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Abstract
β-actin is traditionally considered a structural protein that organizes and maintains the shape of nonmuscle cells, although data now indicate that β-actin is also a signaling molecule. β-actin is directly associated with nitric oxide synthase type 3 (NOS-3) in endothelial cells and platelets, and this interaction increases NOS-3 activity and the affinity of NOS-3 for heat shock protein 90 kD (Hsp90). The β-actin–induced increase in NOS-3 activity may be caused directly by β-actin, the binding of Hsp90 to NOS-3, or both. Alterations in the interaction between β-actin and NOS-3 could be caused by changes either in the availability of β-actin or in the affinity of NOS-3 for β-actin, and these alterations probably contribute to vascular complications and platelet aggregation. Studies examining the interactions between NOS-3, β-actin, and Hsp90 could potentially lead to the discovery of effective peptides for the treatment of diseases associated with impaired NOS-3 activity and nitric oxide release, such as systemic and pulmonary hypertension, atherosclerosis, and thrombotic diseases.
