Experts and Doctors on nitric oxide synthase type iii in United States


Locale: United States
Topic: nitric oxide synthase type iii

Top Publications

  1. Shah V, Chen A, Cao S, Hendrickson H, Weiler D, Smith L, et al. Gene transfer of recombinant endothelial nitric oxide synthase to liver in vivo and in vitro. Am J Physiol Gastrointest Liver Physiol. 2000;279:G1023-30 pubmed
    ..These events were associated with increased ionomycin-stimulated NO release. In summary, this is the first study to demonstrate successful delivery of the recombinant eNOS gene to liver in vivo and in vitro with ensuing NO production...
  2. Smith R, Agata J, Xia C, Chao L, Chao J. Human endothelial nitric oxide synthase gene delivery protects against cardiac remodeling and reduces oxidative stress after myocardial infarction. Life Sci. 2005;76:2457-71 pubmed
    ..This study shows that NO may play an important role in attenuating cardiac remodeling and apoptosis after myocardial infarction via suppression of oxidative stress-mediated signaling pathways. ..
  3. Sullivan J, Smart E, Pollock D, Pollock J. Influence of salt on subcellular localization of nitric oxide synthase activity and expression in the renal inner medulla. Clin Exp Pharmacol Physiol. 2008;35:120-5 pubmed
    ..Expression of NOS3 protein was unaffected by high salt. 4. In conclusion, we hypothesize that NOS1 localization in the intracellular membrane is important in increasing NO production to aid Na(+) and water homeostasis. ..
  4. Guo Y, Li Q, Wu W, Tan W, Zhu X, Mu J, et al. Endothelial nitric oxide synthase is not necessary for the early phase of ischemic preconditioning in the mouse. J Mol Cell Cardiol. 2008;44:496-501 pubmed publisher
    ..Early PC is not eNOS-dependent, at least in this species. ..
  5. Huang Q, Sheibani N. High glucose promotes retinal endothelial cell migration through activation of Src, PI3K/Akt1/eNOS, and ERKs. Am J Physiol Cell Physiol. 2008;295:C1647-57 pubmed publisher
    ..Thus alterations in the proangiogenic properties of retinal EC during diabetes may contribute to the development and pathogenesis of diabetic retinopathy. ..
  6. Wang H, Kohr M, Traynham C, Ziolo M. Phosphodiesterase 5 restricts NOS3/Soluble guanylate cyclase signaling to L-type Ca2+ current in cardiac myocytes. J Mol Cell Cardiol. 2009;47:304-14 pubmed publisher
    ..Our data suggests a novel physiological role for PDE5 in restricting the effects of NOS3/sGC/PKG signaling pathway to modulating beta-AR stimulated I(Ca), while limiting effects on cardiac contraction. ..
  7. Zhang H, Pakeerappa P, Lee H, Fisher S. Induction of PDE5 and de-sensitization to endogenous NO signaling in a systemic resistance artery under altered blood flow. J Mol Cell Cardiol. 2009;47:57-65 pubmed publisher
    ..Treatment with PDE5 antagonists, in contrast to NO donors, may more specifically and effectively increase blood flow to chronically hypo-perfused tissues. ..
  8. Chen W, Druhan L, Chen C, Hemann C, Chen Y, Berka V, et al. Peroxynitrite induces destruction of the tetrahydrobiopterin and heme in endothelial nitric oxide synthase: transition from reversible to irreversible enzyme inhibition. Biochemistry. 2010;49:3129-37 pubmed publisher
    ..Therefore, ONOO(-)-induced eNOS inactivation is primarily due to oxidation of BH(4) and irreversible destruction of the heme/heme center...
  9. Doshi A, Ziolo M, Wang H, Burke E, Lesinski A, Binkley P. A promoter polymorphism of the endothelial nitric oxide synthase gene is associated with reduced mRNA and protein expression in failing human myocardium. J Card Fail. 2010;16:314-9 pubmed publisher
    ..Reduced eNOS expression associated with the promoter polymorphism may contribute to the vascular, contractile, and autonomic responses to ventricular failure. ..

More Information

Publications173 found, 100 shown here

  1. Stuehr D. Mammalian nitric oxide synthases. Biochim Biophys Acta. 1999;1411:217-30 pubmed
    ..This report summarizes some of the current information regarding NO synthase structure-function, reaction mechanism, control of catalysis, and protein interactions. ..
