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首页> 外文期刊>American Journal of Physiology >Ischemia induces alterations in actin filaments in renal vascular smooth muscle cells.
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Ischemia induces alterations in actin filaments in renal vascular smooth muscle cells.

机译：缺血诱导肾血管平滑肌细胞肌动蛋白丝的改变。

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Although altered renal vascular reactivity is known to occur after ischemia, the structural basis explaining the phenomenon has not been clarified. To evaluate for structural damage to the renal vasculature in ischemic acute renal failure (ARF), F-actin in the renal vasculature of rat kidneys and cultured vascular smooth muscle cells was examined using confocal fluorescence microscopy. The left renal artery was clamped for 15 or 45 min in Sprague-Dawley rats. In other experimental groups, 45 min of renal arterial clamping was followed by 1 or 3 h of reperfusion. Control kidneys were procured without any preceding interventional procedure. F-actin was labeled with either fluorescein or Texas red-conjugated phalloidin. Serial optical sections were collected by confocal microscopy, and image volumes were rendered three dimensionally. The degree of cytoskeletal damage in the vasculature was assessed by semiquantitative scoring of the staining for F-actin. Disorganization/disarray of F-actin, reflected by disruption and clumping of the actin filaments, was observed in arteries, arterioles, and the vasa rectae of the kidney after ischemia or ischemia-reperfusion. Smooth muscle cells from arteries and arterioles showed significant damage to F-actin after either 15 or 45 min of ischemia in a duration-dependent manner. The actin cytoskeleton tended to recover from damage from 45 min of ischemia 1 and 3 h after reperfusion. The vasa rectae did not demonstrate significant damage to F-actin after 15- or 45-min ischemia. However, significant damage to the vasa rectae was manifest 3 h after the reperfusion following 45 min of ischemia. In summary, disorganization/disarray of F-actin in vascular smooth muscle cells of the kidney was observed after ischemia or ischemia-reperfusion. A similar finding was observed in cultured vascular smooth muscle cells. We suggest that this disorganization of the actin cytoskeleton may play a contributory role in the loss of autoregulation of renal blood flow and the aberrant vascular reactivity in postischemic ARF.
机译：尽管已知缺血后会发生肾脏血管反应性改变，但尚不清楚解释该现象的结构基础。为了评估缺血性急性肾衰竭（ARF）对肾血管结构的损伤，使用共聚焦荧光显微镜检查了大鼠肾脏和培养的血管平滑肌细胞中F-肌动蛋白的含量。在Sprague-Dawley大鼠中，将左肾动脉夹紧15或45分钟。在其他实验组中，在45分钟的肾动脉夹闭后进行1或3小时的再灌注。无需任何事先干预程序即可购买对照肾脏。 F-肌动蛋白用荧光素或德克萨斯红偶联的鬼笔环肽标记。通过共聚焦显微镜收集连续的光学切片，并将图像体积三维绘制。通过F-肌动蛋白染色的半定量评分来评估脉管系统中细胞骨架损伤的程度。缺血或缺血再灌注后，在肾脏的动脉，小动脉和直肠脉管中观察到F-肌动蛋白的紊乱/紊乱，这反映在肌动蛋白丝的破坏和聚集上。缺血15或45分钟后，来自动脉和小动脉的平滑肌细胞对F-肌动蛋白显示出明显的损伤，并具有持续时间依赖性。肌动蛋白的细胞骨架倾向于从缺血1分钟45分钟和再灌注3小时后的损伤中恢复。在缺血15分钟或45分钟后，直肠脉络膜未显示出对F-肌动蛋白的显着损害。然而，缺血45分钟后3小时再灌注对直肠直肠有明显损害。总之，在缺血或局部缺血-再灌注后，观察到F-肌动蛋白在肾脏的血管平滑肌细胞中的紊乱/混乱。在培养的血管平滑肌细胞中观察到类似的发现。我们建议肌动蛋白细胞骨架的这种失序可能在缺血后ARF中肾血流量的自动调节丧失和异常血管反应性中起重要作用。

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