管ECs,在血小板源性生長因子-BB作用下可分化為VSMCs,因此認(rèn)為Flk-1陽性細(xì)胞是血管ECs和VSMCs的共同前體,然而該理論尚缺乏在體證據(jù)支持。我們通過對(duì)胚胎血管行Flk-1、血小板內(nèi)皮細(xì)胞粘附分子(Platelet endothelial cell adhesion molecule-1,PECAM-1/CD31)、Ⅷ因子相關(guān)抗原及平滑肌α-肌動(dòng)蛋白(Smooth Muscleα-actin,SMα-actin)免疫組織化學(xué)染色,探討上述標(biāo)志物在血管形成初期的表達(dá)時(shí)相及空間位置關(guān)系,為VSMCs的起源提供新的在體實(shí)驗(yàn)依據(jù)。 Flk-1主要分布于ECs、造血細(xì)胞及其前體細(xì)胞,已有報(bào)道Flk-1最早出現(xiàn)于小鼠胚胎6.5 d,在ECs及造血細(xì)胞的發(fā)育中發(fā)揮重要作用;在血管新生生理過程或腫瘤等病理過程中也可觀察到Flk-1呈高表達(dá),但小鼠植入前胚胎是否表達(dá)Flk-1迄今尚未見報(bào)道。本實(shí)驗(yàn)擬初步探討Flk-1在小鼠植入前胚胎發(fā)育過程中的表達(dá)規(guī)律及其在胚胎發(fā)育中的作用。 實(shí)驗(yàn)方法 1.獲取8.5～18.5 d胚胎:將母鼠分別放入公鼠籠內(nèi)過夜、交配。次日清晨檢查到白色陰道栓者為懷孕鼠,該天記為懷孕第0.5 d。在母鼠懷孕第8.5～18.5 d,處死母鼠,取出胚胎。 2.獲取植入前胚胎:母鼠腹腔內(nèi)注射孕馬激素10 U,44～48 h后注射人絨毛膜促性腺激素5 U,隨后將其分別放入公鼠籠內(nèi)過夜、交配。12 h獲取單細(xì)胞期胚胎,36 h獲取2細(xì)胞期胚胎,48 h獲取4細(xì)胞期胚胎,60 h獲取8細(xì)胞期胚胎,84～96 h獲取囊胚。從超排卵母鼠的輸卵管沖出單細(xì)胞期胚胎到8細(xì)胞期胚胎,從子宮中沖出桑椹胚和囊胚。 3. 8.5～18.5 d胚胎標(biāo)本置4%多聚甲醛(Paraformaldehyde,PFA)中室溫固定3 h,按常規(guī)脫水后石蠟包埋,制備橫斷面5μm厚度連續(xù)切片,挑選胸腔部分和腹腔部分的主動(dòng)脈切片染色。 4.植入前胚胎經(jīng)3 g/L聚乙烯基吡咯烷酮/磷酸鹽緩沖液(Polyvinylpyrrolidone/ phosphatebuffered saline,PVP/PBS)中洗滌,2.5% PFA室溫固定15 min,置PVP/PBS液4℃保存,待用。 5. 8.5～18.5 d胚胎切片行蘇木素-伊紅染色,觀察背主動(dòng)脈形態(tài)學(xué)變化。 6. 8.5～18.5 d胚胎切片行Flk-1、CD31、Ⅷ因子相關(guān)抗原及SMα-actin免疫組織化學(xué)染色,觀察胚胎發(fā)育過程中,背主動(dòng)脈ECs及VSMCs標(biāo)記物的表達(dá)變化。 7.收集植入前各期胚胎20個(gè),采用mRNA Capture Kit試劑盒可捕獲總mRNA,行Flk-1的反轉(zhuǎn)錄-聚合酶鏈(Reverse transcription polymerase chain reaction,RT-PCR)反應(yīng),觀察Flk-1的表達(dá)變化規(guī)律。 8.植入前各期胚胎采用微滴操作行Flk-1全胚免疫熒光染色,激光共聚焦顯微鏡下觀察Flk-1的表達(dá)及定位。 9.將8細(xì)胞期胚胎置于含5 mg/L Flk-1中和抗體的胚胎培養(yǎng)液中培養(yǎng) 12 h后,加入綠色熒光標(biāo)記的羊抗大鼠二抗,觀察透明帶是否能通過抗體等大分子物質(zhì)。 10.取8細(xì)胞期胚胎隨機(jī)分3組,實(shí)驗(yàn)組加入Flk-1中和抗體5 mg/L至胚胎培養(yǎng)液中,空白對(duì)照組為胚胎培養(yǎng)液,抗體對(duì)照組加入非中和抗體5 mg/L至胚胎培養(yǎng)液中,培養(yǎng)36 h后計(jì)算囊胚形成率。采用X2檢驗(yàn)對(duì)數(shù)據(jù)作統(tǒng)計(jì)學(xué)分析,P㩳0.05有統(tǒng)計(jì)學(xué)意義。 11. 8細(xì)胞期胚胎采用微滴操作行VEGF全胚免疫熒光染色,激光共聚焦顯微鏡下觀察VEGF的表達(dá)及定位。 實(shí)驗(yàn)結(jié)果 1.