J. Lipid Res.
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A more recent version of this article appeared on February 1, 2004

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J. Lipid Res., doi:10.1194/jlr.R300016-JLR200
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Submitted on September 21, 2003
Revised on November 26, 2003
Accepted on November 26, 2003

Phospholipase A2 in the central nervous system: Implications for neurodegenerative diseases

Grace Y. Sun, Jianfeng Xu, Michael D. Jensen, and Agnes Simonyi

Biochemistry Dept., University of Missouri, Columbia, MO 65211

Corresponding Author: sung{at}health.missouri.edu

Phospholipases A2 (PLA2) belong to a family of enzymes catalyzing the cleavage of fatty acids from the sn-2 position of phospholipids. There are 19+ different isoforms of PLA2 in the mammalian system, but recent studies have focused on three major groups: namely, the group IV cytosolic PLA2 (cPLA2), the group II secretory PLA2 (sPLA2) and the group VI Ca2+-independent PLA2 (iPLA2). These PLA2 are involved in a complex network of signaling pathways linking receptor agonists, oxidative agents and pro-inflammatory cytokines to the release of arachidonic acid (AA) and the synthesis of eicosanoids. PLA2 acting on membrane phospholipids have been implicated in intracellular membrane trafficking, differentiation, proliferation, and apoptotic processes. All major groups of PLA2 are present in the Central Nervous System (CNS). Therefore, this review is focused on PLA2 and AA release in neural cells, especially in astrocytes and neurons. In addition, because many neurodegenerative diseases are associated with increased oxidative and inflammatory responses, an attempt was made to include studies on PLA2 in cerebral ischemia, Alzheimer's disease and neuronal injury due to excitotoxic agents. Information from these studies has provided clear evidence for the important role of PLA2 in regulating physiological and pathological functions in the CNS.


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