Expression of N-methyl-d-aspartate receptor and its effect on nitric oxide production of rat alveolar macrophages

Su, Lihong; Luo, Ziqiang; Deng, XiaoDan; Wang, M.J.; Huang, Furong; Feng, DeYun; Yue, Shaojie

doi:10.1016/j.niox.2010.09.004

Cited by 23 publications

(14 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NMDA applied to the SCN either induced phase delays at peak oscillation times or phase-advances during the trough phase of luminescence demonstrating that the direction and magnitude of the NMDA-induced phase shifts are dependent on the circadian phase [67]. While we have not addressed whether the effect of ketamine on circadian gene expression is mediated by NMDA, it is important to underscore that NMDA receptors are expressed in different types of non-neuronal cells [68]–[72]. Future studies will help to better elucidate the mechanisms of action of ketamine on the circadian system in neuronal and non-neuronal tissues.…”

Section: Discussionmentioning

confidence: 96%

Ketamine Influences CLOCK:BMAL1 Function Leading to Altered Circadian Gene Expression

et al. 2011

View full text Add to dashboard Cite

Major mood disorders have been linked to abnormalities in circadian rhythms, leading to disturbances in sleep, mood, temperature, and hormonal levels. We provide evidence that ketamine, a drug with rapid antidepressant effects, influences the function of the circadian molecular machinery. Ketamine modulates CLOCK:BMAL1-mediated transcriptional activation when these regulators are ectopically expressed in NG108-15 neuronal cells. Inhibition occurs in a dose-dependent manner and is attenuated after treatment with the GSK3β antagonist SB21673. We analyzed the effect of ketamine on circadian gene expression and observed a dose-dependent reduction in the amplitude of circadian transcription of the Bmal1, Per2, and Cry1 genes. Finally, chromatin-immunoprecipitation analyses revealed that ketamine altered the recruitment of the CLOCK:BMAL1 complex on circadian promoters in a time-dependent manner. Our results reveal a yet unsuspected molecular mode of action of ketamine and thereby may suggest possible pharmacological antidepressant strategies.

show abstract

Section: Discussionmentioning

confidence: 96%

Ketamine Influences CLOCK:BMAL1 Function Leading to Altered Circadian Gene Expression

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Its excessive production via iNOS and a subsequent oxidative stress reaction are thought to be critically involved in the pathophysiology of pulmonary sepsis [61]. Increase in iNOS mRNA expression, iNOS activity, and NO secretion have been recorded in alveolar macrophages in hyperoxia-induced lung injury in rat [62]. Conversely, suppression of NO generation via downregulation of iNOS by selective iNOS inhibitors protects from lung injury [63,64].…”

Section: Discussionmentioning

confidence: 99%

Neutrophilic Inflammatory Response and Oxidative Stress in Premenopausal Women Chronically Exposed to Indoor Air Pollution from Biomass Burning

et al. 2011

View full text Add to dashboard Cite

The possibility of inflammation and neutrophil activation in response to indoor air pollution (IAP) from biomass fuel use has been investigated. For this, 142 premenopausal, never-smoking women (median age, 34 years) who cook exclusively with biomass (wood, dung, crop wastes) and 126 age-matched control women who cook with cleaner fuel liquefied petroleum gas (LPG) were enrolled. The neutrophil count in blood and sputum was significantly higher (p < 0.05) in biomass users than the control group. Flow cytometric analysis revealed marked increase in the surface expression of CD35 (complement receptor-1), CD16 (F(C)γ receptor III), and β(2) Mac-1 integrin (CD11b/CD18) on circulating neutrophils of biomass users. Besides, enzyme-linked immunosorbent assay showed that they had 72%, 67%, and 54% higher plasma levels of the proinflammatory cytokines tumor necrosis factor-alpha, interleukin-6, and interleukin-12, respectively, and doubled neutrophil chemoattractant interleukin-8. Immunocytochemical study revealed significantly higher percentage of airway neutrophils expressing inducible nitric oxide synthase, while the serum level of nitric oxide was doubled in women who cooked with biomass. Spectrophotometric analysis documented higher myeloperoxidase activity in circulating neutrophils of biomass users, suggesting neutrophil activation. Flow cytometry showed excess generation of reactive oxygen species (ROS) by leukocytes of biomass-using women, whereas their erythrocytes contained a depleted level of antioxidant enzyme superoxide dismutase (SOD). Indoor air of biomass-using households had two to four times more particulate matter with diameters of <10 μm (PM(10)) and <2.5 μm (PM(2.5)) as measured by real-time laser photometer. After controlling potential confounders, rise in proinflammatory mediators among biomass users were positively associated with PM(10) and PM(2.5) in indoor air, suggesting a close relationship between IAP and neutrophil activation. Besides, the levels of neutrophil activation and inflammation markers were positively associated with generation of ROS and negatively with SOD, indicating a role of oxidative stress in mediating neutrophilic inflammatory response following chronic inhalation of biomass smoke.

