| Literature DB >> 14637156 |
Jun Takahashi1, Yutaka Kagaya, Ichiro Kato, Jun Ohta, Shogen Isoyama, Masahito Miura, Yoshinao Sugai, Masanori Hirose, Yuji Wakayama, Mototsugu Ninomiya, Jun Watanabe, Shin Takasawa, Hiroshi Okamoto, Kunio Shirato.
Abstract
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 degrees C, none of the parameters for Ca(2+) transients and forces of the papillary muscles differed between WT and CD38KO. In contrast, at 27 degrees C, at which cADPR does not work, the peak [Ca(2+)](i) was increased and the decline in [Ca(2+)](i) was accelerated in CD38KO compared with WT. In CD38KO, the protein expression of SR Ca(2+) 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 Ca(2+) homeostasis in cardiac myocytes in vivo. Its deficiency was compensated differentially according to gender.Entities:
Mesh：
Substances：
Year: 2003 PMID： 14637156 DOI： 10.1016/j.bbrc.2003.10.143
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575