  2. Slomiany B, Slomiany A. Platelet-activating factor mediates Helicobacter pylori lipopolysaccharide interference with gastric mucin synthesis. IUBMB Life. 2004;56:41-6 pubmed
    ..Our findings suggest that PAF, through the interference with PI3K-dependent cNOS activation, plays a critical role in influencing the extent of pathological consequences of H. pylori infection on the synthesis of gastric mucin. ..
  3. Yi F, Magness R, Bird I. Simultaneous imaging of [Ca2+]i and intracellular NO production in freshly isolated uterine artery endothelial cells: effects of ovarian cycle and pregnancy. Am J Physiol Regul Integr Comp Physiol. 2005;288:R140-8 pubmed
    ..Thus pregnancy-enhanced eNOS activation in UAE is mediated through [Ca(2+)](i)-insensitive pathways as well as through a greater eNOS sensitivity to [Ca(2+)](i). ..
  4. Douglas G, Reilly C, Dooley M, Page G, Cooper G, Gilkeson G. Angiotensin-converting enzyme (insertion/deletion) and endothelial nitric oxide synthase polymorphisms in patients with systemic lupus erythematosus. J Rheumatol. 2004;31:1756-62 pubmed
    ..These studies emphasize the need to control for ethnicity when investigating genetic polymorphisms and disease. ..
  5. Nowicki P, Caniano D, Hammond S, Giannone P, Besner G, Reber K, et al. Endothelial nitric oxide synthase in human intestine resected for necrotizing enterocolitis. J Pediatr. 2007;150:40-5 pubmed
    ..These vessels were constricted; lack of eNOS-derived NO may contribute to this vasoconstriction. ..
  6. Duckworth L, Hsu L, Feng H, Wang J, Sylvester J, Kissoon N, et al. Physician-diagnosed asthma and acute chest syndrome: associations with NOS polymorphisms. Pediatr Pulmonol. 2007;42:332-8 pubmed
    ..No associations were found between the genotype of the NOS3 T-786C SNP and ACS. Physician-diagnosed asthma is a major risk factor for ACS. NOS1 AAT repeat polymorphism may contribute to physician-diagnosed asthma. ..
  7. Grummer M, Sullivan J, Magness R, Bird I. Vascular endothelial growth factor acts through novel, pregnancy-enhanced receptor signalling pathways to stimulate endothelial nitric oxide synthase activity in uterine artery endothelial cells. Biochem J. 2009;417:501-11 pubmed publisher
  8. Fulton D. Nox5 and the regulation of cellular function. Antioxid Redox Signal. 2009;11:2443-52 pubmed publisher
    ..The goal of this review is to outline recent advances in our knowledge of the genetic regulation, the molecular mechanisms governing its activity, and the functional significance of Nox5 in human physiology and pathophysiology. ..
  9. Gavin K, Seals D, Silver A, Moreau K. Vascular endothelial estrogen receptor alpha is modulated by estrogen status and related to endothelial function and endothelial nitric oxide synthase in healthy women. J Clin Endocrinol Metab. 2009;94:3513-20 pubmed publisher
    ..ER alpha expression may influence vascular endothelial function in women by affecting protein levels and activation of eNOS. ..
  10. Yi F, Boeldt D, Magness R, Bird I. [Ca2+]i signaling vs. eNOS expression as determinants of NO output in uterine artery endothelium: relative roles in pregnancy adaptation and reversal by VEGF165. Am J Physiol Heart Circ Physiol. 2011;300:H1182-93 pubmed publisher
    ..This demonstrates the importance of adaptation of cell signaling over eNOS expression in pregnancy adaptation of uterine endothelial function and further implicates VEGF in the pathophysiology of preeclampsia. ..
  11. Sato W, Tanabe K, Kosugi T, Hudkins K, Lanaspa M, Zhang L, et al. Selective stimulation of VEGFR2 accelerates progressive renal disease. Am J Pathol. 2011;179:155-66 pubmed publisher
    ..In conclusion, prestimulation of VEGFR2 can potentiate subsequent renal injury in mice, an effect enhanced in the setting of nitric oxide deficiency. ..
  12. Sharma S, Sun X, Rafikov R, Kumar S, Hou Y, Oishi P, et al. PPAR-? regulates carnitine homeostasis and mitochondrial function in a lamb model of increased pulmonary blood flow. PLoS ONE. 2012;7:e41555 pubmed publisher
    ..Further, it identifies a new mechanism by which PPAR-? regulates NO signaling through Hsp90. Thus, PPAR-? agonists may have therapeutic potential in preventing the endothelial dysfunction in children with increased pulmonary blood flow. ..
