Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 28, Issue 4, Pages 615-621Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.107.158154
Keywords
thrombospondin-1; CD47; nitric oxide; ischemia; platelet aggregation
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Funding
- NATIONAL CANCER INSTITUTE [Z01SC009172] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL054390, R56HL054390] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM057573] Funding Source: NIH RePORTER
- Intramural NIH HHS Funding Source: Medline
- NHLBI NIH HHS [HL54390, R56 HL054390, R01 HL054390-09A2, R01 HL054390] Funding Source: Medline
- NIGMS NIH HHS [R01 GM057573, GM57573, R01 GM057573-08] Funding Source: Medline
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CD47, originally named integrin-associated protein, is a receptor for thrombospondin-1. A number of important roles for CD47 have been defined in regulating the migration, proliferation, and survival of vascular cells, and in regulation of innate and adaptive immunity. The recent discovery that thrombospondin-1 acts via CD47 to inhibit nitric oxide signaling throughout the vascular system has given new importance and perhaps a unifying mechanism of action to these enigmatic proteins. Here we trace the development of this exciting new paradigm for CD47 function in vascular physiology.
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