Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 79, Issue 1, Pages 95-104Publisher
WILEY
DOI: 10.1189/jlb.0405226
Keywords
inflammation; chemokine; angiogenesis
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Funding
- Intramural NIH HHS Funding Source: Medline
- NATIONAL CANCER INSTITUTE [Z01SC010355, ZIASC010355] Funding Source: NIH RePORTER
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Mast cells (MCs) are common components of inflammatory infiltrates and a source of proangiogenic factors. Inflammation is often accompanied by vascular changes. However, little is known about modulation of MC-derived proangiogenic factors during inflammation. In this study, we evaluated the effects of the proinflammatory mediator prostaglandin E-2 (PGE(2)) on MC expression and release of proangiogenic factors. We report that PGE(2) dose-dependently induces primary MCs to release the proangiogenic chemokine monocyte chemoattractant protein-1 (MCP-1). This release of MCP-1 is complete by 2 h after PGE(2) exposure, reaches levels of MCP-1 at least 15-fold higher than background, and is not accompanied by degranulation or increased MCP-1 gene expression. By immunoelectron microscopy, MCP-1 is detected within MCs at a cytoplasmic location distinct from the secretory granules. Dexamethasone and cyclosporine A inhibit PGE(2)-induced MCP-1 secretion by similar to 60%. Agonists of PGE(2) receptor subtypes revealed that the EP1 and EP3 receptors can independently mediate MCP-1 release from MCs. These observations identify PGE(2)-induced MCP-1 release from MCs as a pathway underlying inflammation-associated angiogenesis and extend current understanding of the activities of PGE(2).
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