Acetylated Low-Density Lipoprotein Stimulates Human Vascular Smooth Muscle Cell Calcification by Promoting Osteoblastic Differentiation and Inhibiting Phagocytosis

Abstract

Background-Vascular

Calcification of Advanced Atherosclerotic Lesions in the Innominate Arteries of ApoE-Deficient Mice

“…ALP activity is increased after exposure of smooth muscle cells to inflammatory factors. [31][32][33] In the present studies, ALP activity was documented only in areas of active calcification and in areas rich in chondrocyte-like cells and suggests that increases in ALP activity plays an active role in the deposition of hydroxyapaptite within the apoEϪ/Ϫ mouse lesions.…”

“…This is consistent with the possibility that smooth muscle cells within the intima are converted to chondrocyte-like cells in response to signals such as elevated levels of P i or factors such as tumor necrosis factor-␣, interleukin-6, and transforming growth factor-␤, which can modulate the smooth muscle cell phenotype. [31][32][33]38 However, it is also feasible that mesenchymal or hematopoietic stem cells are recruited into the plaques and are the source of the chondrocytes. For example, calcifying vascular cells (CVCs) retain a multi-lineage potential that is analogous to mesenchymal stem cells because these cells can be induced to express markers of chondrocytes, smooth muscle cells, and marrow stromal cells.…”

Multifunctional Roles for Serum Protein Fetuin-A in Inhibition of Human Vascular Smooth Muscle Cell Calcification

“…Phagocytosis of vesicles is an important mechanism for their removal with a reduction in phagocytosis of AB associated with increased VSMC calcification (28). Using a quantitative AB binding assay indicative of phagocytosis, we found that VSMC in the presence of fetuin-A had a greater capacity to bind AB than in its absence ( Figure 9) (24,28).…”

Coronary calcification in patients with end-stage renal disease: a novel endocrine disorder?

“…These data imply that arterial calcification of both the intima and the media constitutes a regulated process resembling osteogenesis in many aspects. Moreover, it should be underlined that many of the factors associated with cardiovascular risk and/or vascular calcification in dialysis patients, including high levels of phosphate, 67 calcitriol, 68 urea, 69 lipoproteins, 70,71 homocysteine, 72 parathormone, and parathormone-related peptide 73 promote mineralization of cultured vascular smooth muscle cells. The active, cell-mediated process of vascular calcification in dialysis patients resembles osteogenic differentiation, which is further confirmed by a series of ex vivo experiments.…”