胚胎8.5 d在胸腔部分和腹腔部分均可見左、右背主動(dòng)脈,9.5 d腹腔部分可見單一背主動(dòng)脈,而胸腔部分心臟水平仍然維持左、右背主動(dòng)脈的形態(tài);8.5～9.5 d背主動(dòng)脈呈現(xiàn)Flk-1陽性、CD31陽性、Ⅷ因子相關(guān)抗原陰性、SMα-actin陰性。 2.胚胎10.5 d左、右背主動(dòng)脈在腹腔部分和胸腔下部為一條背主動(dòng)脈,但仍為單層細(xì)胞圍成的管腔,而在心房水平仍然可見左、右背主動(dòng)脈,且呈現(xiàn)SMα-actin、Flk-1、CD31、Ⅷ因子相關(guān)抗原均陽性。 3.胚胎11.5 d背主動(dòng)脈管壁發(fā)育為多層,內(nèi)層細(xì)胞呈Flk-1陽性、SMα-actin陰性,外層細(xì)胞呈Flk-1陰性而SMα-actin陽性,血管與周圍間充質(zhì)無明顯分界,背主動(dòng)脈管壁周圍可見散在SMα-actin陽性細(xì)胞。 4.胚胎11.5 d之后,背主動(dòng)脈管壁VSMCs數(shù)量增多且由不規(guī)則型轉(zhuǎn)變?yōu)榧忓N型,內(nèi)層ECs繼續(xù)呈Flk-1陽性、SMα-actin陰性,外層VSMCs Flk-1陰性、SMα-actin陽性,血管與周圍間充質(zhì)分界清楚,背主動(dòng)脈血管周圍無散在SMα-actin陽性細(xì)胞。 5.在植入前小鼠胚胎中8細(xì)胞期胚胎Flk-1表達(dá)最高,在RT-PCR反應(yīng)28個(gè)循環(huán)時(shí)只有8細(xì)胞期胚胎可檢測到Flk-1;循環(huán)數(shù)增加到32個(gè)時(shí)4細(xì)胞期胚胎也檢測到Flk-1表達(dá)。在單細(xì)胞期、2細(xì)胞期、桑椹胚期和囊胚期胚胎均未檢測到Flk-1表達(dá)。 6. 4細(xì)胞期胚胎的細(xì)胞膜上可見綠色熒光,主要定位于胚胎的外緣和細(xì)胞交界處,胞漿和胞核均未見綠色熒光;8細(xì)胞期胚胎細(xì)胞表面的綠色熒光較4細(xì)胞期胚胎增強(qiáng),蛋白定位同4細(xì)胞期胚胎。單細(xì)胞期、2細(xì)胞期、桑椹胚期、囊胚期表達(dá)呈陰性。 7.取8細(xì)胞期胚胎在含F(xiàn)lk-1中和抗體5 mg/L的胚胎培養(yǎng)液中培養(yǎng)12 h后加入二抗,發(fā)現(xiàn)綠色熒光出現(xiàn)在胚胎的透明帶內(nèi)部,說明透明帶可通過抗體等大分子物質(zhì)。 8.取8細(xì)胞期胚胎在含F(xiàn)lk-1中和抗體5 mg/L的胚胎培養(yǎng)液中培養(yǎng),各組36 h囊胚形成率如下:空白對(duì)照組80.95%(17/21),抗體對(duì)照組81.81%(18/22),實(shí)驗(yàn)組40.00%(10/25)�？瞻讓�(duì)照組和抗體對(duì)照組36 h囊胚形成率無統(tǒng)計(jì)學(xué)差異。實(shí)驗(yàn)組與空白對(duì)照組之間有統(tǒng)計(jì)學(xué)差異。但兩實(shí)驗(yàn)組胚胎在48 h時(shí)仍可發(fā)育為囊胚。 9. 8細(xì)胞期胚胎VEGF表達(dá)呈陽性,蛋白表達(dá)定位于胚胎細(xì)胞的胞漿內(nèi)。 結(jié)論 1.胚胎背主動(dòng)脈的VSMCs可能最早起源于Flk-1、CD31陽性細(xì)胞,后期可能來源于周圍間充質(zhì)細(xì)胞的募集分化。 2.在小鼠植入前胚胎發(fā)育不同階段Flk-1表達(dá)不盡相同,Flk-1的表達(dá)可能與促進(jìn)植入前胚胎發(fā)育有關(guān)。
[Abstract]:Background and purpose of research
