Cell-mediated lipoprotein transport: A novel anti-atherogenic concept
Atherosclerosis. Supplement , Volume 11 - Issue 1 p. 25- 29
Lipoprotein transport is thought to occur in the plasma compartment of the blood, where lipoproteins are modulated by various enzymatic reactions. Subsequently, lipoproteins can migrate through the endothelial barrier to the subendothelial space or are taken up by the liver. The interaction between pro-atherogenic (apoB-containing) lipoproteins and blood cells (especially monocytes and macrophages) in the subendothelial space is well known. This lipoprotein-inflammatory cell interplay is central in the development of the atherosclerotic plaque. In this review, a novel interaction is described between lipoproteins and both leukocytes and erythrocytes in the blood compartment. This lipoprotein-blood cell interaction may also be related to the process of atherosclerosis by inducing inflammatory changes in the case of leukocytes (pro-atherogenic) and as an anti-atherogenic transport-system by adherence to erythrocytes. Triglyceride rich lipoprotein (TRL)-mediated leukocyte activation can lead to an inflammatory situation with generation of oxidative stress and the production of cytokines, ultimately resulting in acute endothelial dysfunction. Binding of apoB containing lipoproteins to erythrocytes may be a potential anti-atherogenic mechanism protecting the vessel wall from the pro-inflammatory effects of these lipoproteins and also playing a role in the removal of these particles from the circulation. One of the proposed mechanisms of this interaction implies complement activation on the lipoprotein surface and binding to the Complement Receptor 1 (CR1) on erythrocytes and leukocytes, followed by clearance by the liver.
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|Organisation||Erasmus MC: University Medical Center Rotterdam|
Bovenberg, S.A, Alipour, A, Elte, J.W.F, Rietveld, A.P, Janssen, J.W.C, van de Geijn, G.J.M, … Castro Cabezas, M. (2010). Cell-mediated lipoprotein transport: A novel anti-atherogenic concept. Atherosclerosis. Supplement, 11(1), 25–29. doi:10.1016/j.atherosclerosissup.2010.04.003