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连接蛋白(Cx)43是构成缝隙连接(GJ)最重要的Cx,GJ是介导胃肠平滑肌细胞(SMC)和Caja1间质细胞(ICC)间电化学信息交流,保证肌肉活动的协调性和同步性的特殊通道。Cx43广泛存在于胃肠Caja1间质细胞与平滑肌细胞之间,在胃肠运动中发挥重要作用。Cx43的异常表达与分布可导致胃肠运动障碍。 相似文献
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缝隙连接和连接蛋白43与动脉粥样硬化 总被引:3,自引:1,他引:2
动脉粥样硬化是一种多因素所致的慢性疾病,发病机理非常复杂。缝隙连接作为细胞间连接的重要方式,在动脉粥样硬化发生发展过程中起着不容忽视的作用。连接蛋白43是主要由血管壁表达的连接蛋白,与内皮细胞凋亡、平滑肌细胞增生及泡沫细胞的生成密切相关,在多种细胞生长及肿瘤分化过程中起重要作用。本文主要就缝隙连接和连接蛋白43在动脉粥样硬化发生中的变化作一综述。 相似文献
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胃肠道各种细胞之间,如平滑肌之间、平滑肌和深部胃肠Cajal间质细胞(ICC-DMP)之间以及ICC-DMP和ICC-DMP之间存在缝隙连接,它主要由连接蛋白43(connexin43,Cx43)构成,其表达的异常与胃肠道疾病的发生密切相关。此文就胃肠道Cx43的研究进展作一综述。 相似文献
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缝隙连接是介导相邻细胞间直接通讯的特殊膜结构.心室肌细胞间的缝隙连接通道主要由连接蛋白43(Cx43)构成.Cx43的磷酸化状态除了快速调节通道的开放/闭合状态(单通道传导性和通道开放概率),还可通过影响Cx43的合成、转运、聚集/解聚和降解等不同环节,改变活化通道数量,最终实现对缝隙连接功能的调控.迄今,已发现多种激酶和蛋白磷酸酶可直接和(或)间接调控Cx43羧基末端的丝氨酸残基和酪氨酸残基的磷酸化状态,从而影响缝隙连接通道的功能.磷酸化/去磷酸化影响Cx43和缝隙连接通道功能的确切作用和具体机制未明.本文就Cx43磷酸化状态与心脏缝隙连接通道功能的关系作一综述. 相似文献
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缝隙连接是介导相邻细胞间直接通讯的特殊膜结构。心室肌细胞间的缝隙连接通道主要由连接蛋白43(Cx43)构成。Cx43的磷酸化状态除了快速调节通道的开放/闭合状态(单通道传导性和通道开放概率),还可通过影响Cx43的合成、转运、聚集/解聚和降解等不同环节,改变活化通道数量,最终实现对缝隙连接功能的调控。迄今,已发现多种激酶和蛋白磷酸酶可直接和(或)间接调控Cx43羧基末端的丝氨酸残基和酪氨酸残基的磷酸化状态,从而影响缝隙连接通道的功能。磷酸化/去磷酸化影响Cx43和缝隙连接通道功能的确切作用和具体机制未明。本文就Cx43磷酸化状态与心脏缝隙连接通道功能的关系作一综述。 相似文献
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风湿性心脏病心房颤动患者左右心耳组织连接蛋白40和连接蛋白43 mRNA水平的对比研究 总被引:2,自引:0,他引:2
心房颤动(房颤)是临床最常见的心律失常,然而造成这种心律失常的发生因素和维持因素尚不明确。缝隙连接是心肌组织动作电位扩布的主要物质基础,其每个通道由2个连接子耦合而成,每个连接子由6个缝隙连接蛋白(connexin,Cx)构成,Cx40、Cx43是人类心房细胞最主要的Cx。本研究观察风湿性心脏病(风心病)房颤患左右心耳Cx40、Cx43mRNA表达水平的变化, 相似文献
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缝隙连接蛋白43(Cx43)是哺乳动物心脏中最主要的连接蛋白,研究表明其对心脏的正常分化和发育发挥着重要作用。Cx43的表达异常可引起多种心血管疾病以及心脏先天性畸形的发生。本文就Cx43的结构、表达及其与心脏发育的最新研究进展予以综述。 相似文献
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目的研究心脏连接蛋白43(Cx43)羧基末端与哪些心肌细胞内蛋白质存在相互作用。方法①通过PCR方法得到编码心脏Cx43羧基末端(AA235-382)的cDNA片段,并在其两端分别加上EcoRI和BamHI酶切位点,应用EcoRI/BamHI酶切PCR产物及pGBKT7空载体,凝胶分离后应用T4连接酶进行连接;②通过化学转化法将pG-BKT7-Cx43-CT转化酵母菌AH109;③通过“尿素/SDS”法从被转化的酵母菌中提取蛋白质;④应用抗C-myc抗体,通过Western blot方法检测”诱饵”蛋白的表达(即Gal4-BD-C-myc-Cx43-CT融合蛋白);⑤检测”诱饵”蛋白自我激活报告基因与否后,将已被“诱饵“质粒转化的AH109与人心脏cDNA文库进行杂交,筛选阳性克隆分离阳性克隆中的cDNA,并测序。结果①诱饵载体测序结果证明pGBKT7中的“Gal4 DNA binding domain-C-myc”与Cx43的羧基末端在同一读框中;②“诱饵”质粒转化AH109酵母菌成功率100%;③从被转化的AH109中能提取到浓度满意的总蛋白;④Western blot能检测到特异性条带,其位置与Gal4-BD-C-myc-Cx43-CT的分子量相当;⑤“诱饵”蛋白不能自激活报告基因Ade2和Mel1,但可自激活His3,5mmol/L的3-AT可有效抑制“诱饵”蛋白本身自激活报告基因His3,以利于下一步的杂交筛选,筛选得到10个准阳性克隆。结论心脏连接蛋白43羧基末端能与心肌细胞中的多种蛋白质存在相互作用,这些蛋白质可能参与对间隙连接通道的功能调控。 相似文献
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Connexin 43 and ischemic preconditioning 总被引:8,自引:0,他引:8
Connexin 43 (Cx43) is the essential protein to form hemichannels and gap junctions in the myocardium. The phosphorylation status of Cx43 which is regulated by a variety of protein kinases and phosphatases determines hemichannel and/or gap junction conductance and permeability. Gap junctions are involved in cell-cell coupling while hemichannels contribute to cardiomyocyte volume regulation. Cx43-formed channels are involved in ischemia/reperfusion injury, since blockade of a large portion of Cx43-formed channels attenuates ischemic hypercontracture, infarct development and post myocardial infarction remodeling. Ischemic preconditioning's protection also depends on functional Cx43-formed channels, since uncoupling of channels or genetic Cx43 deficiency abolishes infarct size reduction by ischemic preconditioning. The exact underlying mechanism(s) how Cx43 mediates protection remain to be established. 相似文献
