Nitric Oxide
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2022 ◽  
Vol 196 ◽  
pp. 113081
Wei-Wei Yu ◽  
Jin-Tao Ma ◽  
Juan He ◽  
Zheng-Hui Li ◽  
Ji-Kai Liu ◽  

2022 ◽  
Vol 231 ◽  
pp. 113197
Junjie He ◽  
Pengfei Cheng ◽  
Jun Wang ◽  
Sheng Xu ◽  
Jianxin Zou ◽  

2022 ◽  
Vol 25 ◽  
pp. 100596
Minh-Thuan Pham ◽  
Truc-Mai T. Nguyen ◽  
Dai-Phat Bui ◽  
Ya-Fen Wang ◽  
Hong-Huy Tran ◽  

Nano Today ◽  
2022 ◽  
Vol 42 ◽  
pp. 101381
Yanfei Li ◽  
Hongliang Qian ◽  
Xin Huang ◽  
Xiang Zhou ◽  
Bingbing Zhao ◽  

Kensuke Fukumitsu ◽  
Hirono Nishiyama ◽  
Yoshihiro Kanemitsu ◽  
Norihisa Takeda ◽  
Ryota Kurokawa ◽  

<b><i>Introduction:</i></b> Inhaled corticosteroids (ICS) are fundamental agents to subside airway inflammation and improve forced expiratory volume in 1 s (FEV<sub>1</sub>) among asthmatics. Alveolar concentrations of nitric oxide (CANO), as well as the classical fraction of exhaled nitric oxide (FeNO50), are associated with the pathophysiology of asthma. However, the association between pretreatment CANO levels and response to anti-asthma treatments, including ICS, remains unknown. <b><i>Methods:</i></b> We retrospectively analyzed 107 patients newly diagnosed with asthma. ICS in combination with long-acting β<sub>2</sub>-agonists (ICS/LABA) was initiated. FEV<sub>1</sub> and FeNO levels were evaluated at diagnosis and were followed up at 6 and 12 months after the treatment intervention. CANO levels were estimated using various expiratory flows of FeNO measurements. Factors associated with annual changes in FEV<sub>1</sub> (ΔFEV<sub>1</sub>) were analyzed. Patients with a ΔFEV<sub>1</sub> &#x3c;–20 mL were defined as “poor-responders.” <b><i>Results:</i></b> FEV<sub>1</sub>, FeNO50, and CANO levels significantly improved by anti-asthma treatments. The average ΔFEV<sub>1</sub> was 85 (176) mL. Eighty-two patients continuously took ICS/LABA treatment. Higher pretreatment CANO levels and continuous use of LABA were independent predictive factors for the improvement of FEV<sub>1</sub> on multivariate analysis. The decline in FeNO50 and CANO levels by the anti-asthma treatments was significantly greater in 81 responders than in 26 poor-responders. CANO, but not FeNO50, levels at 12 months were significantly higher in poor-responders than in responders (<i>p</i> = 0.009). <b><i>Conclusion:</i></b> Levels of CANO, but not FeNO50, predict changes in pulmonary function in ICS-naïve asthmatics. Meanwhile, persistently high levels of CANO may be related to poor responsiveness to treatments assessed by ΔFEV<sub>1</sub>.

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 159
Laurent Kiger ◽  
Julia Keith ◽  
Abdullah Freiwan ◽  
Alfonso G. Fernandez ◽  
Heather Tillman ◽  

Interest in the structure, function, and evolutionary relations of circulating and intracellular globins dates back more than 60 years to the first determination of the three-dimensional structure of these proteins. Non-erythrocytic globins have been implicated in circulatory control through reactions that couple nitric oxide (NO) signaling with cellular oxygen availability and redox status. Small artery endothelial cells (ECs) express free α-globin, which causes vasoconstriction by degrading NO. This reaction converts reduced (Fe2+) α-globin to the oxidized (Fe3+) form, which is unstable, cytotoxic, and unable to degrade NO. Therefore, (Fe3+) α-globin must be stabilized and recycled to (Fe2+) α-globin to reinitiate the catalytic cycle. The molecular chaperone α-hemoglobin-stabilizing protein (AHSP) binds (Fe3+) α-globin to inhibit its degradation and facilitate its reduction. The mechanisms that reduce (Fe3+) α-globin in ECs are unknown, although endothelial nitric oxide synthase (eNOS) and cytochrome b5 reductase (CyB5R3) with cytochrome b5 type A (CyB5a) can reduce (Fe3+) α-globin in solution. Here, we examine the expression and cellular localization of eNOS, CyB5a, and CyB5R3 in mouse arterial ECs and show that α-globin can be reduced by either of two independent redox systems, CyB5R3/CyB5a and eNOS. Together, our findings provide new insights into the regulation of blood vessel contractility.

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