Nitric oxide stimulates endothelial cell proliferation and mobility in the absence of sGC, but increased intracellular cGMP following sGC activation greatly amplifies its angiogenic potential.
Nitric oxide can stimulate endothelial cell proliferation and migration independently of sGC, but sGC activation greatly amplifies its angiogenic potential.
Nitric oxide exerts a stimulatory role during postnatal angiogenesis. Although soluble guanylyl cyclase (sGC) mediates many of the effects of nitric oxide (NO) in the vascular system, the contribution of cGMP-dependent vs cGMP-independent pathways in NO-induced angiogenesis remains unclear. Herein, we determined the effects of a NO donor (sodium nitroprusside; SNP) and a NO-independent sGC activator (BAY 412272) in the growth and migration of rat aortic endothelial cells (RAEC). RAEC lack enzymatically active sGC as suggested by their inability to accumulate cGMP upon exposure to SNP. However, treatment of RAEC with SNP promoted a modest increase in their proliferation and migration that was dependent on extracellular signal regulated kinase1/2 activation. Moreover, when RAEC were exposed to vascular endothelial growth factor we observed an increase in migration that was inhibited by NO synthase, but not sGC, inhibition. Infection of cells with adenoviruses containing sGC greatly increased the efficacy of SNP as a mitogenic and migratory stimulus. We conclude that NO is capable of stimulating EC proliferation and mobility in the absence of sGC; however, increased intracellular levels of cGMP following sGC activation greatly amplify the
Pyriochou et al. (Sun,) conducted a other in Angiogenesis. Nitric oxide donor (sodium nitroprusside) and sGC activator (BAY 41-2272) vs. Control was evaluated on Endothelial cell proliferation and migration. Nitric oxide stimulates endothelial cell proliferation and mobility in the absence of sGC, but increased intracellular cGMP following sGC activation greatly amplifies its angiogenic potential.
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