Nitric oxide synthase signaling mechanism

The interaction of estrogen receptors with signaling systems of the cell membrane that respond to growth factors and mediate nongenomic, fast actions of estrogens will be reviewed as well. These mechanisms have a growing importance in the comprehension of phenomena like the induction of endothelial NOS (nitric oxide synthase) by estrogens (Rubanyi et al. 2002). 

Although NO does not itself use a G-protein for signalling, the mechanism of NO production in vascular endothelium is initiated by IP3 via a G-protein-linked acetylcholine receptor on the cell surface. The IP3 causes activation of nitric oxide synthase via calcium- calmodulin and the NO generated diffuses from the endothelial cell into the adjacent smooth muscle cell where cGMP is produced. 

VI. SIGNALING MECHANISM OF INTERLEUKIN 1-INDUCED EXPRESSION OF NITRIC OXIDE SYNTHASE... 

Akama KT, Van Eldik LJ (2000) Beta-amyloid stimulation of inducible nitric-oxide synthase in astrocytes is interleukin-Ibeta- and tumor necrosis factor-alpha (TNFalpha)-dependent, and involves a TNFalpha receptor-associated factor- and NFkappaB-inducing kinase-dependent signaling mechanism. J Biol Chem 275 7918-7924... 

There are three major isoforms of nitric oxide synthase (NOS). The first to be described is termed inducible, because inflammatory agents such as endotoxin and/or cytokines trigger the de novo transcription and translation of inducible nitric oxide synthase (iNOS) molecules. It is likely that, at least in rodents, every nucleated cell is capable of being triggered to produce iNOS the different sensitivities to signals probably lie only in the differing mechanisms of signal transduction between cell types. 

Chlorine inhalational damage is not restricted to particular cell types, such as epitiielial cells. Injury caused by inhaled chlorine can be complex and involves multiple pathways (Figure 36.1). The loss of vascular tone following chlorine exposure has been linked to dysfunctional nitric oxide (NO)-dependent mechanisms and resulting vasodilation (Honavar et al., 2011). To address the role of NO, Honavar et al. (2014) found that when rats were exposed to a total chlorine concentration of 12,000 ppm X min, isolated pulmonary artery studies showed disruption of vascular tone due to disrupted NO signaling. The balance between endothelial nitric oxide synthase (eNOS)- and inducible nitric oxide s)mthase (iNOS)-derived NO was disrupted by chlorine. The expression and activation of eNOS and iNOS... 

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