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Opposing Effects of Nitric Oxide on Different Connexins Expressed in the Vascular System

机译:一氧化氮对血管系统中表达的不同连接蛋白的拮抗作用

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Gap junctions-clusters of intercellular channels built by connexins (Cx)-are thought to be important for vascular cell functions such as differentiation, control of tone, or growth. In the vascular system, gap junctions can be formed by four different connexins (Cx37, Cx40, Cx43 and Cx45). The permeability of these connexin-formed gap junctions determines the amount of intercellular coupling and can be modulated by several vasoactive substances such as prostacyclin or nitric oxide (NO). We demonstrate here that NO has specific effects on certain connexins. Using two different techniques-injection of a fluorescent dye in single cells as well as detection of the de nova formation of gap junctions by a flow cytometry based technique-we found that NO decreases the functional coupling in Cx37 containing gap junctions whereas it increases the de novo formation of gap junctions containing Cx40. We conclude that NO, in addition to its known vasomotor effects, has a novel role in controlling intercellular coupling resulting in opposing effects depending on the specific connexin expressed in the cells.
机译:连接蛋白(Cx)建立的细胞间通道的间隙连接簇被认为对血管细胞功能(如分化,音调或生长)很重要。在血管系统中,间隙连接可以由四种不同的连接蛋白(Cx37,Cx40,Cx43和Cx45)形成。这些连接蛋白形成的间隙连接的渗透性决定了细胞间偶联的量,并且可以被几种血管活性物质如前列环素或一氧化氮(NO)调节。我们在这里证明NO对某些连接蛋白具有特定作用。使用两种不同的技术-在单个细胞中注入荧光染料以及通过基于流式细胞术的技术检测间隙连接的新形成,我们发现NO降低了含间隙连接的Cx37中的功能偶联,而增加了脱色从头形成包含Cx40的间隙连接。我们得出的结论是,除了已知的血管舒缩作用外,NO还具有控制细胞间偶联的新作用,这取决于细胞中表达的特定连接蛋白而导致相反的作用。

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