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HDL2 interferes with LDL association with arterial proteoglycans: A possible athero-protective effect

Författare och institution:
M. Umaerus (-); B. Rosengren (-); Björn Fagerberg (Wallenberglaboratoriet); E. Hurt-Camejo (-); G. Camejo (-); Atherosclerosis V. P. Mejo G (-); Acta Medica Scandinavica P. Mejo G (-)
Publicerad i:
Atherosclerosis, 225 ( 1 ) s. 115-120
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
Objectives: High levels of large HDL (HDL2) reduce cardiovascular disease risks apparently because it mediates reverse cholesterol transport, and it has anti-inflammatory properties. Here we explored the mechanism behind an additional athero-protective HDL effect related to its capacity to interfere with formation of insoluble LDL-proteoglycans associations, a key step in LDL entrapment in the intima and in atherogenesis. Methods and results: We found that HDL2 levels from type 2 diabetes patients and controls are inversely correlated with complex formation between serum LDL and the arterial proteoglycans versican. Reconstitution experiments indicate that HDL2 was more efficacious inhibitor of the LDL-versican association than the smaller HDL3. This may explain why serum from patients with dyslipidemia of insulin resistance, with low levels of HDL2, have a higher capacity to form insoluble LDL-proteoglycan complex. ApoE enrichment of HDL2 and HDL3 or addition of copies of an apoE peptide with the proteoglycan-binding sequence of this apolipoprotein increased their inhibition of LDL-versican associations. Conclusions: The inhibitory effect of HDL2 and HDL3 on LDL-versican associations was related to formation of apoE-mediated soluble HDL-versican complexes. We speculate that in the intima large, HDL2 subclasses, by forming reversible soluble associations with proteoglycans can compete with formation of irreversible LDL-proteoglycan aggregates. This can contribute to the HDL2 athero-protective effects. In the dyslipidemia of insulin resistance, associated with low levels of HDL2, this athero-protective property may be compromised. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Klinisk medicin ->
LDL, Versican associations, Response to retention hypothesis, HDL subclasses, Inhibition of LDL and, low-density-lipoprotein, cardiovascular-disease, myocardial-infarction, wall proteoglycans, metabolic syndrome, binding, apolipoproteins, biglycan, risk, sphingomyelinase, eung mc, 1982, journal of lipid research, v23, p747
Postens nummer:
Posten skapad:
2012-11-29 12:23

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