Research paperLipoprotein-proteoglycan complexes from injured rabbit aortas accelerate lipoprotein uptake by arterial smooth muscle cells
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Adipocyte-Derived Versican and Macrophage-Derived Biglycan Control Adipose Tissue Inflammation in Obesity
2020, Cell ReportsCitation Excerpt :We have now identified this proteoglycan as versican, a large chondroitin sulfate-rich proteoglycan found in the ECM of most soft tissues (Wight, 2002). Versican is elevated during development and inflammation (Kang et al., 2018; Snyder et al., 2015; Wight et al., 2020) and regulates events associated with adipose tissue inflammation, such as lipoprotein retention (Williams and Tabas, 1995, 1998), lipid uptake, and foam cell formation (Ismail et al., 1994; Llorente-Cortés et al., 2002; Srinivasan et al., 1995). Versican also influences inflammatory processes by interacting with chemokines, growth factors, proteases, and receptors such as CD44, PSGL-1, and TLR2 on the surface of immune cells to provide intrinsic signals and influence the immune cell phenotype (Hirose et al., 2001; Taylor and Gallo, 2006; Wu et al., 2005).
The P2Y<inf>2</inf> receptor mediates uptake of matrix-retained and aggregated low density lipoprotein in primary vascular smooth muscle cells
2016, AtherosclerosisCitation Excerpt :Lipoproteins that are retained in the extracellular matrix are taken up by VSMCs and macrophages, which subsequently results in CE accumulation and foam cell formation [6]. Macrophages become foam cells through the uptake of diversely modified LDLs [7], whereas the aggregation of LDLs seems to be a key condition for lipid accumulation in VSMCs [6,8]. Scavenger receptors on macrophages mediate their transformation to foam cells following uptake of modified and oxidized LDLs (oxLDLs).
Actions of antioxidants in the protection against atherosclerosis
2012, Free Radical Biology and MedicineCitation Excerpt :The oxidative modification hypothesis of atherosclerosis suggests that LDL oxidation initiates disease and that foam cell formation by oxidized LDL represents an early key event in atherogenesis. However, foam cells can arise from LDL modified in ways other than oxidation, such as formation of complexes with proteoglycans [267], indicating that oxidative modification of LDL is not a requirement for atherosclerosis to occur. This notion is concordant with the accumulation of nonoxidized lipids preceding that of oxidized lipids [184] and the fact that several animal studies have dissociated atherosclerosis from arterial lipid oxidation [2].
Lipid loading of human vascular smooth muscle cells induces changes in tropoelastin protein levels and physical structure
2012, Biophysical JournalCitation Excerpt :The incorporation of matrix-retained LDL by macrophages (16,17) and VSMC (18,19) leads to the accumulation of cholesteryl ester (CE) and formation of foam cells. Macrophages become foam cells through the uptake of diversely modified LDLs, whereas the aggregation of LDLs seems to be a key condition for lipid accumulation in VSMCs (21–23). Aggregated LDLs (agLDLs) obtained by vortexing LDL in vitro share structural characteristics with LDL aggregates present in atherosclerotic lesions (24).
Atherosclerosis: From lesion formation to plaque activation and endothelial dysfunction
2000, Molecular Aspects of Medicine