Phospholipase C-δ1 rescues intracellular Ca2+ overload in ischemic heart and hypoxic neonatal cardiomyocytes

Ki Chul Hwang, Soyeon Lim, Hyuck Moon Kwon, Yun Soo Bae, Seok Min Kang, Kwang Hoe Chung, Robert M. Graham, Sue Goo Rhee, Yangsoo Jang

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24 Scopus citations


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.

Original languageEnglish
Pages (from-to)131-138
Number of pages8
JournalJournal of Steroid Biochemistry and Molecular Biology
Issue number3
StatePublished - Jul 2004

Bibliographical note

Funding Information:
This study was supported by a grant of the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea. (HMP-00-GN-01-0001).


  • Hypoxic neonatal cardiomyocytes
  • Ischemic heart
  • Phospholipase C-δ1


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