  13. Oates J, Mashmoushi A, Shaftman S, Gilkeson G. NADPH oxidase and nitric oxide synthase-dependent superoxide production is increased in proliferative lupus nephritis. Lupus. 2013;22:1361-70 pubmed publisher
    ..The markers of SO production used in this study could rationally be used to select SO-modulating therapies and serve as pharmacodynamic indicators for dose titration. ..
  14. Galán M, Kassan M, Kadowitz P, Trebak M, Belmadani S, Matrougui K. Mechanism of endoplasmic reticulum stress-induced vascular endothelial dysfunction. Biochim Biophys Acta. 2014;1843:1063-75 pubmed publisher
    ..Our results indicate that inhibition of ER stress could be a novel therapeutic strategy to attenuate vascular dysfunction during cardiovascular diseases. ..
  15. Wood C, Chen G, Keller Wood M. Expression of nitric oxide synthase isoforms is reduced in late-gestation ovine fetal brainstem. Am J Physiol Regul Integr Comp Physiol. 2005;289:R613-R619 pubmed publisher
    ..We speculate that the reduced expression of NOS in this brain region plays a role in the increased fetal baroreflex activity in late gestation...
  16. Joshi M, Mineo C, Shaul P, Bauer J. Biochemical consequences of the NOS3 Glu298Asp variation in human endothelium: altered caveolar localization and impaired response to shear. FASEB J. 2007;21:2655-63 pubmed
  17. Sen U, Tyagi N, Kumar M, Moshal K, Rodriguez W, Tyagi S. Cystathionine-beta-synthase gene transfer and 3-deazaadenosine ameliorate inflammatory response in endothelial cells. Am J Physiol Cell Physiol. 2007;293:C1779-87 pubmed
    ..However, in vitro DZA and CBS gene therapy successfully treated the HHcy-induced inflammatory reaction in the methionine metabolism pathway. ..
  18. Jones C, Han Z, Presley T, Varadharaj S, Zweier J, Ilangovan G, et al. Endothelial cell respiration is affected by the oxygen tension during shear exposure: role of mitochondrial peroxynitrite. Am J Physiol Cell Physiol. 2008;295:C180-91 pubmed publisher
    ..Hence, the hyperoxia of in vitro EC flow studies, via increased NO and mitochondrial O(2)(*-) production, leads to enhanced ONOO(-) formation intramitochondrially and suppression of respiration. ..
  19. Hu Z, Chen J, Wei Q, Xia Y. Bidirectional actions of hydrogen peroxide on endothelial nitric-oxide synthase phosphorylation and function: co-commitment and interplay of Akt and AMPK. J Biol Chem. 2008;283:25256-63 pubmed publisher
    ..Long term H(2)O(2) exposure decreased eNOS Ser(1179) phosphorylation, and this might account for the loss of eNOS function in cardiovascular diseases where chronic oxidative injury occurs. ..
  20. Pacanowski M, Zineh I, Cooper Dehoff R, Pepine C, Johnson J. Genetic and pharmacogenetic associations between NOS3 polymorphisms, blood pressure, and cardiovascular events in hypertension. Am J Hypertens. 2009;22:748-53 pubmed publisher
    ..The antihypertensive treatment approach did not appear to alter the genetic contribution to either BP control or cardiovascular events. ..
  21. Choi J, Barlow W, Albain K, Hong C, Blanco J, Livingston R, et al. Nitric oxide synthase variants and disease-free survival among treated and untreated breast cancer patients in a Southwest Oncology Group clinical trial. Clin Cancer Res. 2009;15:5258-66 pubmed publisher
    ..These results may mirror the known dual functions of nitric oxide and nitric oxide synthase, depending on oxidative environment. ..
  22. Shen B, Smith R, Hsu Y, Chao L, Chao J. Kruppel-like factor 4 is a novel mediator of Kallistatin in inhibiting endothelial inflammation via increased endothelial nitric-oxide synthase expression. J Biol Chem. 2009;284:35471-8 pubmed publisher
    ..This study provides a new target for modulating endothelial function in vascular disease. ..
  23. Li Q, Verma A, Han P, Nakagawa T, Johnson R, Grant M, et al. Diabetic eNOS-knockout mice develop accelerated retinopathy. Invest Ophthalmol Vis Sci. 2010;51:5240-6 pubmed publisher
  24. Barton Pai A, Feleder C, Johnson A. Tumor necrosis factor-? induces increased lung vascular permeability: a role for GSK3?/?. Eur J Pharmacol. 2011;657:159-66 pubmed publisher
    ..The data indicates that pharmacologic inhibition of GSK3? inhibits TNF induced increased endothelial permeability associated with lung inflammation. ..
