Editorials |
From the Department of Internal Medicine and Cardiovascular Research Center, University of Kentucky, Lexington.
Correspondence to Frederick C. de Beer, Department of Internal Medicine, University of Kentucky Medical Center, 740 S Limestone, Room J-525, Lexington, KY 40536-0284. E-mail fcdebe1@uky.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The secretory phospholipase A2 (sPLA2) family hydrolyzes glycerophospholipids at the sn-2 position to generate lysophospholipids and free fatty acids. Ten members have been described in mammals. These enzymes must be clearly distinguished from the intracellular phospholipase A2s that are involved in intracellular signaling. They are also distinct from lipoprotein-associated phospholipase A2 (Lp-PLA2), which has been shown to be bound predominantly to LDL particles in human plasma, and hydrolyzes oxidized LDL to generate lysophosphatidylcholine and oxidized nonesterified fatty acids.1 Group IIa sPLA2, which was originally isolated from rheumatoid arthritis fluids, is considered to be the prototypic inflammatory sPLA2. Its expression is markedly elevated in many cell types in response to proinflammatory stimuli. The concentration of Group IIa sPLA2 in sera or exudating fluids correlates well with the severity of inflammatory disease. In humans, Group IIa and Group V sPLA2 are tightly linked on chromosome 1 and their gene regulation and functions have largely been viewed as overlapping. Indeed, cross-reactivity of antibodies and molecular probes for these related enzymes has led to confusion in older literature. The study by Rosengren et al, reported in this issue, provides new insights into the expression and functional activity of Group IIa and Group V sPLA2 in the context of atherosclerosis.2
See page 1579
A role for sPLA2s in atherogenic processes has been suggested by epidemiological studies showing that in humans, serum concentrations of Group IIa sPLA2 is an independent risk factor for coronary artery disease and a predictor of
Related Article:
Arterioscler Thromb Vasc Biol 2006 26: 1579-1585.
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