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KMID : 0370220120560060377
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Yakhak Hoeji
2012 Volume.56 No. 6 p.377 ~ p.381
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Regulation of Contraction and Ca2+ Transient by Histidine-rich Ca2+ binding Protein in Ventricular Myocytes
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Son Min-Jeong
Kim Joon-Chul
Kim Seong-Woo
Woo Sun-Hee
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Abstract
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The histidine-rich Ca2+ binding protein (HRC) is a Ca2+ binding protein in the sarcoplasmic reticulum (SR). In this study, we examined whether the HRC is involved in the regulation of cardiac contraction and Ca2+미지 signaling using HRC knock-out (KO) mouse ventricular myocytes. In field-stimulated single mouse ventricular myocytes, cell shortenings and Ca 2+ transients were measured using a video edge detection and a confocal Ca2 imaging, respectively. Compared with the wide-type (WT) myocytes, the magnitudes of cell shortenings were significantly larger in HRC KO cells (P<0.01, WT vs. KO). The rate of contraction and relaxation was significantly accelerated in HRC KO myocytes (P<0.05 and P<0.01, respectively, WT vs. KO). The magnitudes of Ca2+ transients were increased by HRC KO (P<0.01, WT vs. KO). In addition, the decay of the Ca2+ transient was faster in HRC KO cells than in wild-type cells P<0.01, WT vs. KO). These results suggest that HRC may suppress SR Ca2+releases and decay ofCa2+transients during action potentials, thereby attenuating ventricular contraction and relaxation.
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KEYWORD
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histidine-rich Ca2+ binding protein (HRC), contraction, Ca2+ transient, ventricular myocytes, knock-out
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