HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Li, J. Articles by Radice, G. L. Search for Related Content PubMed PubMed Citation Articles by Li, J. Articles by Radice, G. L.

Dysregulation of Cell Adhesion Proteins and Cardiac Arrhythmogenesis

Jifen Li, MD, PhD, Center for Research on Reproduction and Women’s Health, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Vickas V. Patel, MD, PhD, Division of Cardiovascular Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Glenn L. Radice, PhD, Center for Research on Reproduction and Women’s Health, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Reprint Requests: Glenn L. Radice, PhD, Center for Research on Reproduction and Women’s Health, University of Pennsylvania, 1355 Biomedical Research Building II/III, 421 Curie Blvd., Philadelphia, PA 19104, Tel.: 215-898-0164, Fax: 215-573-5408, Email: radice{at}mail.med.upenn.edu

Proper mechanical and electrical coupling of cardiomyocytes is crucial for normal propagation of the electrical impulse throughout the working myocardium.Various proteins on the surface of cardiomyocytes are responsible for the integration of structural information and cell-cell communication. Increasing evidence from diseased myocardium and animal models indicates that alteration in electrical coupling via gap junctions is a critical determinant in the development of an arrhythmogenic substrate. What is less clear is how gap junctions are maintained and regulated in the working myocardium. In this review, we present data from human disease and animal models that support the idea that cell adhesion proteins regulate the stability of the gap junction protein, connexin.

Key Words: Arrhythmia • Cadherin • Connexin • Gap junction • Intercalated disc

This article has been cited by other articles:

				Q. Wang, J. L. C. Lin, B. E. Reinking, H. Z. Feng, F. C. Chan, C. I. Lin, J. P. Jin, E. A. Gustafson-Wagner, T. D. Scholz, B. Yang, et al. Essential Roles of an Intercalated Disc Protein, mXin{beta}, in Postnatal Heart Growth and Survival Circ. Res., May 14, 2010; 106(9): 1468 - 1478. [Abstract] [Full Text] [PDF]

				N. Chauvet, T. El-Yandouzi, M.-N. Mathieu, A. Schlernitzauer, E. Galibert, C. Lafont, P. Le Tissier, I. C Robinson, P. Mollard, and N. Coutry Characterization of adherens junction protein expression and localization in pituitary cell networks J. Endocrinol., September 1, 2009; 202(3): 375 - 387. [Abstract] [Full Text] [PDF]

				X. Liang, Y. Sun, M. Ye, M. C. Scimia, H. Cheng, J. Martin, G. Wang, A. Rearden, C. Wu, K. L. Peterson, et al. Targeted Ablation of PINCH1 and PINCH2 From Murine Myocardium Results in Dilated Cardiomyopathy and Early Postnatal Lethality Circulation, August 18, 2009; 120(7): 568 - 576. [Abstract] [Full Text] [PDF]

				N. J. Severs, A. F. Bruce, E. Dupont, and S. Rothery Remodelling of gap junctions and connexin expression in diseased myocardium Cardiovasc Res, October 1, 2008; 80(1): 9 - 19. [Abstract] [Full Text] [PDF]