  25. Jarajapu Y, Caballero S, Verma A, Nakagawa T, Lo M, Li Q, et al. Blockade of NADPH oxidase restores vasoreparative function in diabetic CD34+ cells. Invest Ophthalmol Vis Sci. 2011;52:5093-104 pubmed publisher
    ..The NADPH oxidase system is a promising target for correcting vasoreparative dysfunction in diabetic EPCs. ..
  26. Peyton K, Liu X, Yu Y, Yates B, Durante W. Activation of AMP-activated protein kinase inhibits the proliferation of human endothelial cells. J Pharmacol Exp Ther. 2012;342:827-34 pubmed publisher
    ..In addition, they show that AMPK regulates endothelial cell migration and differentiation and identify AMPK as an attractive therapeutic target in treating diseases associated with aberrant endothelial cell growth. ..
  27. Kondo S, Tang Y, Scheef E, Sheibani N, Sorenson C. Attenuation of retinal endothelial cell migration and capillary morphogenesis in the absence of bcl-2. Am J Physiol Cell Physiol. 2008;294:C1521-30 pubmed publisher
    ..Thus, bcl-2-mediated cellular functions play important roles not only in survival but also in proangiogenic phenotype of EC with a significant impact on vascular development and angiogenesis. ..
  28. Wang X, Abdel Rahman A. Estrogen modulation of eNOS activity and its association with caveolin-3 and calmodulin in rat hearts. Am J Physiol Heart Circ Physiol. 2002;282:H2309-15 pubmed
    ..Our findings may help to elucidate the molecular mechanism underlying the favorable effects of estrogen on cardiac responses to baroreflex activation. ..
  29. Zhang Y, Lee T, Kolb E, Sun K, Lu X, Sladek F, et al. AMP-activated protein kinase is involved in endothelial NO synthase activation in response to shear stress. Arterioscler Thromb Vasc Biol. 2006;26:1281-7 pubmed
    ..Hence, AMPK, in addition to serving as an energy sensor, also plays an important role in regulating vascular tone. ..
  30. Jackson K, Jackson D, Quadri S, Reitzell M, Navar L. Inhibition of heme oxygenase augments tubular sodium reabsorption. Am J Physiol Renal Physiol. 2011;300:F941-6 pubmed publisher
    ..The results suggest that inhibition of HO promotes water and sodium excretion by a direct tubular action that is independent of renal hemodynamics or the NO system. ..
  31. Chen C, De Pascali F, Basye A, Hemann C, Zweier J. Redox modulation of endothelial nitric oxide synthase by glutaredoxin-1 through reversible oxidative post-translational modification. Biochemistry. 2013;52:6712-23 pubmed publisher
    ..In endothelial cells, Grx1 inhibition or gene silencing increased the level of eNOS S-glutathionylation and decreased the level of cellular NO generation. Thus, Grx1 can exert an important role in the redox regulation of eNOS in cells. ..
  32. Zhang J, Luo B, Tang L, Wang Y, Stockard C, Kadish I, et al. Pulmonary angiogenesis in a rat model of hepatopulmonary syndrome. Gastroenterology. 2009;136:1070-80 pubmed publisher
    ..PTX decreases the angiogenesis, reduces the symptoms of HPS, and downregulates VEGF-A mediated pathways. ..
  33. Church J, Qian J, Kumar S, Black S, Venema R, Papapetropoulos A, et al. Inhibition of endothelial nitric oxide synthase by the lipid phosphatase PTEN. Vascul Pharmacol. 2010;52:191-8 pubmed publisher
    ..We conclude that PTEN is a regulator of eNOS function both when expressed in COS-7 cells and in human endothelial cells, and does so via its effects on the PI3K/Akt pathway. ..
  34. Smith C, Santymire B, Erdely A, Venkat V, Losonczy G, Baylis C. Renal nitric oxide production in rat pregnancy: role of constitutive nitric oxide synthases. Am J Physiol Renal Physiol. 2010;299:F830-6 pubmed publisher
    ..Collectively, these studies suggest that the soluble nNOS? is responsible for the increased renal cortical NO production during pregnancy. ..
  35. Tran Q, Firkins R, Giles J, Francis S, Matnishian V, Tran P, et al. Estrogen Enhances Linkage in the Vascular Endothelial Calmodulin Network via a Feedforward Mechanism at the G Protein-coupled Estrogen Receptor 1. J Biol Chem. 2016;291:10805-23 pubmed publisher
    ..Taken together, E2 generates a feedforward loop via GPER/GPR30, which enhances Ca(2+)/CaM signals and functional linkage in the endothelial CaM target network. ..
