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Am J Physiol Heart Circ Physiol 287: H1705-H1711, 2004. First published June 10, 2004; doi:10.1152/ajpheart.01211.2003
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Regulation of myocardial function by histidine-rich, calcium-binding protein

Guo-Chang Fan,1,* Kimberly N. Gregory,1,* Wen Zhao,1 Woo Jin Park,2 and Evangelia G. Kranias1

1Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267; and 2Department of Life Science and National Research Laboratory of Proteolysis, Kwangju Institute of Science and Technology, Kwangju 500-712, South Korea

Submitted 22 December 2003 ; accepted in final form 4 June 2004

Impaired sarcoplasmic reticulum (SR) Ca release has been suggested to contribute to the depressed cardiac function in heart failure. The release of Ca from the SR may be regulated by the ryanodine receptor, triadin, junctin, calsequestrin, and a histidine-rich, Ca-binding protein (HRC). We observed that the levels of HRC were reduced in animal models and human heart failure. To gain insight into the physiological function of HRC, we infected adult rat cardiac myocytes with a recombinant adenovirus that contains the full-length mouse HRC cDNA. Overexpression (1.7-fold) of HRC in adult rat cardiomyocytes was associated with increased SR Ca load (28%) but decreased SR Ca-induced Ca release (37%), resulting in impaired Ca cycling and depressed fractional shortening (36%) as well as depressed rates of shortening (38%) and relengthening (33%). Furthermore, the depressed basal contractile and Ca kinetic parameters in the HRC-infected myocytes remained significantly depressed even after maximal isoproterenol stimulation. Interestingly, HRC overexpresssion was accompanied by increased protein levels of junctin (1.4-fold) and triadin (1.8-fold), whereas the protein levels of ryanodine receptor, calsequestrin, phospholamban, and sarco(endo)plasmic reticulum Ca-ATPase remained unaltered. Collectively, these data indicate that alterations in expression levels of HRC are associated with impaired cardiac SR Ca homeostasis and contractile function.

sarcoplasmic reticulum; calcium cycling; contractility


Address for reprint requests and other correspondence: E. G. Kranias, Dept. of Pharmacology and Cell Biophysics, Univ. of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0575 (E-mail: Litsa.Kranias{at}uc.edu)




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