本文關(guān)鍵詞：MIF、p-ERK、cyclinD1在肺動(dòng)脈高壓肉雞肺臟中的分布與表達(dá)　出處：《山西農(nóng)業(yè)大學(xué)》2016年碩士論文　論文類型：學(xué)位論文

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【摘要】：[目的]肉雞肺動(dòng)脈高壓(PH)嚴(yán)重影響了我國肉雞產(chǎn)業(yè)的發(fā)展。該病發(fā)生發(fā)展過程的重要環(huán)節(jié)是以肺動(dòng)脈平滑肌細(xì)胞增殖為主的肺動(dòng)脈重構(gòu)。細(xì)胞周期蛋白D1是調(diào)控細(xì)胞增殖的關(guān)鍵因子(之一),該因子是否參與患病肉雞肺動(dòng)脈平滑肌增殖尚未見報(bào)道。據(jù)報(bào)道,激活cyclinD1的信號(hào)通路主要有細(xì)胞外信號(hào)調(diào)節(jié)激酶(ERK);結(jié)合我們前期工作,發(fā)現(xiàn)肺動(dòng)脈高壓肉雞肺臟中巨噬細(xì)胞移動(dòng)抑制因子(MIF)表達(dá)量顯著高于健康肉雞,說明MIF參與了肉雞PH的發(fā)病過程。本試驗(yàn)?zāi)康木褪且砬迦吲c肉雞PH發(fā)病的關(guān)系。[方法]PH組為3-4周齡左右臨床型肺動(dòng)脈高壓肉雞,正常組為同群同日齡健康肉雞,均由山西省大象集團(tuán)AA肉雞養(yǎng)殖場(chǎng)提供。通過HE染色觀察PH組與正常組肺組織血管形態(tài)的區(qū)別,利用免疫組織化學(xué)及免疫印跡技術(shù),對(duì)肉雞肺臟組織MIF、p-ERK、cyclinD1三種蛋白進(jìn)行定位及半定量分析,并對(duì)比PH組與正常組的表達(dá)差異。[結(jié)果]HE染色結(jié)果顯示,正常組肉雞肺臟組織結(jié)構(gòu)清晰、完整,肺血管內(nèi)膜、中膜形態(tài)正常,無明顯增厚現(xiàn)象。與正常組相比,PH組出現(xiàn)動(dòng)脈內(nèi)膜及中膜增厚的現(xiàn)象,其管腔變窄,管壁較正常組顯著增厚。免疫組化結(jié)果顯示,在肉雞肺動(dòng)脈壁上,MIF、p-ERK、cyclinD1三個(gè)蛋白均呈陽性表達(dá)。其中,MIF表達(dá)于血管內(nèi)皮細(xì)胞和中膜平滑肌細(xì)胞胞質(zhì)中;p-ERK和cyclinD1定位于血管中膜平滑肌細(xì)胞胞質(zhì)中。Western-blot結(jié)果顯示,與正常組相比,肺動(dòng)脈高壓組肉雞肺臟MIF、Cyclin D1表達(dá)量顯著升高(P0.01);肺動(dòng)脈高壓組磷酸化ERK(p-ERK)較正常組顯著增多(P0.01),表明ERK通路處于高度激活狀態(tài)。[結(jié)論]肉雞PH發(fā)病過程中,中小型肺動(dòng)脈中膜增厚,其原因可能與肺臟MIF表達(dá)量升高,ERK信號(hào)通路高度活化,cyclinD1表達(dá)量升高等變化有關(guān)。
[Abstract]:[Objective] pulmonary hypertension (PH) has seriously affected the development of broiler industry in China. An important role in the development process of the disease is to pulmonary arterial remodeling in pulmonary arterial smooth muscle cell proliferation mainly. Cyclin D1 is a key factor in the regulation of cell proliferation (one), this factor is involved in the proliferation of pulmonary artery disease chicken muscle has not been reported. According to reports, the activation of cyclinD1 signaling pathway are the main extracellular signal regulated kinase (ERK); combined with our previous work, found that pulmonary hypertension in broilers lung macrophage migration inhibitory factor (MIF) expression was significantly higher than that of healthy broilers, illustrate the pathogenesis of MIF in broiler PH. Relationship method. Group]PH the purpose of this experiment is to understand the pathogenesis of PH and three broilers for 3-4 weeks about clinical pulmonary hypertension in broilers, normal group with the same age group of healthy broilers, from Shanxi Province The elephant group AA broiler farms. The difference was observed in the PH group and the normal group of lung tissue vascular morphology by HE staining by immunohistochemistry and Western blot, p-ERK, MIF in lung tissue of broiler, analysis and semi quantitative cyclinD1 localization of three proteins, and compared with the PH group and the normal group. The difference of expression according to the results of]HE staining, normal group broilers lung tissue structure is clear, complete, pulmonary vascular intima, membrane in normal morphology, no obvious thickening phenomenon. Compared with the normal group, intima and medial thickening phenomenon occurred in the PH group, the narrowing of the lumen wall thickened significantly than the normal group. Immunohistochemistry results showed that in the pulmonary artery wall, MIF, p-ERK, cyclinD1 three protein were positive. The expression of MIF in vascular endothelial cells and smooth muscle cells in the cytoplasm; p-ERK and cyclinD1 in vascular smooth muscle cells .Western-blot results showed that compared with the normal group, pulmonary hypertension group broilers lung MIF, Cyclin D1 expression increased significantly (P0.01); pulmonary hypertension group phosphorylated ERK (p-ERK) significantly increased compared with normal group (P0.01), suggesting that the ERK pathway is highly activated. Conclusion] broilers in the pathogenesis of PH. Small and medium sized pulmonary membrane thickening, which may be associated with lung MIF expression increased, ERK signaling pathway is highly activated, the expression of cyclinD1 was higher in change.

【學(xué)位授予單位】：山西農(nóng)業(yè)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2016
【分類號(hào)】：S858.31

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