  36. Ghosh S, Gachhui R, Crooks C, Wu C, Lisanti M, Stuehr D. Interaction between caveolin-1 and the reductase domain of endothelial nitric-oxide synthase. Consequences for catalysis. J Biol Chem. 1998;273:22267-71 pubmed
    ..We propose that cav-1 binding to eNOS reductase compromises its ability to bind CaM and to donate electrons to the eNOS heme, thereby inhibiting NO synthesis. ..
  37. Zheng J, Wen Y, Chen D, Bird I, Magness R. Angiotensin II elevates nitric oxide synthase 3 expression and nitric oxide production via a mitogen-activated protein kinase cascade in ovine fetoplacental artery endothelial cells. Biol Reprod. 2005;72:1421-8 pubmed
    ..Together with our previous observation that ANG II stimulates OFPAE cell proliferation, these data suggest that ANG II is a key regulator for both vasodilation and angiogenesis in the ovine fetoplacenta. ..
  38. Afolayan A, Eis A, Alexander M, Michalkiewicz T, Teng R, Lakshminrusimha S, et al. Decreased endothelial nitric oxide synthase expression and function contribute to impaired mitochondrial biogenesis and oxidative stress in fetal lambs with persistent pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol. 2016;310:L40-9 pubmed publisher
    ..Knockdown of eNOS decreased ETC protein levels in control PAECs. We conclude that ventilation with 100% O2 amplifies oxidative stress and mitochondrial dysfunction in PPHN, which are partly improved by iNO and weaning of oxygen. ..
  39. Tang L, Luo B, Patel R, Ling Y, Zhang J, Fallon M. Modulation of pulmonary endothelial endothelin B receptor expression and signaling: implications for experimental hepatopulmonary syndrome. Am J Physiol Lung Cell Mol Physiol. 2007;292:L1467-72 pubmed
    ..These findings support that increased pulmonary microvascular endothelial ET(B) receptor expression modulates ET-1-mediated eNOS activation, independent of Akt, and contributes to the development of HPS. ..
  40. Presley T, Vedam K, Druhan L, Ilangovan G. Hyperthermia-induced Hsp90·eNOS preserves mitochondrial respiration in hyperglycemic endothelial cells by down-regulating Glut-1 and up-regulating G6PD activity. J Biol Chem. 2010;285:38194-203 pubmed publisher
  41. d Uscio L, Smith L, Katusic Z. Differential effects of eNOS uncoupling on conduit and small arteries in GTP-cyclohydrolase I-deficient hph-1 mice. Am J Physiol Heart Circ Physiol. 2011;301:H2227-34 pubmed publisher
    ..The results of our study suggest that anatomical origin determines the ability of vessel wall to cope with oxidative stress induced by uncoupling of eNOS. ..
  42. Park S, Ives S, Gifford J, Andtbacka R, Hyngstrom J, Reese V, et al. Impact of age on the vasodilatory function of human skeletal muscle feed arteries. Am J Physiol Heart Circ Physiol. 2016;310:H217-25 pubmed publisher
  43. Hu H, Xin M, Belayev L, Zhang J, Block E, Patel J. Autoinhibitory domain fragment of endothelial NOS enhances pulmonary artery vasorelaxation by the NO-cGMP pathway. Am J Physiol Lung Cell Mol Physiol. 2004;286:L1066-74 pubmed
    ..These results demonstrate that AAF-stimulated vasodilation is mediated via activation of eNOS and enhanced NO-cGMP production in PA and intact lung. ..
  44. Gossl M, Versari D, Hildebrandt H, Bajanowski T, Sangiorgi G, Erbel R, et al. Segmental heterogeneity of vasa vasorum neovascularization in human coronary atherosclerosis. JACC Cardiovasc Imaging. 2010;3:32-40 pubmed publisher
    ..Our results support a possible role of VV neovascularization, VV rupture, and intraplaque hemorrhage in the progression and complications of human coronary atherosclerosis. ..
  45. Sasser J, Akinsiku O, Moningka N, Jerzewski K, Baylis C, LeBlanc A, et al. Sexual dimorphism in development of kidney damage in aging Fischer-344 rats. Gend Med. 2012;9:219-31 pubmed publisher
    ..The kidney damage expressed in aging F344 rats is fairly mild and is not related to loss of renal cortex NOS3 or NOS1 alpha. ..
