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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2010) 34, 415–423 (Printed in Great Britain)
Connexin43 promotes survival of mesenchymal stem cells in ischaemic heart
Deguo Wang, Wenzhi Shen, Fengxiang Zhang, Minglong Chen, Hongwu Chen and Kejiang Cao1
Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Guangzhou Road 300, Nanjing, 210029, Peoples Republic of China

The involvement of connexins in regulating cell growth and death has recently been reported. We have investigated whether Cx43 (connexin43) contributes to MSC (mesenchymal stem cell) survival and improves therapeutic efficacy in MI (myocardial infarction). Genetically modified Cx43 MSCs were exposed to hypoxic conditions or injected intramyocardially into a rat MI model. MSCs overexpressing Cx43, with more Bcl-2 and phosphorylated Akt, but less Bax, were relatively tolerant to hypoxic injury. After transplantation, this Cx43 overexpression enhanced cell survival and reduced infarct size, improving contractile performance. Cx43 inhibition by SiRNA reversed the effects of Cx43 overexpression. Therefore, Cx43 may act as a potential target for improving the therapeutic efficacy of MSCs in ischaemic heart disease.

Key words: apoptosis, Bax, Bcl-2, connexin43, mesenchymal stem cells, myocardial infarction

Abbreviations: Ct, threshold cycle, Cx43, connexin43, EF, ejection fraction, FS, fractional shortening, GAPDH, glyceraldehyde-3-phosphate dehydrogenase, GJ, gap junctions, LAD, left anterior descending, MI, myocardial infarction, MSC, mesenchymal stem cells, PI, propidium iodide

1To whom correspondence should be addressed (email

Received 12 August 2009/19 December 2009; accepted 12 January 2010

Published as Cell Biology International Immediate Publication 12 January 2010, doi:10.1042/CBI20090118

© The Author(s) Journal compilation © 2010 Portland Press Limited

ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)