Abstract
Rat and mouse aortic rings produced angiogenic outgrowths in collagen gel cultures in response to the injury of the dissection procedure. Neovessels were composed of endothelial cells and surrounding pericytes. Pericyte recruitment along endothelial sprouts was enhanced by treating cultures with angiopoeitin‐1 (Ang‐1). Analysis of gene expression in Ang‐1 stimulated cultures revealed upregulated expression of several inflammatory cytokines, including monocyte chemotactic protein‐1 (MCP‐1). Recombinant MCP‐1 dose‐dependently increased pericyte number while anti‐MCP‐1 antibody depleted vessels of pericytes and abrogated Ang‐1 mediated pericyte recruitment. Mouse aortas deficient for MCP‐1 or its receptor CCR2 had fewer pericytes than controls. MCP‐1 deficiency also impaired the pericyte recruitment activity of Ang‐1. These results implicate MCP‐1 as a mediator of Ang‐1 effects on the development and maturation of the vessel wall during angiogenesis following injury. Supported by NHLBI‐HL52585, and a Merit Review Grant from the Department of Veterans Affairs.
Published Version
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