  46. Zhao X, He G, Chen Y, Pandian R, Kuppusamy P, Zweier J. Endothelium-derived nitric oxide regulates postischemic myocardial oxygenation and oxygen consumption by modulation of mitochondrial electron transport. Circulation. 2005;111:2966-72 pubmed
    ..The marked myocardial hyperoxygenation in reperfused myocardium may be a critical factor that triggers postischemic remodeling. ..
  47. Cardounel A, Cui H, Samouilov A, Johnson W, Kearns P, Tsai A, et al. Evidence for the pathophysiological role of endogenous methylarginines in regulation of endothelial NO production and vascular function. J Biol Chem. 2007;282:879-87 pubmed
    ..Thus, MAs are critical mediators of vascular dysfunction following vascular injury. ..
  48. Newcomer S, Taylor J, McAllister R, Laughlin M. Effects of chronic nitric oxide synthase inhibition on endothelium-dependent and -independent relaxation in arteries that perfuse skeletal muscle of swine. Endothelium. 2008;15:17-31 pubmed publisher
  49. Krupp J, Boeldt D, Yi F, Grummer M, Bankowski Anaya H, Shah D, et al. The loss of sustained Ca(2+) signaling underlies suppressed endothelial nitric oxide production in preeclamptic pregnancies: implications for new therapy. Am J Physiol Heart Circ Physiol. 2013;305:H969-79 pubmed publisher
    ..Thus novel clinical therapy aimed at restoring function in vivo may be possible. ..
  50. Zhang Y, Li J, Partovian C, Sellke F, Simons M. Syndecan-4 modulates basic fibroblast growth factor 2 signaling in vivo. Am J Physiol Heart Circ Physiol. 2003;284:H2078-82 pubmed
    ..In conclusion, enhanced syndecan-4 expression in mouse cardiac endothelial cells results in preferential augmentation of FGF2 but not VEGF-A(165)-induced NO release. ..
  51. Gifford S, Grummer M, Pierre S, Austin J, Zheng J, Bird I. Functional characterization of HUVEC-CS: Ca2+ signaling, ERK 1/2 activation, mitogenesis and vasodilator production. J Endocrinol. 2004;182:485-99 pubmed
    ..In conclusion, HUVEC-CS are indeed endothelial cells and appear to be functionally very similar to primary HUVEC. These cells will prove a valuable tool for future studies in both basic and therapeutic sciences. ..
  52. Sheffield M, Mabry S, Thibeault D, Truog W. Pulmonary nitric oxide synthases and nitrotyrosine: findings during lung development and in chronic lung disease of prematurity. Pediatrics. 2006;118:1056-64 pubmed
    ..Nitric oxide synthase ontogeny shows no significant changes in abundance or distribution with advancing gestational age nor with chronic lung disease. Nitrotyrosine is significantly increased in severe chronic lung disease. ..
  53. Kan W, Hsu J, Ba Z, Schwacha M, Chen J, Choudhry M, et al. p38 MAPK-dependent eNOS upregulation is critical for 17beta-estradiol-mediated cardioprotection following trauma-hemorrhage. Am J Physiol Heart Circ Physiol. 2008;294:H2627-36 pubmed publisher
    ..The salutary effects of E2 on cardiac functions and tissue protection following trauma-hemorrhage are mediated, in part, through activation of p38 MAPK and subsequent eNOS expression and phosphorylation. ..
  54. Su Y, Edwards Bennett S, Bubb M, Block E. Regulation of endothelial nitric oxide synthase by the actin cytoskeleton. Am J Physiol Cell Physiol. 2003;284:C1542-9 pubmed
    ..These results suggest that eNOS is associated with actin in PAEC and that actin and its polymerization state play an important role in the regulation of eNOS activity. ..
  55. Cale J, Tsoi S, Toppe M, Grummer M, Ochiai M, Magness R, et al. Molecular cloning of ovine endothelial nitric oxide synthase and expression in COS-7 cells. J Soc Gynecol Investig. 2005;12:156-68 pubmed
  56. Newcomer S, Taylor J, Bowles D, Laughlin M. Endothelium-dependent and -independent relaxation in the forelimb and hindlimb vasculatures of swine. Comp Biochem Physiol A Mol Integr Physiol. 2007;148:292-300 pubmed
    ..The current results of this investigation suggest that the forelimb and hindlimb vasculatures of swine have relatively similar vasorelaxation responses to both endothelium-dependent and -independent vasodilators. ..
