Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation Research
Search: search_blue_button Advanced Search
Circulation Research. 2003;93:381-383
doi: 10.1161/01.RES.0000091364.90121.0C
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kohl, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kohl, P.
Related Collections
Right arrow Structure
Right arrow Arrythmias-basic studies
Right arrow Cell biology/structural biology
Right arrow CV surgery: transplantation, ventricular assistance, cardiomyopathy
(Circulation Research. 2003;93:381.)
© 2003 American Heart Association, Inc.


Editorials

Heterogeneous Cell Coupling in the Heart

An Electrophysiological Role for Fibroblasts

Peter Kohl

From the University Lab of Physiology, Oxford, UK.

Correspondence to Peter Kohl, MD, PhD, University Lab of Physiology, Parks Road, Oxford OX1 3PT, UK. E-mail peter.kohl@physiol.ox.ac.uk


Key Words: cardiomyocytes • cardiac fibroblasts • gap junctions • in vitro • in vivo


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

The heart is a muscle. Muscles are made up of myocytes. These may differ in form and function, but—in essence—they are the cells in which we are interested when we consider the structural makeup of the heart. Likewise, when we assess electrical coupling of cardiac cells by connexins, we are often content to assume that gap junctions occur exclusively—or at least in the overwhelming majority of cases—between homologous cell types.

It is sobering, in this context, to reflect on the fact that cardiac myocytes form a minority of cells in the heart, insofar as cell numbers are concerned (which, for cell coupling, is more relevant than total volume occupied by a cell population). A meticulous study by Adler et al1 demonstrated that myocyte and connective tissue cell numbers increase at a similar rate in early human development, from about 0.5x109 at 28 weeks of fetal development to 2 to 3x109 several weeks postpartum. Thereafter, myocyte cell numbers remain stable, while the connective tissue cell count increases with cardiac weight to {approx}7x109 at 2 months of age.

This mitotic potential of cardiac fibroblasts is maintained after cell isolation and is the key reason for which fibroblasts are omnipresent in primary cardiac cell cultures. This is not for lack of effort to eliminate nonmyocytes. Measures to enrich myocyte content in cardiac cell culture include addition of mitotic inhibitors, substrate restrictions, and, most prominently, preplating steps (occasionally in the presence of antibodies against muscle cell surface adhesion . . . [Full Text of this Article]




This article has been cited by other articles:


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
N. Morita, A. A. Sovari, Y. Xie, M. C. Fishbein, W. J. Mandel, A. Garfinkel, S.-F. Lin, P.-S. Chen, L.-H. Xie, F. Chen, et al.
Increased susceptibility of aged hearts to ventricular fibrillation during oxidative stress
Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1594 - H1605.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
Y. Xie, A. Garfinkel, J. N. Weiss, and Z. Qu
Cardiac alternans induced by fibroblast-myocyte coupling: mechanistic insights from computational models
Am J Physiol Heart Circ Physiol, August 1, 2009; 297(2): H775 - H784.
[Abstract] [Full Text] [PDF]


Home page
Phil Trans R Soc BHome page
K. K Parker and D. E Ingber
Extracellular matrix, mechanotransduction and structural hierarchies in heart tissue engineering
Phil Trans R Soc B, August 29, 2007; 362(1484): 1267 - 1279.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
H. C. Cho, Y. Kashiwakura, and E. Marban
Creation of a Biological Pacemaker by Cell Fusion
Circ. Res., April 27, 2007; 100(8): 1112 - 1115.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
T. A. Baudino, W. Carver, W. Giles, and T. K. Borg
Cardiac fibroblasts: friend or foe?
Am J Physiol Heart Circ Physiol, September 1, 2006; 291(3): H1015 - H1026.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
R. B. Driesen, G. D. Dispersyn, F. K. Verheyen, S. M. van den Eijnde, L. Hofstra, F. Thone, P. Dijkstra, W. Debie, M. Borgers, and F. C.S. Ramaekers
Partial cell fusion: A newly recognized type of communication between dedifferentiating cardiomyocytes and fibroblasts
Cardiovasc Res, October 1, 2005; 68(1): 37 - 46.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
P. Camelliti, T. K. Borg, and P. Kohl
Structural and functional characterisation of cardiac fibroblasts
Cardiovasc Res, January 1, 2005; 65(1): 40 - 51.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
P. Camelliti, G. P Devlin, K. G Matthews, P. Kohl, and C. R Green
Spatially and temporally distinct expression of fibroblast connexins after sheep ventricular infarction
Cardiovasc Res, May 1, 2004; 62(2): 415 - 425.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
P. Camelliti, C. R. Green, I. LeGrice, and P. Kohl
Fibroblast Network in Rabbit Sinoatrial Node: Structural and Functional Identification of Homogeneous and Heterogeneous Cell Coupling
Circ. Res., April 2, 2004; 94(6): 828 - 835.
[Abstract] [Full Text] [PDF]