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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


ROLE OF CONNEXIN43 DURING ISCHEMIC PRECONDITIONING IN NORMAL AND HYPERLIPIDAEMIC RAT HEARTS
Abstract number: OF22-87

Gorbe1 A., Shultz1 R., Csont1 T., Ferdinandy1 P.

1Department of Biochemistry, Faculty of Medicine, University of Szeged, Szeged, [email protected]

Aims: 

The loss of early preconditioning was subsequently confirmed by our group in hearts isolated from rats exposed to dietary cholesterol. Information exchange via Connexin43 (Cx43) gap junctions located mainly in the intercalated disc in the hearts, could be involved as an effector molecule in ischemic preconditioning (IP). The aim of the study was to detect expression and intracellular migration of Cx43 during IP in hyperlipidemic rats.

Methods: 

Male Wistar rats were fed laboratory chow enriched with 2% cholesterol or standard chow for 12 weeks and after diet period hearts were isolated and perfused according to Langendorf. IP protocol (3X5 min ischaemia/ reperfusion) or 10 min perfusion was applied, which was followed by 30 min global ischaemia and 5 min reperfusion. Cx43 expression was detected by immunohistochemistry or western blotting (WB) in total hearts and by WB in isolated mitochondria.

Results: 

Cx43 expression did not change significantly in hyperlipidaemia. Cx43 content of mitochondria significantly increased (p < 0.05) due to ischaemia and reduced (p < 0.05) following PC in both groups. Intracellular migration of connexins from intercalated discs was observed in hyperlipidaemic hearts, which further decreased (p < 0.05) after IP.

Conclusion: 

Intracellular migration of Cx43 was detected in hyperlipidaemic hearts, and altered intracellular pattern of connexins after IP, which could be involved in lost preconditioning in cholesterol-fed rats.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :OF22-87

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