  57. Standley P, Stanley M, Senechal P. Activation of mitogenic and antimitogenic pathways in cyclically stretched arterial smooth muscle. Am J Physiol Endocrinol Metab. 2001;281:E1165-71 pubmed
    ..These two molecules regulate each other's secretory rates, providing tight regulation of VSMC proliferation. These data may have profound implications in understanding vascular growth alterations in vascular injury and hypertension...
  58. Mehta V, Zhou Y, Radulescu A, Besner G. HB-EGF stimulates eNOS expression and nitric oxide production and promotes eNOS dependent angiogenesis. Growth Factors. 2008;26:301-15 pubmed publisher
    ..Thus, activation of eNOS appears to be one of the key signaling pathways necessary for HB-EGF mediated angiogenesis. These novel findings highlight an important role for HB-EGF as a regulator of endothelial cell function. ..
  59. Song Y, Wang K, Chen D, Magness R, Zheng J. Suppression of protein phosphatase 2 differentially modulates VEGF- and FGF2-induced signaling in ovine fetoplacental artery endothelial cells. Placenta. 2009;30:907-13 pubmed publisher
    ..These data also suggest that signaling molecules other than ERK1/2, AKT1, and p38 MAPK are important mediators for VEGF- and FGF2-stimulated OFPAE cell proliferation after PPP2CA suppression. ..
  60. Mohan S, Wu C, Shin S, Fung H. Continuous exposure to L-arginine induces oxidative stress and physiological tolerance in cultured human endothelial cells. Amino Acids. 2012;43:1179-88 pubmed publisher
    ..These studies suggest that ARG-induced oxidative stress may be a primary causative factor for the development of cellular ARG tolerance. ..
  61. Nakagawa T. Uncoupling of the VEGF-endothelial nitric oxide axis in diabetic nephropathy: an explanation for the paradoxical effects of VEGF in renal disease. Am J Physiol Renal Physiol. 2007;292:F1665-72 pubmed
  62. Sud N, Kumar S, Wedgwood S, Black S. Modulation of PKCdelta signaling alters the shear stress-mediated increases in endothelial nitric oxide synthase transcription: role of STAT3. Am J Physiol Lung Cell Mol Physiol. 2009;296:L519-26 pubmed publisher
    ..In conclusion, shear decreases PKCdelta activity and, subsequently, reduces STAT3 binding to the eNOS promoter. This signaling pathway plays a previously unidentified role in the regulation of eNOS expression by shear stress. ..
  63. Foster J, Carmines P, Pollock J. PP2B-dependent NO production in the medullary thick ascending limb during diabetes. Am J Physiol Renal Physiol. 2009;297:F471-80 pubmed publisher
    ..In conclusion, while NO bioavailability in mTALs is reduced during diabetes, free radical scavenging with tempol unmasks increased NO production that involves PP2B-dependent activation of NOS1 and NOS2...
  64. Alpers C, Hudkins K. Mouse models of diabetic nephropathy. Curr Opin Nephrol Hypertens. 2011;20:278-84 pubmed publisher
    ..A model that allows testing of interventions that modulate podocyte loss and regeneration, such as the BTBR ob/ob mouse, may be of particular benefit in developing therapeutics for diabetic nephropathy. ..
  65. Woodman C, Schrage W, Rush J, Ray C, Price E, Hasser E, et al. Hindlimb unweighting decreases endothelium-dependent dilation and eNOS expression in soleus not gastrocnemius. J Appl Physiol (1985). 2001;91:1091-8 pubmed
    ..These data indicate that HLU decreases endothelium-dependent vasodilation, eNOS expression, and SOD-1 expression primarily in arteries of Sol muscle where blood flow is reduced during HLU...
  66. Tanimoto T, Jin Z, Berk B. Transactivation of vascular endothelial growth factor (VEGF) receptor Flk-1/KDR is involved in sphingosine 1-phosphate-stimulated phosphorylation of Akt and endothelial nitric-oxide synthase (eNOS). J Biol Chem. 2002;277:42997-3001 pubmed
    ..These data are the first to establish a critical role of Flk-1/KDR in S1P-stimulated eNOS phosphorylation and activation. ..
  67. Khorram O, Lessey B. Alterations in expression of endometrial endothelial nitric oxide synthase and alpha(v)beta(3) integrin in women with endometriosis. Fertil Steril. 2002;78:860-4 pubmed
    ..The nitric oxide pathway may play a role in the pathogenesis of endometriosis. ..
