ArticleArteriosclerosis, thrombosis, and vascular biology2009
The capacity of group V sPLA2 to increase atherogenicity of ApoE-/- and LDLR-/- mouse LDL in vitro predicts its atherogenic role in vivo.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Novel genetic approach to investigate the role of plasma secretory phospholipase A2 (sPLA2)-V isoenzyme in coronary heart disease: modified Mendelian randomization analysis using PLA2G5 expression levels.Circulation. Cardiovascular genetics · 2014Pooled it
- Regulatory Roles of Phospholipase AFrontiers in immunology · 2022Review
- Group V secreted phospholipase AThe Journal of biological chemistry · 2020Article
- Group IID, IIE, IIF and III secreted phospholipase ABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Harmful and protective roles of group V phospholipase ABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- The Roles of the Secreted Phospholipase AAdvances in immunology · 2016Review
- Metabolic regulation by secreted phospholipase AInflammation and regeneration · 2016Review
- A new era of secreted phospholipase A₂.Journal of lipid research · 2015Article
- Immunization with advanced glycation end products modified low density lipoprotein inhibits atherosclerosis progression in diabetic apoE and LDLR null mice.Cardiovascular diabetology · 2014Article
- The (G>A) rs11573191 polymorphism of PLA2G5 gene is associated with premature coronary artery disease in the Mexican Mestizo population: the genetics of atherosclerotic disease Mexican study.BioMed research international · 2014Article
- Regulation of plasma cholesterol esterification by sphingomyelin: effect of physiological variations of plasma sphingomyelin on lecithin-cholesterol acyltransferase activity.Biochimica et biophysica acta · 2012Article
- Biallelic mutations in PLA2G5, encoding group V phospholipase A2, cause benign fleck retina.American journal of human genetics · 2011Article
- Group V phospholipase A2 in bone marrow-derived myeloid cells and bronchial epithelial cells promotes bacterial clearance after Escherichia coli pneumonia.The Journal of biological chemistry · 2011Article
- Secreted phospholipase A2, lipoprotein hydrolysis, and atherosclerosis: integration with lipidomics.Analytical and bioanalytical chemistry · 2011Review
- A novel anti-inflammatory role for secretory phospholipase A2 in immune complex-mediated arthritis.EMBO molecular medicine · 2010Article
- Bioactive products generated by group V sPLA(2) hydrolysis of LDL activate macrophages to secrete pro-inflammatory cytokines.Cytokine · 2010Article
- The vicious circle between oxidative stress and inflammation in atherosclerosis.Journal of cellular and molecular medicine · 2010Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveIn vitro data indicate that human LDL modified by Group V secretory phospholipase A(2) (GV sPLA(2)) is proatherogenic. Consistent with this, gain and loss of function studies demonstrated that GV sPLA(2) promotes atherosclerosis in LDLR(-/-) mice. The current study investigates whether GV sPLA(2) promotes atherosclerotic processes in apoE(-/-) mice. METHODS AND
resultsLDL (d=1.019 to 1.063) from apoE(-/-) and LDLR(-/-) mice fed chow or Western diet were hydrolyzed by GV sPLA(2). Phosphatidylcholine on LDL from LDLR(-/-) mice fed either a chow or Western diet was hydrolyzed to a greater extent (61.1+/-0.4% and 45.3+/-4.6%) than the corresponding fractions from apoE(-/-) mice (41.7+/-3.6% and 39.4+/-1.2%). ApoE(-/-) LDL induced macrophage foam cell formation in vitro without modification by GV sPLA(2), whereas hydrolysis of LDLR(-/-) LDL was a prerequisite for foam cell formation. In contrast to findings in LDLR(-/-) mice, GV sPLA(2) deficiency did not significantly reduce atherosclerosis in apoE(-/-) mice, although collagen content was significantly reduced in lesions of apoE(-/-) mice lacking GV sPLA(2).
conclusionsThe ability of GV sPLA(2) to promote atherosclerotic lipid deposition in apoE(-/-) and LDLR(-/-) mice may be related to its ability to increase the atherogenic potential of LDL from these mice as assessed in vitro.
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Registered trials
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