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首页> 外文期刊>American Journal of Physiology >Roles for alphaB-crystallin and HSPB2 in protecting the myocardium from ischemia-reperfusion-induced damage in a KO mouse model.
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Roles for alphaB-crystallin and HSPB2 in protecting the myocardium from ischemia-reperfusion-induced damage in a KO mouse model.

机译：在KO小鼠模型中，alphaB-crystallin和HSPB2在保护心肌免受缺血再灌注诱导的损伤中的作用。

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摘要

Overexpression studies have shown that the small heat shock proteins (sHSP) protect the myocardium from ischemia-reperfusion (I/R)-induced damage. However, gene deletion studies are necessary to demonstrate whether sHSPs are required for protection. The genes for alphaB-crystallin (alphaBC) and HSPB2, two sHSPs that are expressed in high levels in the heart, are in close proximity to one another; as a result, both genes were disrupted in a recently generated knockout (KO) mouse line. The alphaBC/HSPB2 KO mouse line is currently the only model that features disruption of sHSPs normally expressed in the heart. Accordingly, we examined the cardiac morphology, function, and response to I/R-induced stress in alphaBC-HSPB2 KO mice. Initial gross, light microscopic and echocardiographic characterization showed that the morphological and functional properties of hearts from adult KO mice were indistinguishable from age-matched wild-type (WT) mice. Electron microscopy showed that, compared with WT mouse hearts,KO mouse heart sarcomeres were relatively normal. Isolated perfused KO mouse hearts displayed normal contractility; however, when compared with WT, after I/R, KO mouse hearts exhibited a twofold reduction in contractile recovery, as well as increased necrosis and apoptosis. Additionally, when compared with WT, KO mouse hearts exhibited 43% less reduced glutathione, which is known to protect from I/R-induced damage. Thus, whereas neither alphaBC nor HSPB2 is essential for myocardial development and function under nonstressful conditions, one or both are required for maximal functional recovery and protection from I/R-induced necrosis and apoptosis.
机译：过度表达研究表明，小的热激蛋白（sHSP）保护心肌免受缺血再灌注（I / R）诱导的损害。但是，必须进行基因缺失研究来证明是否需要sHSP才能进行保护。 alphaB-crystallin（alphaBC）和HSPB2的基因是两种在心脏中高水平表达的sHSP，彼此之间非常接近。结果，这两个基因在最近产生的基因敲除（KO）小鼠品系中均被破坏。 alphaBC / HSPB2 KO小鼠系目前是唯一具有正常心脏中表达的sHSP破坏的模型。因此，我们检查了alphaBC-HSPB2 KO小鼠的心脏形态，功能和对I / R诱导的应激的反应。最初的总体，光学显微镜和超声心动图特征表明，成年KO小鼠心脏的形态和功能特性与年龄匹配的野生型（WT）小鼠没有区别。电子显微镜显示，与WT小鼠心脏相比，KO小鼠心脏肉瘤相对正常。离体的灌注KO小鼠心脏显示出正常的收缩力。但是，与WT相比，I / R后，KO小鼠心脏收缩恢复降低了两倍，坏死和凋亡增加。此外，与WT相比，KO小鼠心脏的还原型谷胱甘肽减少了43％，这可以防止I / R诱导的损伤。因此，尽管alphaBC和HSPB2都不是非应激条件下心肌发育和功能所必需的，但最大程度的功能恢复和I / R诱导的坏死和细胞凋亡的保护都需要一个或两个。

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