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VEGF Activates Nitric Oxide Pathway in Asthma Model

Results in mice suggest nitric oxide pathway may be therapeutic target in VEGF-driven inflammation and asthma

TUESDAY, July 11 (HealthDay News) -- Vascular endothelial growth factor (VEGF) stimulation of the nitric oxide pathway is key to events in the lung that lead to inflammation and the onset of asthma, according to a report published online July 10 in the Proceedings of the National Academy of Sciences Early Edition.

Jack A. Elias, M.D., of the Yale University School of Medicine in New Haven, Conn., and colleagues used transgenic mice that overexpress VEGF in the lung, producing asthma-like symptoms, to study the role of the nitric oxide pathway.

Pulmonary edema, inflammation, mucus metaplasia and airway hyperresponsiveness observed in VEGF-overexpressing mice all were reduced by using an inhibitor of nitric oxide synthesis. The investigators also showed that both endothelial- and inducible-type nitric oxide synthases are required for these effects.

VEGF plays a role in many diseases, including tumor neovascularization, asthma, cystic fibrosis, viral infections, psoriasis, pulmonary edema, atherosclerosis and retinopathies of the newborn and diabetic, they write. Since their data now link VEGF to nitric oxide production, the authors suggest the VEGF-nitric oxide pathway may be a "worthwhile site for future investigations designed to identify therapeutic agents that can be used in the treatment of these disorders."

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