No ischemic preconditioning in heterozygous connexin 43-deficient mice

Protein kinase C (PKC) plays a central role in ischemic preconditioning (IP) in mice and rabbits, and activated PKC colocalizes with and phosphorylates connexin43 (Cx43) in rats and humans. Whether or not Cx43 contributes to the mechanism(s) of IP in vivo is yet unknown. Therefore, wild-type (n = 8)...

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Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 2002-10, Vol.52 (4), p.H1740
Main Authors: Schwanke, Uwe, Konietzka, Ina, Duschin, Alexej, Li, Xiaokui
Format: Article
Language:English
Subjects:
Anatomy & physiology
Cardiology
Clinical trials
Rodents
Online Access:Get full text
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Summary:Protein kinase C (PKC) plays a central role in ischemic preconditioning (IP) in mice and rabbits, and activated PKC colocalizes with and phosphorylates connexin43 (Cx43) in rats and humans. Whether or not Cx43 contributes to the mechanism(s) of IP in vivo is yet unknown. Therefore, wild-type (n = 8) and heterozygous Cx43-deficient mice (n = 8) were subjected to 30 min occlusion and 120 min reperfusion of the left anterior descending coronary artery. IP was induced by one cycle of 5 min occlusion and 10 min reperfusion (n = 8/8 mice) before the sustained occlusion. Infarct size was reduced by IP in wild-type mice [11.3 plus minus 3.4% vs. 23.7 plus minus 7.2% of the left ventricle (LV), P < 0.05] but not in Cx43-deficient mice (26.0 plus minus 6.0% vs. 25.1 plus minus 3.8% of LV). Also, three cycles of 5 min occlusion and 10 min reperfusion (n = 5) did not induce protection in Cx43-deficient mice (27.6 plus minus 5.5 % of LV). Thus Cx43 contributes to the protection of IP in mice in vivo.
ISSN:0363-6135
1522-1539