首页> 外文期刊>American Journal of Physiology >Impaired flow-induced dilation in mesenteric resistance arteries from receptor protein tyrosine phosphatase-mu-deficient mice.
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Impaired flow-induced dilation in mesenteric resistance arteries from receptor protein tyrosine phosphatase-mu-deficient mice.

机译:受体蛋白酪氨酸磷酸酶-μ缺陷小鼠的肠系膜阻力动脉血流诱导的扩张受损。

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The transmembrane receptor-like protein tyrosine phosphatase-mu (RPTPmu) is thought to play an important role in cell-cell adhesion-mediated processes. We recently showed that RPTPmu is predominantly expressed in the endothelium of arteries and not in veins. Its involvement in the regulation of endothelial adherens junctions and its specific arterial expression suggest that RPTPmu plays a role in controlling arterial endothelial cell function and vascular tone. To test this hypothesis, we analyzed myogenic responsiveness, flow-induced dilation, and functional integrity of mesenteric resistance arteries from RPTPmu-deficient (RPTPmu(-/-)) mice and from wild-type littermates. Here, we show that cannulated mesenteric arteries from RPTPmu(-/-) mice display significantly decreased flow-induced dilation. In contrast, mechanical properties, myogenic responsiveness, responsiveness to the vasoconstrictors phenylephrine or U-46619, and responsiveness to the endothelium-dependent vasodilators methacholine or bradykinin were similar in both groups. Our results imply that RPTPmu is involved in the mechanotransduction or accessory signaling pathways that control shear stress responses in mesenteric resistance arteries.
机译:跨膜受体样蛋白酪氨酸磷酸酶-mu(RPTPmu)被认为在细胞-细胞粘附介导的过程中起重要作用。我们最近发现RPTPmu主要在动脉内皮而不是静脉中表达。它参与了对内皮粘附连接的调节及其特定的动脉表达,提示RPTPmu在控制动脉内皮细胞功能和血管紧张中起作用。若要测试此假设,我们分析了RPTPmu缺陷型(RPTPmu(-/-))小鼠和野生型同窝仔的肠系膜阻力动脉的肌源性反应性,血流诱导的扩张和功能完整性。在这里,我们显示从RPTPmu(-/-)小鼠的空心肠系膜动脉显示明显减少的血流诱发的扩张。相比之下,两组的机械特性,肌源性反应性,对血管收缩剂去氧肾上腺素或U-46619的反应性以及对内皮依赖性血管扩张剂的乙酰甲胆碱或缓激肽的反应性相似。我们的结果表明,RPTPmu参与了机械转导或辅助信号传导途径,这些途径控制着肠系膜阻力动脉的切应力响应。

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