Role of phospholipase A2 in the release of free fatty acids during ischemia-reperfusion in the rat cerebral cortex
Section snippets
Acknowledgements
Supported by USPHS Grant No. NS26912-09.
References (12)
Effects of ischemia and electroconvulsive shock on free fatty acid pool in the brain
Biochim. Biophys. Acta
(1970)Diversity of group types, regulation and function of phospholipase A2
J. Biol. Chem.
(1994)- et al.
Control of arachidonic acid accumulation in bone marrow derived macrophages by acyltransferases
J. Biol. Chem.
(1981) - et al.
A possible role for phospholipases in the release of neurotransmitter amino acids from ischemic rat cerebral cortex
Neurosci. Lett.
(1995) - et al.
Enhanced prostaglandin synthesis due to phospholipid breakdown in ischemic reperfused myocardium
J. Mol. Cell. Cardiol.
(1986) - et al.
Molecular cloning of rat cDNA for cytosolic phospholipase A2 and the increased gene expression in the dentate gyrus following transient forebrain ischemia
Mol. Brain Res.
(1994)
Cited by (41)
Astrocytic phospholipase A2 contributes to neuronal glutamate toxicity
2014, Brain ResearchCitation Excerpt :The neuronal production of extracellular H2O2 in response to chronic glutamate exposure might not be involved in astrocytic PLA2 activation (Fig. 3A–D). Both cPLA2 activity and protein levels are significantly increased during the ischemic period (Saluja et al., 1997). The inhibition and overexpression of PLA2 activity in neuronal disorders has been investigated using knockout (Kennedy et al., 1995; Tabuchi et al., 2003) and transgenic (Grass et al., 1996) mice.
Influence of experimental subarachnoid hemorrhage on nicotine-induced contraction of the rat basilar artery in relation to arachidonic acid metabolites signaling pathway
2013, Journal of Stroke and Cerebrovascular DiseasesCitation Excerpt :It was reported that cPLA2 enzymatic activity and immunoreactivity (Western blot) in the cerebral artery significantly increased after 10 or 20 minutes of global cerebral ischemia (no reperfusion) in male Sprague-Dawley rats. Both PLA2 activity and protein expression returned to control levels following 20 minutes of reperfusion.48 AACOCF3 (10−5 to 3 × 10−5 mol/L) treatment of SAH (1 hour and 1 week) arteries inhibited contraction more than in normal arteries, suggesting that exposure to SAH (1 hour and 1 week) decreases cPLA2 activity in the RBA.
Role of PI3Kα and sarcolemmal ATP-sensitive potassium channels in epoxyeicosatrienoic acid mediated cardioprotection
2012, Journal of Molecular and Cellular CardiologyCitation Excerpt :In recent years, it has become evident that metabolites of polyunsaturated fatty acids act as critical intracellular mediators, maintaining cardiac homeostasis and initiating protective responses to cellular stress. Arachidonic acid (AA) is a polyunsaturated fatty acid normally found esterified to cell membranes that can be released in response to several stimuli including ischemia [1]. Free AA is further metabolized by cyclooxygenases, lipoxygenases, and cytochrome P450 (CYP) epoxygenases to numerous products collectively termed eicosanoids with differing cellular function in health and disease [2].
Pathways involved in the generation of reactive oxygen and nitrogen species during glucose deprivation and its role on the death of cultured hippocampal neurons
2010, NeuroscienceCitation Excerpt :In agreement with these observations, a role of 12-LOX on neuronal death induced by GD and glucose reperfusion has been recently demonstrated (Nagasawa et al., 2007). The present results agree with previous observations supporting the role of cPLA2 and XaO on ROS generation and neuronal death during ischemia/reperfusion (Owada et al., 1994; Saluja et al., 1997; Arai et al., 2001; Lin and Phillis, 1991; Abramov et al., 2007), and suggests that the activation of these enzymes is related to the hypoglycemic component of the ischemic episode. In the present experimental conditions activation of these Ca2+-dependent enzymes would result from the increase in the intracellular concentration of calcium recorded during the GD episode.
Epoxyeicosatrienoic acids limit damage to mitochondrial function following stress in cardiac cells
2009, Journal of Molecular and Cellular CardiologyCitation Excerpt :The majority of endogenous EETs (> 85%) are esterified to membrane glycerophospholipids, particularly phosphatidylcholine and phosphatidylinositol, where they are generally considered inactive until their release [2]. Ischemia has been shown to activate cytosolic phospholipase A2 which will release free fatty acid from membrane stores [3]. Modulation of EET levels can occur via reincorporation into phospholipid membranes or by β-oxidation to smaller reactive epoxides; however, the predominant pathway occurs through metabolism to inactive vicinal diol compounds by epoxide hydrolases, such as soluble epoxide hydrolase (sEH or Ephx2) [4].