Lipids Sample Clauses

Lipids. The interaction between lipids and CRP is diverse. It has been suggested that CRP could be the factor linking lipoprotein deposition and complement activation in atherosclerotic plaques. Binding of tissue-deposited CRP to enzymatically degraded LDL (e-LDL) enhances complement activation, which may be relevant to the development and progression of the atherosclerotic lesion, particularly at early stages of atherosclerosis when low concentrations of e-LDL are present38,39. The reports on interaction between CRP and oxLDL are conflicting40,41, but complement activation as a result of this interaction is generally considered unlikely. The majority of foam cells below the endothelium show positive staining for CRP27. Zwaka et al42 demonstrated that native LDL co-incubated with CRP was taken up by macrophages via macropinocytosis. It was concluded that foam cell formation in human atherogenesis might be caused in part by uptake of CRP-opsonized native LDL. High levels of high-density lipoprotein (HDL) are atheroprotective since HDL is involved in transporting cholesterol from the periphery to the liver. HDL might also protect the endothelium since the CRP-induced upregulation of inflammatory adhesion molecules in HUVECs was completely blocked by HDL. So, HDL neutralizes CRP induced proinflammatory activity43. HDL also inhibits atherosclerosis through prevention of oxidation of LDL. It is not known whether CRP has an effect on the oxidative status of LDL.
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