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1 Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY, USA
2 Department of Neuroanatomy and Molecular Brain Research, Ruhr-University, Bochum, Germany
3 Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY, USA; Department of Cardiology, Albert Einstein College of Medicine, Bronx, NY, USA
* To whom correspondence should be addressed. E-mail: diacobas{at}aecom.yu.edu.
We have used mouse 27k cDNA arrays to compare gene expression patterns in four sets of three hearts each of neonatal wildtype and four sets of three hearts each of littermates lacking the major cardiac gap junction protein, Cx43. Each individual set of hearts was hybridized against aliquots of an RNA standard prepared from selected mouse tissues, allowing calculation of variability and coordination of gene expression among the samples from both genoypes. Overall variance of gene expression was found to be markedly higher in wildtype hearts than in those from Cx43 null littermates. Expression levels of 586 of 5613 adequately quantifiable distinct genes with known protein products were statistically altered in the Cx43 null hearts, 38 up-regulated and 548 down-regulated compared to wildtypes. Down-regulation was confirmed for seven tested genes by qRT-PCR. Functions of proteins encoded by the altered genes encompassed all functional categories, with largest percent changes in genes involved in intracellular transport and transcription factors. Among the down-regulated genes in the Cx43 null hearts were those related to neuronal and glial function, suggesting that cardiac innervation might be compromised as a consequence of Cx43 deletion. This was supported by immunodetection of sympathetic innervation using antibodies to the synaptic vesicle protein synaptophysin and to the adrenergic nerve terminal marker tyrosine hydroxylase. These findings reinforce the proposal that the cardiac abnormality in Cx43 null animals may be contributed by altered innervation and indicate that Cx43 deletion has consequences in addition to reduced intercellular communication.
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