Deficit of CD38/cyclic ADP-ribose is differentially compensated in hearts by gender.
Deficit of CD38/cyclic ADP-ribose is differentially compensated in hearts by gender.
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DOI：
10.1016/j.bbrc.2003.10.143
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发表时间：
2003-12
影响因子：
3.1
通讯作者：
J. Takahashi;Y. Kagaya;I. Kato;J. Ohta;S. Isoyama;M. Miura;Y. Sugai;M. Hirose;Y. Wakayama;M. Ninomiya;J. Watanabe;S. Takasawa;H. Okamoto;K. Shirato
中科院分区：
文献类型：
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作者：
J. Takahashi;Y. Kagaya;I. Kato;J. Ohta;S. Isoyama;M. Miura;Y. Sugai;M. Hirose;Y. Wakayama;M. Ninomiya;J. Watanabe;S. Takasawa;H. Okamoto;K. Shirato
为了阐明心肌 CD38/环 ADP-核糖 (cADPR) 信号传导是否发挥生理作用，我们研究了 CD38 敲除小鼠 (CD38KO) 的心脏。在CD38KO中，与野生型小鼠(WT)相比，心肌cADPR含量降低了85%。心脏肥大只发生在男性中。在 36°C 时，WT 和 CD38KO 之间的 Ca2+ 瞬变参数和乳头肌力均无差异。相反，在cADPR不起作用的27°C下，与WT相比，CD38KO中的[Ca2+]i峰值增加，并且[Ca2+]i下降加速。在CD38KO中，与WT相比，SR Ca2+ATP酶2型(SERCA2)的蛋白表达以及SERCA2与受磷蛋白的比率增加。与野生型相比，兰尼碱受体蛋白仅在雌性CD38KO中增加。这些数据表明 CD38/cADPR 信号传导在体内心肌细胞的细胞内 Ca2+ 稳态中发挥重要作用。它的缺陷根据性别有差别地得到补偿。
To elucidate whether myocardial CD38/cyclic ADP-ribose (cADPR) signaling plays a physiological role, we investigated the heart of CD38 knockout mice (CD38KO). In CD38KO, the myocardial cADPR content was reduced by 85% compared with wild-type mice (WT). Cardiac hypertrophy developed only in males. At 36°C, none of the parameters for Ca2+transients and forces of the papillary muscles differed between WT and CD38KO. In contrast, at 27°C, at which cADPR does not work, the peak [Ca2+]iwas increased and the decline in [Ca2+]iwas accelerated in CD38KO compared with WT. In CD38KO, the protein expression of SR Ca2+ATPase type2 (SERCA2) and the SERCA2-to-phospholamban ratio were increased compared with WT. The ryanodine receptor protein was increased only in female CD38KO compared with WT. These data suggest that the CD38/cADPR signaling plays an important role in intracellular Ca2+homeostasis in cardiac myocytes in vivo. Its deficiency was compensated differentially according to gender.