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B-crystallin and HSPB2 in Protecting the Myocardium from Ischemia/Reperfusion-Induced Damage in a KO Mouse Model
1 The SDSU Heart Institute and The Department of Biology, San Diego State University, San Diego, CA, USA
2 National Eye Institute, National Institutes of Health, Bethesda, MD, USA
* To whom correspondence should be addressed. E-mail: cglembotski{at}sciences.sdsu.edu.
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 
B-crystallin (BC) 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 BC/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 BC/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 to WT mouse hearts, KO mouse heart sarcomeres were relatively normal. Isolated perfused KO mouse hearts displayed normal contractility, however, compared to WT, following I/R, KO mouse hearts exhibited a two-fold reduction in contractile recovery, as well as increased necrosis and apoptosis. Additionally, compared to WT, KO mouse hearts exhibited 43% less reduced glutathione, which is known to protect from I/R-induced damage. Thus, while neither BC nor HSPB2 is essential for myocardial development and function under non-stressful conditions, one or both are required for maximal functional recovery and protection from I/R-induced necrosis and apoptosis.
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