Deficit of CD38/cyclic ADP-ribose is differentially compensated in hearts by gender

Jun Takahashi, 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

Research output: Contribution to journalArticlepeer-review

25 Citations (Scopus)


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+]i was increased and the decline in [Ca2+]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 Ca2+ homeostasis in cardiac myocytes in vivo. Its deficiency was compensated differentially according to gender.

Original languageEnglish
Pages (from-to)434-440
Number of pages7
JournalBiochemical and biophysical research communications
Issue number2
Publication statusPublished - 2003 Dec 12


  • CD38
  • Calcium cycling
  • Cyclic ADP-ribose
  • Gender difference
  • Hypertrophy

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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