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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Upregulation of CaMKIIδ during ischaemia- reperfusion is associated with reperfusioninduced arrhythmias and mechanical dysfunction of the rat heart: Involvement of sarcolemmal Ca 2+-cycling proteins
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Upregulation of CaMKIIδ during ischaemia- reperfusion is associated with reperfusioninduced arrhythmias and mechanical dysfunction of the rat heart: Involvement of sarcolemmal Ca 2+-cycling proteins

机译：缺血-再灌注过程中CaMKIIδ的上调与再灌注引起的心律不齐和大鼠心脏机械功能障碍有关：肌膜Ca 2+循环蛋白的参与

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Although Ca 2+/calmodulin-dependent protein kinase II delta (CaMKIIδ) has been implicated in development of different phenotypes of myocardial ischaemia-reperfusion injury, its involvement in arrhythmogenesis and cardiac stunning is not sufficiently elucidated. Moreover, the mechanisms by which Camkiiδ mediates disturbances in excitation-contraction coupling, are not exactly known. To investigate this, KN-93 (0.5 μmol/L), a CaMKII inhibitor, was administered before induction of global ischaemia and reperfusion in isolated Langendorff-perfused rat hearts. Expression of CaMKIIδ and the sarcollemal Ca 2+-cycling proteins, known to be activated during reperfusion, was analyzed using immunoblotting. KN-93 reduced reperfusion-induced ectopic activity and the incidence of ventricular fibrillation. Likewise, the severity of arrhythmias was lower in KN-treated hearts. During the pre-ischaemia phase, neither inotropic nor chronotropic effects were elicited by KN-93, whereas post-ischaemic contractile recovery was significantly improved. Ischaemia-reperfusion increased the expression of CaMKIIδ and sodium-calcium exchanger (NCX1) proteins without any influence on the protein content of alpha 1c, a pore-forming subunit of L-type calcium channels (LTCCs). On the other hand, inhibition of CaMKII normalized changes in the expression of CaMKIIδ and NCX1. Taken together, CaMKIIδ seems to regulate its own turnover and to be an important component of cascade integrating NCX1, rather than LTCCs that promote ischaemia-reperfusion-induced contractile dysfunction and arrhythmias.
机译：尽管Ca 2 + /钙调蛋白依赖性蛋白激酶IIδ（CaMKIIδ）参与了心肌缺血再灌注损伤的不同表型的发生，但仍未充分阐明其在心律失常和心脏电击中的作用。而且，尚不清楚Camkiiδ介导激励-收缩耦合中的干扰的机制。为了对此进行研究，在诱导局部缺血和在离体的Langendorff灌注大鼠心脏中进行再灌注之前，先给予CaMKII抑制剂KN-93（0.5μmol/ L）。使用免疫印迹分析了已知在再灌注过程中被激活的CaMKIIδ和肌膜Ca 2+循环蛋白的表达。 KN-93减少了再灌注诱导的异位活性和心室纤颤的发生率。同样，在接受KN治疗的心脏中，心律不齐的严重程度较低。在缺血前阶段，KN-93既不会引起正性变力作用也不会引起变时性作用，而缺血后的收缩力恢复则明显改善。缺血再灌注增加了CaMKIIδ和钠钙交换剂（NCX1）的表达，而对L型钙通道（LTCCs）的成孔亚基alpha 1c的蛋白质含量没有任何影响。另一方面，抑制CaMKII可以使CaMKIIδ和NCX1表达的变化正常化。两者合计，CaMKIIδ似乎调节自己的营业额，是级联整合NCX1的重要组成部分，而不是促进缺血再灌注引起的收缩功能障碍和心律失常的LTCC。

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