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Divison of Cardiothoracic Surgery, University of Colorado Health Sciences Center, Denver, Colorado 80262
Although monocyte chemotactic protein-1
(MCP-1) is best known for its ability to recruit mononuclear cells, few
studies have examined the effects of this chemokine on other events in
the vascular response to injury. The purpose of the present study was
to determine the influence of MCP-1 on human vascular smooth muscle
(VSMC) proliferation. MCP-1 induced concentration-dependent VSMC
proliferation as measured by bromodeoxyuridine (BrdU) uptake. Direct
cell counting demonstrated a twofold increase in VSMC after stimulation
with MCP-1. This mitogenic effect was similar to that observed with the
prototypical atherogenic cytokine platelet-derived growth factor.
Immunohistochemistry and Western blot analysis revealed that MCP-1
increased both proliferating nuclear cell antigen and cyclin A
expression. Whereas MCP-1 did not promote nuclear factor-
B
activation, MCP-1-induced VSMC proliferation appeared to be dependent
on phosphotidylinositol 3-kinase activation. In conclusion, MCP-1
directly induces VSMC growth, which is associated with activation of
cell cycle proteins and intracellular proliferative signals. Within the
inflammatory paradigm of vascular remodeling, these data suggest that
MCP-1 is more than simply a chemokine but also a potent mitogen for
VSMC proliferation.
chemokine; platelet-derived growth factor; proliferating cellular
nuclear antigen; nuclear factor-B; phosphotidylinositol 3-kinase
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