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1 Institut für Pathophysiologie, Universitätsklinikum Essen, essen, Germany
2 Institut für Pathophysiologie, Universitätsklinikum Essen, Essen, Germany
3 Hospital Universitari Vall d'Hebron, Servicio de Cardiologia, Barcelona, Spain
* To whom correspondence should be addressed. E-mail: kerstin.boengler{at}uk-essen.de.
Connexin 43 (Cx43) is localized at left ventricular (LV) gap junctions and in cardiomyocyte mitochondria. A genetically-induced reduction of Cx43 as well as blockade of mitochondrial Cx43 import abolishes the infarct size (IS) reduction by ischemic preconditioning (IP). With progressing age, Cx43 content in ventricular and atrial tissue homogenates is reduced. We now investigated whether or not 1) the mitochondrial Cx43 content is reduced in aged mice hearts, and 2) IS reduction by IP is lost in aged mice hearts in vivo.
Confirming previous results, sarcolemmal Cx43 content was reduced in aged (>13 months) compared to young (<3 months) C57Bl/6 mice hearts, whereas the expression levels of protein kinase C 
and endothelial nitric oxide synthase remained unchanged. Also in mitochondria isolated from aged mice LV myocardium, Western blot analysis indicated a 40% decrease in Cx43 content compared to mitochondria isolated from young mice hearts.
In young mice hearts, IP by one cycle of 10 min ischemia and 10 min reperfusion reduced IS
(% of area at risk) following 30 min regional ischemia and 120 min reperfusion from 67.7±3.3 (n=17) to 34.2±6.6 (n=5, p<0.05). In contrast, IP's cardioprotection was lost in aged mice hearts, since IS in non-preconditioned (57.5±4.0, n=10) and preconditioned hearts (65.4±6.3, n=8, p=ns) was not different.
In conclusion, mitochondrial Cx43 content is decreased in aged mouse hearts. The reduced levels of Cx43 may contribute to the age-related loss of cardioprotection by IP.
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