We are analyzing https://link.springer.com/article/10.1007/s10495-006-4937-1.

Title:
Actin cytoskeleton derangement induces apoptosis in renal ischemia/reperfusion | Apoptosis
Description:
This study evaluated whether cytoskeletal alterations during the ischemic conditions associated with kidney preservation could determine apoptosis. Cytoskeletal alterations are among the main effects of ischemia and may induce apoptosis. Rat kidneys were preserved in University of Wisconsin (UW) solution for 24 h. Some groups of animals underwent 45 min of warm ischemia (WI) to evaluate its effect on both the actin cytoskeleton and apoptosis (assessed by caspase-3 activity and TUNEL staining). Swinholide A (SwinA) and Latrunculin B (LB), two actin cytoskeleton-targeted agents, were administered to assess the effect of direct actin disruption on apoptosis. Jasplakinolide (JP), a compound that stabilizes actin filaments, was administered to evaluate the effect of actin stabilization. Apoptosis was evaluated at 3 h of ex vivo reperfusion using the isolated perfused rat kidney (IPK) model. Results: Apoptosis increased during reperfusion with WI or administration of actin disruptor agents. Administration of stabilizing agents reversed apoptosis in kidneys that had previously undergone WI or had received an actin disruptor agent. Conclusion: The disruption of the actin cytoskeleton during ischemic conditions associated with kidney preservation induces apoptosis upon reperfusion through caspase-3 activation.
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Keywords {🔍}

google, scholar, pubmed, cas, article, apoptosis, actin, renal, kidney, cell, cytoskeleton, physiol, ischemiareperfusion, cells, function, ischemia, disruption, injury, epithelial, tubular, privacy, cookies, content, hotter, effects, access, acute, nephrol, proximal, failure, publish, search, induces, kidneys, reperfusion, isolated, induced, biol, molitoris, invest, res, data, information, log, journal, research, derangement, march, genescà, sola,

Topics {✒️}

month download article/chapter cd10/neutral endopeptidase expression ischemia-induced cell injury long-term renal function renal ischemia–reperfusion injury cold ischemia/reperfusion injury initial ischemia/reperfusion injury actin cytoskeleton-targeted agents altered membrane-cytoskeleton linkage nonheart-beating kidney donation pressure-induced actin polymerization related subjects van de water ischemia-reperfusion prevents inflammation full article pdf tubular epithelial cells actin cytoskeletal derangement vascular smooth muscle renal tubular epithelium article apoptosis aims renal epithelial cells proximal tubule na ischemia induces alterations privacy choices/manage cookies renal ischemia/reperfusion acute renal failure focal adhesion kinase major energy drain actin disruptor agents molitoris ba dentate granule cells hl-60 line cells isolated mitochondria leads rho protein regulation delayed graft function ischemia-induced loss human monocytes stimulated heart-beating donors actin disruptor agent anti-actin drugs actin-atp hydrolysis actin modulating substances cofilin-actin complex european economic area scope submit manuscript animals underwent 45 min proapoptotic genes increases hippocampal slice cultures reactive oxygen intermediates dos remedios cg

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         headline:Actin cytoskeleton derangement induces apoptosis in renal ischemia/reperfusion
         description:This study evaluated whether cytoskeletal alterations during the ischemic conditions associated with kidney preservation could determine apoptosis. Cytoskeletal alterations are among the main effects of ischemia and may induce apoptosis. Rat kidneys were preserved in University of Wisconsin (UW) solution for 24 h. Some groups of animals underwent 45 min of warm ischemia (WI) to evaluate its effect on both the actin cytoskeleton and apoptosis (assessed by caspase-3 activity and TUNEL staining). Swinholide A (SwinA) and Latrunculin B (LB), two actin cytoskeleton-targeted agents, were administered to assess the effect of direct actin disruption on apoptosis. Jasplakinolide (JP), a compound that stabilizes actin filaments, was administered to evaluate the effect of actin stabilization. Apoptosis was evaluated at 3 h of ex vivo reperfusion using the isolated perfused rat kidney (IPK) model. Results: Apoptosis increased during reperfusion with WI or administration of actin disruptor agents. Administration of stabilizing agents reversed apoptosis in kidneys that had previously undergone WI or had received an actin disruptor agent. Conclusion: The disruption of the actin cytoskeleton during ischemic conditions associated with kidney preservation induces apoptosis upon reperfusion through caspase-3 activation.
         datePublished:2006-03-09T00:00:00Z
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      headline:Actin cytoskeleton derangement induces apoptosis in renal ischemia/reperfusion
      description:This study evaluated whether cytoskeletal alterations during the ischemic conditions associated with kidney preservation could determine apoptosis. Cytoskeletal alterations are among the main effects of ischemia and may induce apoptosis. Rat kidneys were preserved in University of Wisconsin (UW) solution for 24 h. Some groups of animals underwent 45 min of warm ischemia (WI) to evaluate its effect on both the actin cytoskeleton and apoptosis (assessed by caspase-3 activity and TUNEL staining). Swinholide A (SwinA) and Latrunculin B (LB), two actin cytoskeleton-targeted agents, were administered to assess the effect of direct actin disruption on apoptosis. Jasplakinolide (JP), a compound that stabilizes actin filaments, was administered to evaluate the effect of actin stabilization. Apoptosis was evaluated at 3 h of ex vivo reperfusion using the isolated perfused rat kidney (IPK) model. Results: Apoptosis increased during reperfusion with WI or administration of actin disruptor agents. Administration of stabilizing agents reversed apoptosis in kidneys that had previously undergone WI or had received an actin disruptor agent. Conclusion: The disruption of the actin cytoskeleton during ischemic conditions associated with kidney preservation induces apoptosis upon reperfusion through caspase-3 activation.
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