doi: 10.1161/hc0502.102969
(Circulation. 2002;105:650.)
© 2002 American Heart Association, Inc.
Basic Science Reports |
Monocyte/Macrophage Regulation of Vascular Calcification In Vitro
From the Departments of Medicine (Y.T., J.P., M.T., T.S., F.P., L.L.D.) and Physiology (L.L.D.), UCLA School of Medicine, Los Angeles, Calif.
Correspondence to Yin Tintut, PhD, Division of Cardiology, UCLA School of Medicine, 47-123 Center for the Health Sciences, 10833 Le Conte Ave, Los Angeles, CA 90095-1679. E-mail ytintut{at}ucla.edu
Background— Calcification is a common complication of atherosclerosis and other chronic inflammatory processes that involves infiltration of monocytes and accumulation of macrophages.
Methods and Results— To determine whether these cells modulate vascular calcification in vitro, calcifying vascular cells (CVCs), a subpopulation of osteoblast-like cells derived from the artery wall, were cocultured with human peripheral blood monocytes for 5 days. Results showed that alkaline phosphatase (ALP) activity, a marker of osteoblastic differentiation, was significantly greater in cocultures than in cultures of CVCs or monocytes alone. Both ALP activity and matrix mineralization increased in proportion to the number of monocytes added. Activation of monocyte/macrophages (M/Ms) by oxidized LDL further increased ALP activity in cocultures. However, neither conditioned medium from oxidized-LDL–activated M/Ms or transwell coculture had this effect on CVCs, which suggests a need for cell-to-cell contact. In contrast, conditioned medium from lipopolysaccharide-activated M/Ms increased ALP activity of CVCs. ELISA showed that lipopolysaccharide-activated M/Ms secreted tumor necrosis factor-
, and neutralizing antibody to tumor necrosis factor- attenuated the induction of ALP activity by the conditioned media.
Conclusions— These results suggest that M/Ms enhance in vitro vascular calcification via 2 independent mechanisms: cell-cell interaction and production of soluble factors such as tumor necrosis factor-.
Key Words: muscle, smooth • lipids • atherosclerosis • leukocytes
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