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Endothelial cell and macrophage regulation of vascular smooth muscle cell calcification modulated by cholestane‐3β, 5α, 6β‐triol
Author(s) -
Liu Hongmei,
Yuan Lan,
Xu Shanjin,
Wang Kui
Publication year - 2007
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2007.02.009
Subject(s) - calcification , vascular smooth muscle , oxysterol , microbiology and biotechnology , chemistry , extracellular , stimulation , macrophage , extracellular matrix , in vitro , endothelial stem cell , biochemistry , endocrinology , biology , medicine , cholesterol , smooth muscle
The cellular and molecular mechanisms that mediate vascular calcification remain poorly understood. In our previous study, oxysterol cholestane‐3β, 5α, 6β‐triol (Triol) was shown to promote vascular smooth muscle cells (VSMCs) calcification. In this study, by using direct coculture, non‐contact transwell coculture, and culture with conditioned media, we investigated the roles of endothelial cells (ECs) and macrophages in the regulation of VSMCs calcification in the absence or presence of Triol. In vitro calcification was induced by incubation of VSMCs with β‐glycerophosphate. The results showed that ECs inhibited VSMCs calcification, as manifested by the reduction of calcium deposition in extracellular matrix. This effect of ECs on calcification was via the secreted soluble factors. Furthermore, the stimulation of ECs by Triol had no influence on ECs inhibition of calcification. On the other hand, macrophages promoted VSMCs calcification via the secreted soluble factors such as reactive oxygen species, which was further enhanced by Triol. Our results supported the roles for ECs and macrophages in vascular calcification, modulated by oxysterols in atherosclerotic plaque.