show abstract

“…In rat lungs, NOS2 up-regulation in hyperoxia has been noted in alveolar epithelial cells and macrophages (9,18,59). Possible differences in alveolar macrophages obtained from adult (2 mo old) and NB (PN7) rats in response to hyperoxia, with the latter having increased production of NO, have been suggested (16). Cell source-specific source of up-regulation of NOS2 has been proposed to explain the differential effects of NOS2 inhibition in HALI (20,60).…”

Section: Nos2mentioning

confidence: 99%

“…The inflammatory response in HALI is initiated and propagated, to a large extent, by the release of cytokines (1), which are known to induce NOS (6,7). Most data suggest that hyperoxia exposure up-regulates inducible NOS (NOS2) and endothelial NOS (NOS3) expression in adult (8)(9)(10)(11)(12)(13)(14)(15)(16) and neonatal (7,(16)(17)(18)(19) lungs. In ALI and cell death, the endogenous production of NO is said to be mostly contributed by up-regulation of NOS2 in the lung (20)(21)(22).…”

mentioning

confidence: 99%

Increased Hyperoxia-Induced Lung Injury in Nitric Oxide Synthase 2 Null Mice Is Mediated via Angiopoietin 2

Bhandari

Choo-Wing

Harijith

et al. 2012

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Supplemental oxygen is frequently prescribed. However, prolonged exposure to high concentrations of oxygen causes hyperoxic acute lung injury (HALI), which manifests as acute respiratory distress syndrome in adults and leads to bronchopulmonary dysplasia in newborns (NBs). Nitric oxide (NO), NO synthases (NOSs), and angiopoietin (Ang) 2 have been implicated in the pathogenesis of HALI. However, the mechanisms of the contributions of NOS/NO and the relationship(s) between NOS/NO and Ang2 have not been addressed. In addition, the relevance of these moieties in adults and NBs has not been evaluated. To address these issues, we compared the responses in hyperoxia of wild-type (NOS [1/1]) and NOS null (2/2) young adult and NB mice. When compared with NOS21/1 adult controls, NOS2 2/2 animals manifest exaggerated alveolar-capillary protein leak and premature death. These responses were associated with enhanced levels of structural cell death, enhanced expression of proapoptotic regulatory proteins, and Ang2. Importantly, silencing RNA knockdown of Ang2 decreased the levels of cell death and the expression of proapoptotic mediators. These effects were at least partially NOS2 specific, and were development dependent, because survival was similar in adult NOS3 1/1 and NOS3 2/2 mice and NB NOS2 1/1 and NOS2 2/2 mice, respectively. These studies demonstrate that NOS2 plays an important protective role in HALI in adult animals. They also demonstrate that this response is mediated, at least in part, by the ability of NOS2 to inhibit hyperoxia-induced Ang2 production and thereby decrease Ang2-induced tissue injury.Keywords: cytokines; hyperoxia; lung Supplemental oxygen is commonly employed to counteract tissue hypoxemia. Although this is lifesaving in most circumstances, prolonged exposure to high concentrations of oxygen can lead to untoward effects. In the lung, exposure to hyperoxia is characterized by an inflammatory response (mediated by cytokines) and breakdown of the alveolar-capillary barrier, leading to pulmonary edema and endothelial and epithelial cell injury/ death (1). In adults, hyperoxic acute lung injury (HALI) causes acute respiratory distress syndrome (2). In neonates, HALI has been shown to lead to a pulmonary phenotype suggestive of bronchopulmonary dysplasia (3). Hence, HALI is a major cause of morbidity and mortality in both adult (2) and neonatal (3,4) populations.In addition, nitric oxide (NO) is known to have oxidant effects (5), and has been implicated in the pathogenesis of HALI. NO is generated via the action of NO synthases (NOSs). The inflammatory response in HALI is initiated and propagated, to a large extent, by the release of cytokines (1), which are known to induce NOS (6, 7). Most data suggest that hyperoxia exposure up-regulates inducible NOS (NOS2) and endothelial NOS (NOS3) expression in adult (8-16) and neonatal (7,(16)(17)(18)(19) lungs. In ALI and cell death, the endogenous production of NO is said to be mostly contributed by up-regulation of NOS2 in the lung (20)(21)(22).Previous work...

show abstract

Expression of N-methyl-d-aspartate receptor and its effect on nitric oxide production of rat alveolar macrophages

Cited by 23 publications

References 26 publications

Ketamine Influences CLOCK:BMAL1 Function Leading to Altered Circadian Gene Expression

Ketamine Influences CLOCK:BMAL1 Function Leading to Altered Circadian Gene Expression

Neutrophilic Inflammatory Response and Oxidative Stress in Premenopausal Women Chronically Exposed to Indoor Air Pollution from Biomass Burning

Increased Hyperoxia-Induced Lung Injury in Nitric Oxide Synthase 2 Null Mice Is Mediated via Angiopoietin 2

Contact Info

Product

Resources

About