| First Author | Takahashi J | Year | 2003 |
| Journal | Biochem Biophys Res Commun | Volume | 312 |
| Issue | 2 | Pages | 434-40 |
| PubMed ID | 14637156 | Mgi Jnum | J:86745 |
| Mgi Id | MGI:2681398 | Doi | 10.1016/j.bbrc.2003.10.143 |
| Citation | Takahashi J, et al. (2003) Deficit of CD38/cyclic ADP-ribose is differentially compensated in hearts by gender. Biochem Biophys Res Commun 312(2):434-40 |
| abstractText | 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. |
