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Phospholipases A2 and Inflammatory Responses in the Central Nervous System

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Abstract

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.

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Abbreviations

AD:

Alzheimer’s disease

APP:

Amyloid precursor protein

AA:

Arachidonic acid

BEL:

Bromoenol lactone

CaMKII:

Ca2+/Calmodulin-dependent protein kinase II

CNS:

Central nervous system

CSF:

Cerebrospinal fluid

COX-2:

Cyclooxygenase-2

DHA:

Docosahexaenoic acid

ERK:

Extracellular signal-regulated kinases

HNE:

4-Hydroxynonenal

hsp90:

Heat shock protein 90

iNOS:

Inducible nitric oxide synthase

IFNγ:

Interferon-γ

IL-1β:

Interleukin 1β

INAD:

Infantile neuroaxonal dystrophy

LPS:

Lipopolysaccharide

MAPK:

Mitogen-activated protein kinase

MNK1:

MAPK-interacting kinase

MRI:

Magnetic resonance imaging

NBIA:

Idiopathic neurodegeneration with brain iron accumulation

NMDA:

N-Methyl-d-aspartic acid

NO:

Nitric oxide

NPD1:

Neuroprotectin 1

PACOCF3:

Palmitoyl trifluoromethyl ketone

PIP2:

Phosphatidylinositol-4,5-bisphosphate

PGE2:

prostglandin E2

PKC:

Protein kinase C

PLA2:

Phospholipases A2

SMase:

sphingomyelinase

ROS:

Reactive oxygen species

TBHP:

tert-Butylhydroperoxide

TNFα:

Tumor necrosis factor-alpha

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Acknowledgment

This study was supported by P01 AG018357 from NIH.

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  1. Department of Biochemistry, University of Missouri, 117 Schweitzer Hall, Columbia, MO, 65211, USA

    Grace Y. Sun, Phullara B. Shelat, Michael B. Jensen, Yan He & Agnes Simonyi

  2. Department of Pathology and Anatomical Sciences, University of Missouri, Columbia, MO, 65211, USA

    Grace Y. Sun & Albert Y. Sun

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Correspondence to Grace Y. Sun.

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Sun, G.Y., Shelat, P.B., Jensen, M.B. et al. Phospholipases A2 and Inflammatory Responses in the Central Nervous System. Neuromol Med 12, 133–148 (2010). https://doi.org/10.1007/s12017-009-8092-z

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