2003年12月
Deficit of CD38/cyclic ADP-ribose is differentially compensated in hearts by gender
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- 巻
- 312
- 号
- 2
- 開始ページ
- 434
- 終了ページ
- 440
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/j.bbrc.2003.10.143
- 出版者・発行元
- ACADEMIC PRESS INC ELSEVIER SCIENCE
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 wildtype mice (WT). Cardiac hypertrophy developed only in mates. At 36degreesC, none of the parameters for Ca2+ transients and forces of the papillary muscles differed between WT and CD38KO. In contrast, at 27degreesC, 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 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. (C) 2003 Elsevier Inc. All rights reserved.
- リンク情報
- ID情報
-
- DOI : 10.1016/j.bbrc.2003.10.143
- ISSN : 0006-291X
- eISSN : 1090-2104
- Web of Science ID : WOS:000186987000025