Increased cardiac contractility by decreased HAX-1 expression
© Zhao; licensee BioMed Central Ltd. 2012
Published: 17 October 2012
The HS-1 associated protein X-1 (HAX-1) is a ubiquitously expressed protein that protects cardiomyocytes from programmed cell death. HAX-1 is mainly located in cardiac mitochondria and sarcoplasmic reticulum. Recently, it has been recognized that HAX-1 serves as a binding partner of phospholamban, which plays a fundamental role in controlling basal contractility and constitutes a key downstream effector of the β-adrenergic signaling cascade. However, the functional significance of HAX-1 in the heart remains unclear. Our previous studies have shown that overexpression of HAX-1 in vitro or in vivo by adenoviruses and transgenesis reduced cardiac myocyte contractility and calcium transients under basal condition without significant alterations of isoproterenol response. Conversely, in vitro downregulation of HAX-1 enhanced calcium kinetics and mechanics under basal conditions.
Methods and results
These results indicate that decreased HAX-1 expression in the heart is associated with increased cardiac contractility and calcium handling, suggesting that HAX-1 may be a novel regulator in cardiac contractile performance.
The author thanks Dr. Evangelia G. Kranias, who is from University of Cincinnati College of Medicine, for her constructive suggestion in the current study. This work was supported by the Starting Package of Zhengzhou University for Wen Zhao.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.