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lüll Thrombospondin-1: a physiological regulator of nitric oxide signaling Isenberg JS; Frazier WA; Roberts DDCell Mol Life Sci 2008[Mar]; 65 (5): 728-42Thrombospondin-1 is a secreted protein that modulates vascular cell behavior via several cell surface receptors. In vitro, nanomolar concentrations of thrombospondin-1 are required to alter endothelial and vascular smooth muscle cell adhesion, proliferation, motility, and survival. Yet, much lower levels of thrombospondin-1 are clearly functional in vivo. This discrepancy was explained with the discovery that the potency of thrombospondin-1 increases more than 100-fold in the presence of physiological levels of nitric oxide (NO). Thrombospondin-1 binding to CD47 inhibits NO signaling by preventing cGMP synthesis and activation of its target cGMP-dependent protein kinase. This potent antagonism of NO signaling allows thrombospondin-1 to acutely constrict blood vessels, accelerate platelet aggregation, and if sustained, inhibit angiogenic responses. Acute antagonism of NO signaling by thrombospondin-1 is important for hemostasis but becomes detrimental for tissue survival of ischemic injuries. New therapeutic approaches targeting thrombospondin-1 or CD47 can improve recovery from ischemic injuries and overcome a deficit in NO-responsiveness in aging. (Part of a Multi-author Review).|*Signal Transduction[MESH]|Animals[MESH]|Humans[MESH]|Neovascularization, Physiologic[MESH]|Nitric Oxide/*metabolism[MESH]|Thrombospondin 1/*physiology[MESH] |