Phospholipase A2 in astrocytes |
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| Authors: | Grace Y Sun Jianfeng Xu Michael D Jensen Sue Yu W Gibson Wood Fernando A González Agnes Simonyi Albert Y Sun Gary A Weisman |
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| Institution: | (1) Department of Biochemistry, University of Missouri-Columbia, Columbia, MO;(2) Department of Medical Pharmacology and Physiology, University of Missouri-Columbia, Columbia, MO;(3) Division of Experimental Medicine, Harvard Institute of Medicine and Beth Israel Deaconess Medical Center, Boston, MA;(4) Department of Pharmacology and Geriatric Research, Education and Clinical Center, VA Medical Center, University of Minnesota School of Medicine, Minneapolis, MN;(5) Department of Chemistry, University of Puerto Rico, Rio Piedras, Puerto Rico |
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| Abstract: | Astrocytes comprise the major cell type in the central nervous system (CNS) and they are essential for support of neuronal
functions by providing nutrients and regulating cell-to-cell communication. Astrocytes also are immune-like cells that become
reactive in response to neuronal injury. Phospholipases A2 (PLA
2) are a family of ubiquitous enzymes that degrade membrane phospholipids and produce lipid mediators for regulating cellular
functions. Three major classes of PLA
2 are expressed in astrocytes: group IV calcium-dependent cytosolic PLA
2 (cPLA2), group VI calcium-independent PLA
2 (iPLA2), and group II secretory PLA
2 (sPLA2). Upregulation of PLA
2 in reactive astrocytes has been shown to occur in a number of neurodegenerative diseases, including stroke and Alzheimer’s
disease. This review focuses on describing the effects of oxidative stress, inflammation, and activation of G protein-coupled
receptors on PLA
2 activation, arachidonic acid (AA) release, and production of prostanoids in astrocytes. |
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| Keywords: | Phospholipases A2 oxidative stress cytokines arachidonic acid prostaglandin E2 astrocyte reactive gliosis |
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