Vascular dysregulation is a common clinical pathological process, such as atherosclerosis, vascular remodeling, stent restenosis after allograft, percutaneous balloon angioplasty, and the origin of Vascular smooth muscle cells (VSMCs), which is helpful for the treatment of angiopathy. The origin of VSMCs in the embryo was previously believed. Neural crest and embryonic mesoderm; recently, VSMCs may also be derived from adult bone marrow stem cells or progenitor cells, peripheral blood mononuclear cells, skeletal muscle adult stem cells and endothelial cells (Endothelium cells, ECs) and other.Yamashita J in vitro studies confirmed that embryonic stem cells derived from fetal liver kinase -1 (Fetal liver kinase-1, Flk-1), that is, Vascular endothelial growth factor receptor -2 positive cells can differentiate into vascular ECs under the action of vascular endothelial growth factor (Vascular endothelial growth factor, VEGF), and can differentiate into VSMCs under the action of platelet derived growth factor -BB. Therefore, the Flk-1 positive cells are the common precursors of vascular ECs and VSMCs. However, the theory is still lacking in body. Evidence is supported by immunohistochemical staining of Flk-1, platelet endothelial cell adhesion molecule (Platelet endothelial cell adhesion molecule-1, PECAM-1/CD31), factor VIII associated antigen and smooth muscle alpha actin (Smooth Muscle alpha -actin, SM alpha -actin), to explore the expression of the above markers at the early stage of angiogenesis. The relationship between the time and space position provides a new experimental basis for the origin of VSMCs.
Flk-1 is mainly distributed in ECs, hematopoietic cells and progenitor cells. It has been reported that Flk-1 was first appeared in mouse embryo 6.5 D and plays an important role in the development of ECs and hematopoietic cells. The high expression of Flk-1 can be observed during the physiological process of angiogenesis or in the pathological process of tumor, but the expression of Flk-1 in the preimplantation embryo of mice has not yet been found yet. This report intends to preliminarily explore the expression pattern of Flk-1 in mouse preimplantation embryo development and its role in embryonic development.
