scholarly journals Enhanced notch signaling modulates unproductive revascularization in response to nitric oxide‐angiopoietin signaling in a mouse model of peripheral ischemia

2019 ◽  
Vol 26 (6) ◽  
Author(s):  
Maria J. C. Machado ◽  
Rachel Boardman ◽  
Federica Riu ◽  
Costanza Emanueli ◽  
Andrew V. Benest ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mouse Model ◽  
Notch Signaling ◽  
Peripheral Ischemia

Deficiency of Nitric Oxide Synthase 2 Results in Increased Neointima Formation in a Mouse Model of Vascular Injury

2003 ◽  
Vol 41 (6) ◽  
pp. 897-902 ◽  
Author(s):  
Allan Sirsjö ◽  
Anders Löfving ◽  
Göran K. Hansson ◽  
Dick Wågsäter ◽  
Shinichi Tokuno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mouse Model ◽  
Vascular Injury ◽  
Neointima Formation ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

scholarly journals Nitric oxide enhances the anti-inflammatory and anti-atherogenic activity of atorvastatin in a mouse model of accelerated atherosclerosis

2012 ◽  
Vol 94 (3) ◽  
pp. 428-438 ◽  
Author(s):  
Stefania Momi ◽  
Angela Monopoli ◽  
Paolo Francesco Alberti ◽  
Emanuela Falcinelli ◽  
Teresa Corazzi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mouse Model ◽  
Accelerated Atherosclerosis ◽  
Anti Inflammatory

Mechanisms of vascular instability in a transgenic mouse model of sickle cell disease

2000 ◽  
Vol 279 (6) ◽  
pp. R1949-R1955 ◽  
Author(s):  
K. A. Nath ◽  
V. Shah ◽  
J. J. Haggard ◽  
A. J. Croatt ◽  
L. A. Smith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Lipid Peroxidation ◽  
Sickle Cell Disease ◽  
Mouse Model ◽  
Systolic Blood Pressure ◽  
Transgenic Mouse ◽  
Sickle Cell ◽  
Transgenic Mouse Model ◽  
Cell Disease

We investigated a transgenic mouse model of sickle cell disease, homozygous for deletion of mouse β-globin and containing transgenes for human βSand βS-antillesglobins linked to the transgene for human α-globin. In these mice, basal cGMP production in aortic rings is increased, whereas relaxation to an endothelium-dependent vasodilator, A-23187, is impaired. In contrast, aortic expression of endothelial nitric oxide synthase (NOS) is unaltered in sickle mice, whereas expression of inducible NOS is not detected in either group; plasma nitrate/nitrite concentrations and NOS activity are similar in both groups. Increased cGMP may reflect the stimulatory effect of peroxides (an activator of guanylate cyclase), because lipid peroxidation is increased in aortae and in plasma in sickle mice. Despite increased vascular cGMP levels in sickle mice, conscious systolic blood pressure is comparable to that of aged-matched controls; sickle mice, however, evince a greater rise in systolic blood pressure in response to nitro-l-arginine methyl ester, an inhibitor of NOS. Systemic concentrations of the vasoconstrictive oxidative product 8-isoprostane are increased in sickle mice. We conclude that vascular responses are altered in this transgenic sickle mouse and are accompanied by increased lipid peroxidation and production of cGMP; we suggest that oxidant-inducible vasoconstrictor systems such as isoprostanes may oppose nitric oxide-dependent and nitric oxide-independent mechanisms of vasodilatation in this transgenic sickle mouse. Destabilization of the vasoactive balance in the sickle vasculature by clinically relevant states may predispose to vasoocclusive disease.

scholarly journals Inhibition of calcium-calmodulin kinase restores nitric oxide production and signaling in submandibular glands of a mouse model of salivary dysfunction

2004 ◽  
Vol 143 (8) ◽  
pp. 1058-1065 ◽  
Author(s):  
Florencia Rosignoli ◽  
Valeria Roca ◽  
Roberto Meiss ◽  
Nicolás Pregi ◽  
Claudia Pérez Leirós
Keyword(s):  
Nitric Oxide ◽  
Mouse Model ◽  
Nitric Oxide Production ◽  
Submandibular Glands ◽  
Oxide Production ◽  
Calmodulin Kinase

scholarly journals Regulatory Role of GSK-3βon NF-κB, Nitric Oxide, and TNF-αin Group A Streptococcal Infection

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Yu-Tzu Chang ◽  
Chia-Ling Chen ◽  
Chiou-Feng Lin ◽  
Shiou-Ling Lu ◽  
Miao-Huei Cheng ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mouse Model ◽  
Group A Streptococcus ◽  
Glycogen Synthase ◽  
Critical Issue ◽  
No Production ◽  
Group A ◽  
Oxide Synthase

Group A streptococcus (GAS) imposes a great burden on humans. Efforts to minimize the associated morbidity and mortality represent a critical issue. Glycogen synthase kinase-3β(GSK-3β) is known to regulate inflammatory response in infectious diseases. However, the regulation of GSK-3βin GAS infection is still unknown. The present study investigates the interaction between GSK-3β, NF-κB, and possible related inflammatory mediators in vitro and in a mouse model. The results revealed that GAS could activate NF-κB, followed by an increased expression of inducible nitric oxide synthase (iNOS) and NO production in a murine macrophage cell line. Activation of GSK-3βoccurred after GAS infection, and inhibition of GSK-3βreduced iNOS expression and NO production. Furthermore, GSK-3βinhibitors reduced NF-κB activation and subsequent TNF-αproduction, which indicates that GSK-3βacts upstream of NF-κB in GAS-infected macrophages. Similar to the in vitro findings, administration of GSK-3βinhibitor in an air pouch GAS infection mouse model significantly reduced the level of serum TNF-αand improved the survival rate. The inhibition of GSK-3βto moderate the inflammatory effect might be an alternative therapeutic strategy against GAS infection.

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