In a recent interesting paper Babaei and Stewart [1] demonstrated that coculture of endothelial cells (ECs) with smooth muscle cells (SMCs) may result in the formation of extensive capillary-like structure. However, the effect was observed only when SMCs were previously transfected with vector containing the endothelial nitric oxide synthase (eNOS) cDNA. Such an in vitro angiogenic-like events were abrogated by l-NAME, a NOS inhibitor. A similar angiogenic response has been observed when SMCs were transfected with plasmids containing VEGF121 cDNA, the effect again being inhibited by l-NAME. Similarly, in a Boyden chamber model the EC migration was potently enhanced in the presence of SMC transfected with eNOS or VEGF121, and was significantly attenuated by l-NAME.
Much evidence indicates that NO plays an integral role in VEGF signaling (see Ref. [1]). It has …
Jozef Dulak, Alicja Józkowicz, A. Dembińska-Kieć, Ibeth Guevara, Anna Zdzienicka, Danuta Zmudzinska-Grochot, Izabela Florek, Anna K. Wójtowicz, Andrzej Szuba, John P. Cooke
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