View : 1041 Download: 0
Phospholipase C-δ1 rescues intracellular Ca2+ overload in ischemic heart and hypoxic neonatal cardiomyocytes
- Title
- Phospholipase C-δ1 rescues intracellular Ca2+ overload in ischemic heart and hypoxic neonatal cardiomyocytes
- Authors
- Hwang K.-C.; Lim S.; Kwon H.M.; Bae Y.S.; Kang S.-M.; Chung K.-H.; Graham R.M.; Rhee S.G.; Jang Y.
- Ewha Authors
- 이서구; 배윤수
- SCOPUS Author ID
- 이서구; 배윤수
- Issue Date
- 2004
- Journal Title
- Journal of Steroid Biochemistry and Molecular Biology
- ISSN
- 0960-0760
- Citation
- Journal of Steroid Biochemistry and Molecular Biology vol. 91, no. 3, pp. 131 - 138
- Indexed
- SCI; SCIE; SCOPUS
- Document Type
- Article
- Abstract
- Ischemia and simulated ischemic conditions cause intracellular Ca 2+ overload in the myocardium. The relationship between ischemia injury and Ca2+ overload has not been fully characterized. The aim of the present study was to investigate the expression and characteristics of PLC isozymes in myocardial infarction-induced cardiac remodeling and heart failure. In normal rat heart tissue, PLC-δ1 (about 44 ng/mg of heart tissue) was most abundant isozymes compared to PLC-γ1 (6.8 ng/mg) and PLC-β1 (0.4 ng/mg). In ischemic heart and hypoxic neonatal cardiomyocytes, PLC-δ1, but not PLC-β1 and PLC-γ1, was selectively degraded, a response that could be inhibited by the calpain inhibitor, calpastatin, and by the caspase inhibitor, zVAD-fmk. Overexpression of the PLC-δ1 in hypoxic neonatal cardiomyocytes rescued intracellular Ca2+ overload by ischemic conditions. In the border zone and scar region of infarcted myocardium, and in hypoxic neonatal cardiomyocytes, the selective degradation of PLC-δ1 by the calcium sensitive proteases may play important roles in intracellular Ca2+ regulations under the ischemic conditions. It is suggested that PLC isozyme-changes may contribute to the alterations in calcium homeostasis in myocardial ischemia. © 2004 Elsevier Ltd. All rights reserved.
- DOI
- 10.1016/j.jsbmb.2004.02.009
- Appears in Collections:
- 일반대학원 > 생명·약학부 > Journal papers
- Files in This Item:
There are no files associated with this item.
- Export
- RIS (EndNote)
- XLS (Excel)
- XML