히스티딘-리치 Ca2+ 결합 단백질에 의한 심실근세포 수축 및 Ca2+ Transient의 조절

Regulation of Contraction and Ca2+ Transient by Histidine-rich Ca2+-binding Protein in Ventricular Myocytes

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+ signaling using HRC knock-out (KO) mouse ventricular myocytes. In field-stimulated single mouse ventricular myocytes, cell shortenings and Ca2+ 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 of Ca2+ transients during action potentials, thereby attenuating ventricular contraction and relaxation.