Experimental method
1. to get 8.5 to 18.5 D embryos: the female rats were put into the cage for the night and mating. The next morning, the white vaginal suppositories were checked as pregnant rats. The day was recorded as the 0.5 D. pregnancy of the pregnant mouse, and the pregnant mouse was killed and the embryo was removed.
2. to obtain preimplantation embryos: intraperitoneal injection of gestational hormone 10 U intraperitoneally, 44~48 h after injection of human chorionic gonadotropin 5 U, then put them into the male rat cage overnight, mating.12 h to obtain single cell stage embryos, 36 h to obtain 2 cell stage embryos, 48 h to obtain 4 cell stage embryos, 60 h to obtain 8 cell stage embryos, 84~96 h acquisition blastocysts. From super Oviductal ovulation of ovulation female rats rushed out of single cell stage embryos to 8 cell stage embryos, and blastocysts and blastocysts were released from the womb.
3. 8.5 ~ 18.5 D embryos were placed in 4% paraformaldehyde (Paraformaldehyde, PFA) for 3 h at room temperature. The thickness of 5 mu section of the transverse section was prepared by paraffin embedded after routine dehydration. The section of the aorta of the thoracic cavity and the abdominal part were selected and stained with the section of the aorta.
4. the preimplantation embryos were washed in 3 g/L polyvinylpyrrolidone / phosphate buffer (Polyvinylpyrrolidone/ phosphatebuffered saline, PVP/PBS), 2.5% PFA was fixed at room temperature 15 min, and PVP/PBS solution was stored at 4 C for use.
5. 8.5 to 18.5 D embryos were stained with hematoxylin eosin to observe the morphological changes of the dorsal aorta.
6. 8.5 ~ 18.5 D embryos sections were stained with Flk-1, CD31, factor VIII related antigen and SM alpha -actin immunohistochemical staining. The expression of ECs and VSMCs markers in the dorsal aorta during the development of the embryo was observed.
7. a total of 20 preimplantation embryos were collected, and the mRNA Capture Kit kit was used to capture the total mRNA, and the reaction of Flk-1 reverse transcription polymerase chain (Reverse transcription polymerase chain reaction, RT-PCR) was used to observe the regularity of the expression of Flk-1.
8. pre implantation embryos were immunized with Flk-1 whole embryo immunofluorescence staining and laser scanning confocal microscopy was used to observe the expression and localization of Flk-1.
9. the 8 cell stage embryos were cultured in the embryo culture medium containing 5 mg/L Flk-1 neutralizing antibody.
After 12 h, the green fluorescent labeled Goat anti rat two antibody was added to observe whether the zona pellucida could pass macromolecules such as antibody.
10. the 8 cell stage embryos were randomly divided into 3 groups, the experimental group added Flk-1 neutralization antibody 5 mg/L to the embryo culture solution, the blank control group was the embryo culture solution, the antibody control group added non neutralizing antibody in 5 mg/L to the embryo culture solution, and then cultured 36 h to calculate the blastocyst formation rate. The data were statistically analyzed by X2 test, and P 0.05 had statistical significance.
11.8 cell stage embryos were immunized with VEGF whole embryo immunofluorescence staining by microdroplet operation. The expression and localization of VEGF were observed under confocal laser scanning microscope.
experimental result
1. the 8.5 D of the embryo had left and right dorsal aorta in the thoracic cavity and the abdominal part, and the single dorsal aorta in the abdominal cavity of 9.5 D, while the level of the thoracic cavity still maintained the left and right dorsal aorta, and the 8.5 to 9.5 D dorsal aorta showed Flk-1 positive, CD31 positive, and negative of the child associated antigen, and SM alpha -actin negative.
