Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:1011-1017
© 1997 American Heart Association, Inc.
Articles |
Cellular Consequences of the Association of ApoB Lipoproteins With Proteoglycans
Potential Contribution to Atherogenesis
From the Wallenberg Laboratory for Cardiovascular Research, Faculty of Medicine, University of Gothenburg, (E.H.-C., U.O., O.W., G.B., G.C.), and Astra Hässle AB, Preclinical Research Laboratories, Mölndal (G.C.), Sweden.
Correspondence to Germán Camejo, Astra Hässle AB, Preclinical Research Laboratories, Mölndal, S-431 83, Sweden.
Key Words: proteoglycans • atherogenesis • apoB lipoproteins
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ApoB Lipoproteins in the Intima and Atherosclerosis |
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The hypothesis of a causal relation between disturbances of apoB lipoprotein metabolism and atherosclerosis is consistent with results from recent intervention studies with drugs that lower circulating levels of the lipoproteins.1 2 3 However, the molecular and cellular mechanisms by which apoB lipoproteins (LDL and VLDL) contribute to atherosclerosis are still unclear. Faber4 in 1949 concluded, with remarkable intuition, that cholesterol carried by lipoproteins colocalizes with CSs of the intima and that this accumulation contributes to lesion development. All sulfated polysaccharides, the GAGs, occur in the arterial intima and media as glycoproteins known generically as PGs.5 Immunohistochemical studies confirm the colocalization of the lipoproteins with extracellular GAGs in human and animal lesions.6 7 Hollander8 in 1976 suggested that GAGs of the intima are central for apoB lipoprotein accumulation in the extracellular intima and the subsequent tissue response. Analysis of lipids and lipoproteins indicates that most of the extracellular lipids of human lesions originate from plasma apoB lipoproteins.9 Isolation of only partially altered apoB lipoproteins from lesions also indicates that they are mostly associated with extracellular matrix elements, because if taken up by cells they should be rapidly degraded.10 11 12 13 14 Quantitative autoradiography likewise reveals that a large fraction of LDL in arteries resides in the extracellular intima in rabbits.15 Remarkable electron micrographs obtained by Nievelstein-Post et al16 also indicate that in rabbit intima LDL is associated with extracellular fibrillar structures, probably PGs. With the aid of high-resolution immunogold, Galis et al17 demonstrated that also in rabbits apoB lipoproteins colocalize with CSPG.
However, deposition and colocalization
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