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Review Role of secretory phospholipases in atherogenesis. 2008
Jönsson-Rylander AC, Lundin S, Rosengren B, Pettersson C, Hurt-Camejo E. · AstraZeneca, R&D, Bioscience, Mölndal S-431 83, Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska University Hospital, Gotheburg, Sweden. · Curr Atheroscler Rep. · Pubmed #18489854 No free full text.
Abstract: Elevated circulating levels of secretory phospholipase A(2) (sPLA(2)) are associated with atherosclerotic cardiovascular disease. sPLA(2) can contribute to atherogenesis by hydrolyzing phospholipids of circulating lipoproteins and lipoproteins entrapped in the arterial wall and/or in cells that reside in the intima and that participate in the inflammatory response to lipoprotein deposition. This article reviews differences and similarities between sPLA(2)-IIA, sPLA(2)-V, and sPLA(2)-X, all of which are members of this family of enzymes with reported potential proatherogenic features. Published data suggest that each of the enzymes has a distinct profile characterized by differences in tissue expression and localization, capacity to act on phospholipids of cell membranes and lipoproteins, and their interaction with arterial proteoglycans. In addition, the article discusses results from the authors' laboratory showing that diet-induced or gene-induced hyperlipidemia in mice enhances the expression of sPLA(2)-V in different tissues, but not sPLA(2)-IIA. Such differences indicate that these enzymes may have different roles in atherosclerotic cardiovascular disease through their distinct profiles.
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Review Distinctiveness of secretory phospholipase A2 group IIA and V suggesting unique roles in atherosclerosis. 2006
Rosengren B, Jönsson-Rylander AC, Peilot H, Camejo G, Hurt-Camejo E. · AstraZeneca, R&D, Molecular Pharmacology, Mölndal S-431 83, Sweden. · Biochim Biophys Acta. · Pubmed #17070102 No free full text.
Abstract: Clinical observations strongly support an association of circulating levels of secretory phospholipases A(2) (sPLA(2)) in atherosclerotic cardiovascular disease (ACVD). Two modes of action can provide causal support for these statistical correlations. One is the action of the enzymes on circulating lipoproteins and the other is direct action on the lipoproteins once in the arterial extracellular intima. In this review we discuss results suggesting a distinct profile of characteristics related to localization, action on plasma lipoproteins and interaction with arterial proteoglycans for sPLA(2)-IIA and sPLA(2)-V. The differences observed indicate that these enzymes may contribute to atherosclerosis through dissimilar pathways. Furthermore, we comment on recent animal studies from our laboratory indicating that the expression of type V enzyme is up-regulated by genetically and nutritionally-induced dyslipidemias but not the group type IIA enzyme, which is well known to be up-regulated by acute inflammation. The results suggest that if similar up-regulation occurs in humans in response to hyperlipidemia, it may create a distinctive link between the group V enzyme and the disease.
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