1,721,171 research outputs found
Role of nitric oxide in the angiogenesis of avascular tissue
No full textA number of independent lines of evidence converge indicating a role for nitric oxide (NO) in angiogenesis. Our data support the existence of an autocrine loop exerted by microvascular endothelium in angiogenesis which involves NO production, cyclic GMP elevation and fibroblast growth factor-2 (FGF-2) expression. Our results indicate that NO production significantly contributes to the growth-promoting effect of vasodilating peptides and vascular endothelial growth factor (VEGF), but not for that of FGF-2. On these basis, the nitric oxide pathway appears to be a promising target to be considered in pro- and anti-angiogenic therapeutic strategies
Nitric oxide and angiogenesis
No full textThe steps required for new vessel growth are biologically complex and require coordinate regulation of contributing components, including modifications of cell--cell interactions, proliferation and migration of endothelial cells and matrix degradation. The observation that in vivo angiogenesis is accompanied by vasodilation, that many angiogenesis effectors possess vasodilating properties and that tumor vasculature is in a persistent state of vasodilation, support the existence of a molecular/biochemical link between vasodilation and angiogenesis. Several pieces of evidence converge in the indication of a role for nitric oxide (NO), the factor responsible for vasodilation, in physiological and pathological angiogenesis. Data originated in different labs indicate that NO can act both as an 'actor' of angiogenesis and as a 'director of angiogenesis', both functions being equally expressed during physiological and pathological processes. NO significantly contributes to the prosurvival/proangiogenic program of capillary endothelium by triggering and transducing cell growth and differentiation via endothelial-constitutive NO synthase (ec-NOS) activation, cyclic GMP (cGMP) elevation, mitogen activated kinase (MAPK) activation and fibroblast growth factor-2 (FGF-2) expression. Re-establishment of a balanced NO production in the central nervous system results in a reduction of cell damage during inflammatory and vascular diseases. Elevation of NOS activity in correlation with angiogenesis and tumor progression has been extensively reported in experimental and human tumors. In the brain, tumor expansion and edema formation are sensitive to NOS inhibition. On this basis, the nitric oxide pathway appears to be a promising target for consideration in pro- and anti-angiogenic therapeutic strategies. The use of NOS inhibitors seems appropriate to reduce edema, block angiogenesis and facilitate antitumor drug delivery
Constitutive and inducible nitric oxide synthase: role in angiogenesis
No full textSince the initial report of nitric oxide (NO) activity, enormous progress has been made over the last two decades in the field of NO research. Whereas most physiological responses triggered by moderate concentrations of NO are mediated by soluble guanylate cyclase activation and the subsequent production of cyclic GMP as the major signaling messenger, recent studies have provided evidence of alternative signaling pathways triggered by high concentrations of NO. These signals operate in part through redox-sensitive regulation of transcription factors, gene expression, transcription, cellular activation, proliferation, and cell death. Numerous results converge to indicate a role for NO in physiological and pathological angiogenesis. Experimental data indicate that NO synthase, depending on the isoforms, the timing, and the degree of activation, may display contradictory effects, expressed during both physiological and pathological angiogenesis. The dual personality of NO will be reviewed in the context of the angiogenesis process
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