Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 283, Issue 4, Pages H1455-H1461Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00188.2002
Keywords
chemokine; platelet-derived growth factor; proliferating cellular nuclear antigen; nuclear factor-kappa B; phosphotidylinositol 3-kinase
Ask authors/readers for more resources
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-kappaB 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available