Selective hydrolysis of plasmalogen phospholipids by Ca2 -independent PLA2 in hypoxic ventricular myocytes

Jane McHowat, Shi Liu, Michael Creer

Research output: Contribution to journalArticle

Abstract

Accelerated phospholipid catabolism occurs early after the onset of myocardial ischemia and is likely to be mediated by the activation of one or more phospholipases in ischemic tissue. We hypothesized that hypoxia increases phospholipase A2 (PLA2) activity in isolated ventricular myocytes, resulting in increased lysophospholipid and arachidonic acid production, contributing to arrhythmogenesis in ischemic heart disease. The majority of ventricular myocyte arachidonic acid was found in plasmalogen phospholipids. Hypoxia increased membrane-associated, Ca2 -independent, plasmalogen-selective PLA2 activity, resulting in increased arachidonic acid release and lysoplasmenylcholine production. Pretreatment with the specific Ca2Mndependent PLA2 inhibitor bromoenol lactone blocked hypoxia-induced increases in PLA2 activity, arachidonic acid release, and lysoplasmenylcholine production. Lysoplasmenylcholine produced action potential derangements, including shortening of action potential duration, and induced early and delayed afterdepolarizations in normoxic myocytes. The electrophysiological alterations induced by lysoplasmenylcholine would likely contribute to the initiation of arrhythmogenesis in the ischemic heart.

Original languageEnglish (US)
JournalAmerican Journal of Physiology
Volume274
Issue number6 PART 1
StatePublished - Dec 1 1998

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Plasmalogens
Phospholipases A2
Arachidonic Acid
Muscle Cells
Phospholipids
Hydrolysis
Action Potentials
Myocardial Ischemia
Lysophospholipids
Phospholipases
Membranes
lysoplasmalogens
Hypoxia

All Science Journal Classification (ASJC) codes

  • Physiology (medical)

Cite this

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abstract = "Accelerated phospholipid catabolism occurs early after the onset of myocardial ischemia and is likely to be mediated by the activation of one or more phospholipases in ischemic tissue. We hypothesized that hypoxia increases phospholipase A2 (PLA2) activity in isolated ventricular myocytes, resulting in increased lysophospholipid and arachidonic acid production, contributing to arrhythmogenesis in ischemic heart disease. The majority of ventricular myocyte arachidonic acid was found in plasmalogen phospholipids. Hypoxia increased membrane-associated, Ca2 -independent, plasmalogen-selective PLA2 activity, resulting in increased arachidonic acid release and lysoplasmenylcholine production. Pretreatment with the specific Ca2Mndependent PLA2 inhibitor bromoenol lactone blocked hypoxia-induced increases in PLA2 activity, arachidonic acid release, and lysoplasmenylcholine production. Lysoplasmenylcholine produced action potential derangements, including shortening of action potential duration, and induced early and delayed afterdepolarizations in normoxic myocytes. The electrophysiological alterations induced by lysoplasmenylcholine would likely contribute to the initiation of arrhythmogenesis in the ischemic heart.",
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Selective hydrolysis of plasmalogen phospholipids by Ca2 -independent PLA2 in hypoxic ventricular myocytes. / McHowat, Jane; Liu, Shi; Creer, Michael.

In: American Journal of Physiology, Vol. 274, No. 6 PART 1, 01.12.1998.

Research output: Contribution to journalArticle

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