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Connexin (Cx) 43 is the predominant protein forming gap junctions and non-junctional hemichannels in ventricular myocardium. The Cx43 proteins are central to the cardioprotection afforded by ischaemic preconditioning (IP). The specific role of mitochondrial Cx43 in protection by IP is reviewed. 相似文献
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The connexin 43 ( Cx43 ) proteins, which is the predominant protein that can form gap junctions and non- junctional hemichannels in ventricular myocardium, are central to the cardioprotection afforded by ischemic preconditioning (IP) and maybe ischemic postconditioning ( PC ) too. Recent studies showed that recruitment of Cx43 to the mitochondria in IP might play a role in the production of reactive oxygen species (ROS) that mediates IP. The localization of Cx43 at mitochondria appears to be important for the achieved cardioprotection and opens a new door for us to reveal the exact mechanisms of ischemia/reperfusion (I/R) injury and cardioprotection, and it might be new targets of pharmacological modulator to achieved cardioprotection. 相似文献
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Schulz R Boengler K Totzeck A Luo Y Garcia-Dorado D Heusch G 《Heart failure reviews》2007,12(3-4):261-266
Connexin 43 (Cx43) is the predominant protein forming gap junctions and non-junctional hemichannels in ventricular myocardium,
but Cx43 is also localized at the inner membrane of cardiomyocyte mitochondria. In cardiomyocytes, Cx43 is involved in the
formation of reactive oxygen species, which are central to the signal transduction cascade of ischemic preconditioning’s protection.
Accordingly, genetically-induced or age-related loss of Cx43 abolishes infarct size reduction by ischemic preconditioning.
Similarly, mitochondrial import inhibition of Cx43 completely blocks infarct size reduction by pharmacological preconditioning
with diazoxide. In contrast to its importance for preconditioning-induced cardioprotection, Cx43 is not important for infarct
size reduction by ischemic postconditioning. In summary, Cx43––especially Cx43 localized in mitochondria––appears to be one
key element of the signal transduction cascade of the protection by preconditioning.
The authors’ studies were supported by the German Research Foundation (Schu843/7-1). 相似文献
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Background Stem cells have multilineage differentiation capacity,which makes bone marrow mesenchymal stem cells(BMSCs) derived relatively easy and provides a promising alternative treatment for myocardial infarction(MI).The in vivo cardiac differentiation and functional effects of unmodified BMSCs after MI are controversial.Poor moderate survival benefits of BMSCs-implanted rats were caused by incomplete electromechanical integration induced by tissue heterogeneity between myocytes and engrafted BMSCs in th... 相似文献
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胃肠功能和动力障碍研究进展 总被引:9,自引:0,他引:9
柯美云 《现代消化及介入诊疗》2004,9(1):1-4
近年提出的功能性胃肠病(FGID)的罗马Ⅱ诊断标准和胃肠动力障碍(DGIM)的新分类已为国内外普遍接受,并有助于国内外的交流。这里将讨论FGID和DGIM的研究热点、方法学及诊治的进展。 相似文献