2. the 2. embryo was 10.5 d left, the right dorsal aorta was a dorsal aorta in the part of the abdominal cavity and the lower part of the thoracic cavity, but it was still a lumen enclosed by the monolayer cells, while the left and right dorsal aorta remained at the level of the atrium, and the SM alpha -actin, Flk-1, CD31, and factor VIII related antigens were all positive.
3. the wall of the dorsal aorta of 11.5 D of the embryo was multilayered, the inner layer cells were Flk-1 positive, SM alpha -actin was negative, the outer cells were Flk-1 negative and SM alpha -actin positive. There was no clear demarcation between the blood vessels and the surrounding mesenchyme, and the SM a -actin positive cells were scattered around the wall of the dorsal aorta.
4. after 11.5 D of the embryo, the number of VSMCs in the wall of the dorsal aorta increased and changed from irregular type to spindle type. The inner ECs continued to be Flk-1 positive, SM alpha -actin negative, the outer VSMCs Flk-1 negative, the SM alpha -actin positive, the blood vessels and the surrounding mesenchyme clear, and the circumference of the dorsal aorta did not scatter in SM alpha -actin positive cells.
5. the expression of Flk-1 was highest in the 8 cell stage embryo of the preimplantation mouse embryo. Only 8 cell stage embryos could detect Flk-1 in the 28 cycles of RT-PCR reaction; the expression of Flk-1 was also detected in 4 cell stage embryos when the number of cycles increased to 32. The Flk-1 expression was not detected at the single cell stage, 2 cell stage, morula and blastocyst stage embryos.
The green fluorescence was found on the membrane of the 6.4 cell stage embryo, mainly located at the outer edge of the embryo and the junction of the cell, the cytoplasm and the nucleus were not green fluorescence, the green fluorescence of the 8 cell stage embryo cells was stronger than the 4 cell stage embryo, the protein localization was with the 4 cell stage embryo, the single cell stage, the 2 cell stage, the morula stage, and the blastocyst expression were negative. Sex.
7. the 8 cell stage embryos were cultured 12 h in the embryo culture medium containing Flk-1 neutralization antibody 5 mg/L and added two resistance. It was found that the green fluorescence appeared in the zona pellucid zone of the embryo, indicating that the zona pellucida could pass through the antibody and other macromolecules.
8. the 8 cell stage embryos were cultured in the embryo culture medium containing Flk-1 neutralization antibody 5 mg/L. The formation rate of 36 h blastocysts in each group was as follows: the blank control group was 80.95% (17/21), the antibody control group was 81.81% (18/22), and the experimental group was 40% (10/25). There was no statistical difference between the blank control group and the antibody control group in the 36 h blastocyst formation rate. Between the experimental group and the blank control group, there was a significant difference between the experimental group and the blank control group. Statistical difference. But two of embryos in the experimental group could still develop into blastocysts at 48 h.
9.8 the expression of VEGF was positive in cell stage embryos, and the protein expression was localized in the cytoplasm of embryonic cells.
conclusion
1. the VSMCs of embryonic dorsal aorta probably originated from Flk-1 and CD31 positive cells. Later, it may originate from recruitment and differentiation of peripheral mesenchymal cells.
2. the expression of Flk-1 is different in different stages of mouse preimplantation embryo development, and the expression of Flk-1 may be related to the development of preimplantation embryos.
【學(xué)位授予單位】：大連醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2007
【分類號(hào)】：R363

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7 柳和培;侯燕鳴;;血管平滑肌線粒體超微結(jié)構(gòu)圖像分析研究[A];第九次全國電子顯微學(xué)會(huì)議論文摘要集（Ⅰ）[C];1996年

8 姬媛媛;劉俊田;劉娜;王志東;;血管緊張肽Ⅱ?qū)Υ笫笱芷交〖?xì)胞TLR4及基質(zhì)金屬蛋白酶-9表達(dá)的影響[A];中國藥理學(xué)會(huì)第九次全國會(huì)員代表大會(huì)暨全國藥理學(xué)術(shù)會(huì)議論文集[C];2007年

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