NeuroMolecular Medicine

, Volume 12, Issue 2, pp 133–148 | Cite as

Phospholipases A2 and Inflammatory Responses in the Central Nervous System

  • Grace Y. Sun
  • Phullara B. Shelat
  • Michael B. Jensen
  • Yan He
  • Albert Y. Sun
  • Agnes Simonyi


Phospholipases A2 (PLA2s) belong to a superfamily of enzymes responsible for hydrolyzing the sn-2 fatty acids of membrane phospholipids. These enzymes are known to play multiple roles for maintenance of membrane phospholipid homeostasis and for production of a variety of lipid mediators. Over 20 different types of PLA2s are present in the mammalian cells, and in snake and bee venom. Despite their common function in hydrolyzing fatty acids of phospholipids, they are diversely encoded by a number of genes and express proteins that are regulated by different mechanisms. Recent studies have focused on the group IV calcium-dependent cytosolic cPLA2, the group VI calcium-independent iPLA2, and the group II small molecule secretory sPLA2. In the central nervous system (CNS), these PLA2s are distributed among neurons and glial cells. Although the physiological role of these PLA2s in regulating neural cell function has not yet been clearly elucidated, there is increasing evidence for their involvement in receptor signaling and transcriptional pathways that link oxidative events to inflammatory responses that underline many neurodegenerative diseases. Recent studies also reveal an important role of cPLA2 in modulating neuronal excitatory functions, sPLA2 in the inflammatory responses, and iPLA2 with childhood neurologic disorders associated with brain iron accumulation. The goal for this review is to better understand the structure and function of these PLA2s and to highlight specific types of PLA2s and their cross-talk mechanisms in these inflammatory responses under physiological and pathological conditions in the CNS.


Cytosolic phospholipases A2 Calcium-independent phospholipases A2 Secretory phospholipases A2 NADPH oxidase NMDA receptor Inflammatory responses Cerebral ischemia Cytokines Alzheimer’s disease 



Alzheimer’s disease


Amyloid precursor protein


Arachidonic acid


Bromoenol lactone


Ca2+/Calmodulin-dependent protein kinase II


Central nervous system


Cerebrospinal fluid




Docosahexaenoic acid


Extracellular signal-regulated kinases




Heat shock protein 90


Inducible nitric oxide synthase




Interleukin 1β


Infantile neuroaxonal dystrophy




Mitogen-activated protein kinase


MAPK-interacting kinase


Magnetic resonance imaging


Idiopathic neurodegeneration with brain iron accumulation


N-Methyl-d-aspartic acid


Nitric oxide


Neuroprotectin 1


Palmitoyl trifluoromethyl ketone




prostglandin E2


Protein kinase C


Phospholipases A2




Reactive oxygen species




Tumor necrosis factor-alpha



This study was supported by P01 AG018357 from NIH.


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Copyright information

© Humana Press Inc. 2009

Authors and Affiliations

  • Grace Y. Sun
    • 1
    • 2
  • Phullara B. Shelat
    • 1
  • Michael B. Jensen
    • 1
  • Yan He
    • 1
  • Albert Y. Sun
    • 2
  • Agnes Simonyi
    • 1
  1. 1.Department of BiochemistryUniversity of MissouriColumbiaUSA
  2. 2.Department of Pathology and Anatomical SciencesUniversity of MissouriColumbiaUSA

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