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http://purl.uniprot.org/citations/20360257http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20360257http://www.w3.org/2000/01/rdf-schema#comment"

Rationale

Plasma apolipoprotein (apo)M is mainly associated with high-density lipoprotein (HDL). HDL-bound apoM is antiatherogenic in vitro. However, plasma apoM is not associated with coronary heart disease in humans, perhaps because of a positive correlation with plasma low-density lipoprotein (LDL).

Objective

We explored putative links between apoM and very-low-density (VLDL)/LDL metabolism and the antiatherogenic potential of apoM in vivo.

Methods and results

Plasma apoM was increased approximately 2.1 and approximately 1.5 fold in mice lacking LDL receptors (Ldlr(-/-)) and expressing dysfunctional LDL receptor-related protein 1 (Lrp1(n2/n2)), respectively, but was unaffected in apoE-deficient (ApoE(-/-)) mice. Thus, pathways controlling catabolism of VLDL and LDL affect plasma apoM. Overexpression (approximately 10-fold) of human apoM increased (50% to 70%) and apoM deficiency decreased ( approximately 25%) plasma VLDL/LDL cholesterol in Ldlr(-/-) mice, whereas apoM did not affect plasma VLDL/LDL in mice with intact LDL receptors. Moreover, plasma clearance of apoM-enriched VLDL/LDL was slower than that of control VLDL/LDL in mice lacking functional LDL receptors and LRP1, suggesting that apoM impairs the catabolism of VLDL/LDL that occurs independently of the LDL receptor and LRP1. ApoM overexpression decreased atherosclerosis in ApoE(-/-) (60%) and cholate/cholesterol-fed wild-type mice (70%). However, in Ldlr(-/-) mice the antiatherogenic effect of apoM was attenuated by its VLDL/LDL-raising effect.

Conclusion

The data suggest that defect LDL receptor function leads to increased plasma apoM concentrations, which in turn, impairs the removal of VLDL/LDL from plasma. This mechanism opposes the otherwise antiatherogenic effect of apoM."xsd:string
http://purl.uniprot.org/citations/20360257http://purl.org/dc/terms/identifier"doi:10.1161/circresaha.109.211086"xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/author"Gordts P.L."xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/author"Christoffersen C."xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/author"Dahlback B."xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/author"Nielsen L.B."xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/author"Roebroek A.J."xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/author"Pedersen T.X."xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/name"Circ Res"xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/pages"1624-1634"xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/title"Opposing effects of apolipoprotein m on catabolism of apolipoprotein B-containing lipoproteins and atherosclerosis."xsd:string
http://purl.uniprot.org/citations/20360257http://purl.uniprot.org/core/volume"106"xsd:string
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http://purl.uniprot.org/uniprot/#_G3UWW2-mappedCitation-20360257http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20360257
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