Disease relevance of NOS3

• After balloon injury of the left anterior descending (LAD) coronary artery, animals received an intramural injection of adenovirus (1.5 X 10(9) PFU) carrying either the NOS3 cDNA (AdCMVNOS3, n = 12), the PAI-1 cDNA (AdCMVPAI-1, n = 12), the TK cDNA (AdMLPItk, n = 12), or no cDNA (AdpL+, n = 12) [1].
• We tested the hypothesis that hypoxia up-regulates endothelial nitric oxide synthase (NOS3, type III) protein expression in fetal hearts similar to that observed in adult hearts as a cardioprotective adaptation [2].
• The development of NOS-3 dysfunction in resistance level PAs may contribute to the progression of chronic hypoxia-induced pulmonary hypertension in newborn piglets [3].
• Our objective, therefore, was to determine whether cNOS, i.e. ecNOS (NOS-3) and nNOS (NOS-1) are still active in vessels of pigs treated with lipopolysaccharide (LPS) from Escherichia coli [4].

High impact information on NOS3

• After 10 days of hypoxia, NO function is impaired in PAs despite preserved levels of NOS-3, HSP90, and caveolin-1 [3].
• Immunoblot analysis showed stress-induced upregulation of NOS2, but not NOS1 or NOS3 [5].
• NOS 3 was expressed in endothelial cells only, and NOS 1 expression was not observed in the granulation tissue [6].
• The expression of NOS2 and NOS3 in the myocardium did not differ between the groups [7].
• These findings suggest that oocyte NOS-3 is promoted for the synthesis of NO by E2 without increases in NOS-3 expression, but the synthesis of NO is suppressed, at least in the oocytes of early antral follicles [8].

Anatomical context of NOS3

• Positive immunostaining of NOS3 protein of fetal hearts was localized in both cardiomyocytes and endothelial cells [2].
• CONCLUSION: Contrary to our hypothesis, the hypoxia-induced decrease in fetal guinea pig heart NOS3 protein contrasts to the protein levels measured in either adult hearts or fetal carotid arteries [2].
• The endothelial type (NOS-3) of three isoforms of nitric oxide (NO) synthase occurs in porcine oocytes and granulosa cells, but the regulation of NO synthesis in oocytes remains unknown [8].
• Thioglycolate-elicited rat peritoneal macrophages and coronary endothelium of isolated guinea pig heart were used as assay systems for NOS-2 and NOS-3, respectively [9].

Associations of NOS3 with chemical compounds

• A23187-induced alterations of APD and I(Ks) were strongly suppressed by a NOS3 inhibitor, but barely affected by a NOS1 inhibitor, suggesting that NOS3 was responsible for NO release in this phenomenon [10].
• Analyses of RT-PCR and Western blotting showed that E2 did not increase NOS-3 expression [8].
• A significant synthesis of NO by oocytes was observed in the presence of ionomycin, but not in the absence of ionomycin, indicating that oocyte NOS-3 functions in response to transient elevations in the intracellular calcium level [11].

Other interactions of NOS3

• HPX decreased NOS3 protein levels in fetal guinea pig hearts by 29% after 28 days compared to NMX controls [2].

Analytical, diagnostic and therapeutic context of NOS3

• NOS3 protein was extracted from all tissues and quantified using Western blot analysis [2].
• Fetal heart samples were also prepared for localization of NOS3 protein using immunohistochemistry [2].

References