Copyright © 2004, European Society of Cardiology
Annexins and Ca2+ handling in the heart
INSERM U572, IFR Circulation, Hôpital Lariboisière, 41 Bd de la Chapelle, 75475 Paris cedex 10, France
* Corresponding author. Tel.: +33 1 446 31725; fax: +33 1 487 42315. Email address: daniele.charlemagne{at}larib.inserm.fr
Annexins are a family of 13 proteins known to bind phospholipids (PL) in a Ca2+-dependent way. They are ubiquitous proteins and share a similar structure characterized by a conserved C-terminal domain with Ca2+ binding sites and a variable N-terminal domain. Depending on Ca2+ concentration, they have been reported to participate in a variety of membrane-related events such as exocytosis, endocytosis, apoptosis and binding to cytoskeletal proteins. They have also been reported to regulate protein activities. This review will focus on annexins in the heart, and particularly on annexins A2, A5, A6 and A7. Annexin A2 has been found in endothelial cells and reported to play a central role in control of plasmin-mediated processes. Annexin A5 is mainly localized in cardiomyocytes. However, it could be relocated to interstitial tissue in ischemic and failing hearts or it could be externalized and exhibit a proapoptotic effect in cardiomyocytes. Annexin A6 is the most abundant annexin in the heart, and has been localized in various cell types including myocytes. Overexpression of annexin A6 has underlined physiological alterations in contractile mechanics leading to dilated cardiomyopathy, whereas knockout has been found to induce faster changes in Ca2+ transient and increased contractility, suggesting a negative inotropic role for annexin A6. Annexin A7 is expressed in heart and skeletal muscle. In annexin A7 null mutant mice decreases in the force–frequency relationship were observed in adult cardiomyocytes, consistent with regulation of Ca2+ handling. In conclusion, while annexin A2 was involved in regulation of fibrin homeostasis, alterations in expression and activity of annexins A5, A6 and A7 have been associated with regulation of Ca2+ handling in the heart, but the target of each annexin has not yet been identified.
KEYWORDS Annexin; Ca2+ handling; Heart
Time for primary review 40 days
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  T. Urashima, M. Zhao, R. Wagner, G. Fajardo, S. Farahani, T. Quertermous, and D. Bernstein Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H1351 - H1368. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M Mihm, P J Baker, L M Fleming, A M Monteiro, and P J O'Shaughnessy Differentiation of the bovine dominant follicle from the cohort upregulates mRNA expression for new tissue development genes Reproduction, February 1, 2008; 135(2): 253 - 265. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Ravassa, A. Gonzalez, B. Lopez, J. Beaumont, R. Querejeta, M. Larman, and J. Diez Upregulation of myocardial Annexin A5 in hypertensive heart disease: association with systolic dysfunction Eur. Heart J., November 2, 2007; 28(22): 2785 - 2791. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Hofstra and S. Heymans Annexin A5 and the failing heart; lost or found in translation? Eur. Heart J., November 2, 2007; 28(22): 2695 - 2696. [Full Text] [PDF]
|
|