  68. Sullivan J, Pardieck J, Brinson K, Kang K. Effects of estradiol on renal cyclic guanosine monophosphate and oxidative stress in spontaneously hypertensive rats. Gend Med. 2009;6:498-510 pubmed publisher
    ..In vivo manipulations of estradiol levels influenced renal cortical NO bioavailability, as assessed indirectly by cGMP measurements. The decrease in cGMP following OVX was not due to alterations in the activity or expression of NOS. ..
  69. Gu M, Roy S, Raina K, Agarwal C, Agarwal R. Inositol hexaphosphate suppresses growth and induces apoptosis in prostate carcinoma cells in culture and nude mouse xenograft: PI3K-Akt pathway as potential target. Cancer Res. 2009;69:9465-72 pubmed publisher
  70. Park S, Dimaio T, Scheef E, Sorenson C, Sheibani N. PECAM-1 regulates proangiogenic properties of endothelial cells through modulation of cell-cell and cell-matrix interactions. Am J Physiol Cell Physiol. 2010;299:C1468-84 pubmed publisher
    ..Thus PECAM-1 expression modulates proangiogenic properties of EC, and these activities are significantly influenced by alternative splicing of its cytoplasmic domain. ..
  71. Adluri R, Thirunavukkarasu M, Zhan L, Akita Y, Samuel S, Otani H, et al. Thioredoxin 1 enhances neovascularization and reduces ventricular remodeling during chronic myocardial infarction: a study using thioredoxin 1 transgenic mice. J Mol Cell Cardiol. 2011;50:239-47 pubmed publisher
    ..Hence, Trx1 and other proteins identified in our study may prove to be potential therapeutic targets in the treatment of ischemic heart disease. ..
  72. Headley C, Disilvestro D, Bryant K, Hemann C, Chen C, Das A, et al. Nitrones reverse hyperglycemia-induced endothelial dysfunction in bovine aortic endothelial cells. Biochem Pharmacol. 2016;104:108-17 pubmed publisher
    ..Our findings demonstrate that the nitrones reverse the deleterious effects of hyperglycemia in BAEC. We believe that in vivo testing of these nitrone compounds in models of cardiometabolic disease is warranted. ..
  73. Ahn J, Ambrosone C, Kanetsky P, Tian C, Lehman T, Kropp S, et al. Polymorphisms in genes related to oxidative stress (CAT, MnSOD, MPO, and eNOS) and acute toxicities from radiation therapy following lumpectomy for breast cancer. Clin Cancer Res. 2006;12:7063-70 pubmed
    ..Regression trees may be useful in future studies to examine the contributions of multiple factors to individual susceptibility to adverse effects of cancer treatment. ..
  74. Zineh I, Beitelshees A, Haller M. NOS3 polymorphisms are associated with arterial stiffness in children with type 1 diabetes. Diabetes Care. 2007;30:689-93 pubmed
    ..002, R2 = 0.40). This is the first reported association between -786T-->C and arterial stiffness in type 1 diabetes. Larger studies are needed to confirm this observation for potential translation to risk assessment. ..
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    ..We conclude that UA-induced arginase activation is a potential mechanism for reduction of NO production in PAEC. ..
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    ..Together, these data suggest that the inhibition of Sp1 activity, possibly through loss of zinc in the protein, plays a role in the H(2)O(2)-induced inhibition of eNOS promoter activity. ..
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    ..These results suggest that atheroprotective flow, via AMPK and SIRT1, increases NO bioavailability in endothelium. ..
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    ..These findings indicate a novel role of kallistatin in the protection against vascular injury and oxidative stress-induced endothelial apoptosis via the activation of Akt-dependent eNOS signaling. ..
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    ..1 and sod-3 synthesis in C. elegans. These in vitro and in vivo studies provide significant insights into the role and mechanism of kallistatin in vascular senescence and aging by regulating miR-34a-SIRT1 pathway...
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    ..The results indicate that the activation of TLR2 and the generation of ROS/RNS mediates LTA-induced barrier dysfunction in PMEM. ..
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    ..This process takes place in injured, but not in normal, SECs. ..
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    ..We conclude that HDL binding to SR-BI stimulates eNOS by increasing intracellular ceramide levels and is independent of an increase in intracellular calcium or Akt kinase phosphorylation. ..
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    ..5. Myristoylated peptides can be considered a new class of activators of NO production in endothelial cells and that using mPS as a specific inhibitor of PKC should be done with caution, especially in endothelial cells. ..
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    ..15, p = 0.01, respectively). In conclusion, our findings suggest that high-risk genotypes of the PON1 Q192R and eNOS E298D polymorphisms are independently associated with a significantly earlier occurrence of coronary events. ..