alexa Molecular Investigation into the Human Atrioventricular
ISSN: 2161-0940

Anatomy & Physiology: Current Research
Open Access

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Research Article

Molecular Investigation into the Human Atrioventricular Node in Heart Failure

Halina Dobrzynski1*, Andrew Atkinson1, Zoltan Borbas1, Christina M Ambrosi2 and Igor R Efimov2*

1Institute of Cardiovascular Sciences, University of Manchester, 46 Grafton Street, Manchester, UK

2Department of Biomedical Engineering, Washington University, One Brookings Drive, St. Louis, MO, USA

*Corresponding Author:
Halina Dobrzynski
Institute of Cardiovascular Sciences
University of Manchester, 46 Grafton Street
Manchester, M13 9NT, UK
Tel: +44 (0)161-275 1182
E-mail: [email protected]

Igor R. Efimov
Department of Biomedical Engineering
Washington University, Campus box 1097
One Brookings Drive, St. Louis, MO 63130, USA
Tel: 5-8612
E-mail: [email protected]

Received date: July 23, 2014; Accepted date: November 17, 2014; Published date: November 20, 2014

Citation: Dobrzynski H, Atkinson A, Borbas Z, Ambrosi CM, Efimov IR (2015) Molecular Investigation into the Human Atrioventricular Node in Heart Failure . Anat Physiol 5:164. doi:10.4172/2161-0940.1000164

Copyright: © 2015 Dobrzynski, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

 

Abstract

The atrioventricular node (AVN), the molecular basis has been studied in animal models; however, the human AVN remains poorly explored at the molecular level in heart failure patients. We studied ex vivo donor human hearts rejected for transplantation (n=6) and end-stage failing hearts with cardiomyopathy of various etiologies (n=6). Microdissection and quantitative PCR (qPCR) were used to anatomically map mRNA expression in both failing and non-failing hearts from tissue sections through the AVN, atrial and ventricular muscle. In the failing ventricle significant (P<0.05) downregulation is apparent for vimentin, hERG and Kir3.4 and trend to downregulation for Nav1.5, Cav1.2, Tbx3, Kir2.1, NCX1, Cx43 and Cx45. In the failing atrium, there is non-significant trend in upregulation for Nav1.5, HCN2, Cav3.1, Kv1.5, Kir3.1, RYR2 and significant upregulation for Cx40 and trend in downregulation for hERG, Kir2.1 and NCX1, and significant downregulation for HCN4 and Kir3.4. In the failing AVN there is significant (P<0.05) downregulation for vimentin, collagen, Tbx3, Kir3.1, Kir3.4, Cx45 and HCN4; there is also trend toward downregulation for HCN2, Kv1.5, Kir2.1 and RYR2. In the failing AVN there is significant (P<0.05) upregulation for Cx40, HCN1 and Cav3.1; and trend in upregulation for Nav1.5 and Cx43. For several transcripts, we also analysed corresponding protein expression via immunofluorescence. The protein expression data on the AVN for HCN1, Cav3.1 and Cx40 support qPCR data. Remodelling of AVN in heart failure might contribute to prolonged AV conduction time and could explain the prolonged PR interval that occurs in heart failure patients.

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