Developmental loss of parvalbumin-positive cells in the prefrontal cortex and psychiatric anxiety after intermittent hypoxia exposures in neonatal rats might be mediated by NADPH oxidase-2

2016 ◽  
Vol 296 ◽  
pp. 134-140 ◽  
Author(s):  
Dong Liang ◽  
Guowei Li ◽  
Xingzhi Liao ◽  
Dawei Yu ◽  
Jing Wu ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Nadph Oxidase ◽  
Intermittent Hypoxia ◽  
Neonatal Rats ◽  
Nadph Oxidase 2

Intermittent Hypoxia-Induced Parvalbumin-Immunoreactive Interneurons Loss and Neurobehavioral Impairment is Mediated by NADPH-Oxidase-2

2015 ◽  
Vol 40 (6) ◽  
pp. 1232-1242 ◽  
Author(s):  
Liang Yuan ◽  
Jing Wu ◽  
Jiang Liu ◽  
Guowei Li ◽  
Dong Liang
Keyword(s):  
Nadph Oxidase ◽  
Intermittent Hypoxia ◽  
Nadph Oxidase 2

scholarly journals NADPH Oxidase 2 Mediates Intermittent Hypoxia-Induced Mitochondrial Complex I Inhibition: Relevance to Blood Pressure Changes in Rats

2011 ◽  
Vol 14 (4) ◽  
pp. 533-542 ◽  
Author(s):  
Shakil A. Khan ◽  
Jayasri Nanduri ◽  
Guoxiang Yuan ◽  
Brian Kinsman ◽  
Ganesh K. Kumar ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nadph Oxidase ◽  
Complex I ◽  
Intermittent Hypoxia ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Nadph Oxidase 2 ◽  
Pressure Changes

scholarly journals Hypoxia-inducible factor 1 mediates increased expression of NADPH oxidase-2 in response to intermittent hypoxia

2011 ◽  
Vol 226 (11) ◽  
pp. 2925-2933 ◽  
Author(s):  
Guoxiang Yuan ◽  
Shakil A. Khan ◽  
Weibo Luo ◽  
Jayasri Nanduri ◽  
Gregg L. Semenza ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Intermittent Hypoxia ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1 ◽  
Nadph Oxidase 2

scholarly journals Intermittent hypoxia inhibits mandibular cartilage growth with reduced TGF-β and SOX9 expressions in neonatal rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kochakorn Lekvijittada ◽  
Jun Hosomichi ◽  
Hideyuki Maeda ◽  
Haixin Hong ◽  
Chidsanu Changsiripun ◽  
...  
Keyword(s):  
Bone Mineral ◽  
Intermittent Hypoxia ◽  
Hyaline Cartilage ◽  
Body Weight Gain ◽  
Mandibular Condyle ◽  
Neonatal Rats ◽  
Sprague Dawley ◽  
Cartilage Growth ◽  
Condylar Cartilage ◽  
Sprague Dawley Rats

AbstractIntermittent hypoxia (IH) has been associated with skeletal growth. However, the influence of IH on cartilage growth and metabolism is unknown. We compared the effects of IH on chondrocyte proliferation and maturation in the mandibular condyle fibrocartilage and tibial hyaline cartilage of 1-week-old male Sprague–Dawley rats. The rats were exposed to normoxic air (n = 9) or IH at 20 cycles/h (nadir, 4% O2; peak, 21% O2; 0% CO2) (n = 9) for 8 h each day. IH impeded body weight gain, but not tibial elongation. IH also increased cancellous bone mineral and volumetric bone mineral densities in the mandibular condylar head. The mandibular condylar became thinner, but the tibial cartilage did not. IH reduced maturative and increased hypertrophic chondrocytic layers of the middle and posterior mandibular cartilage. PCR showed that IH shifted proliferation and maturation in mandibular condyle fibrocartilage toward hypertrophic differentiation and ossification by downregulating TGF-β and SOX9, and upregulating collagen X. These effects were absent in the tibial growth plate hyaline cartilage. Our results showed that neonatal rats exposed to IH displayed underdeveloped mandibular ramus/condyles, while suppression of chondrogenesis marker expression was detected in the growth-restricted condylar cartilage.

scholarly journals NADPH Oxidase Is Required for the Sensory Plasticity of the Carotid Body by Chronic Intermittent Hypoxia

2009 ◽  
Vol 29 (15) ◽  
pp. 4903-4910 ◽  
Author(s):  
Y.- J. Peng ◽  
J. Nanduri ◽  
G. Yuan ◽  
N. Wang ◽  
E. Deneris ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Carotid Body ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Sensory Plasticity

scholarly journals NADPH Oxidase 2-Mediated Insult in the Auditory Cortex of Zucker Diabetic Fatty Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Zheng-De Du ◽  
Wei Wei ◽  
Shukui Yu ◽  
Qing-Ling Song ◽  
Ke Liu ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Nadph Oxidase ◽  
Auditory Cortex ◽  
Auditory System ◽  
Auditory Brainstem ◽  
Secondary Symptom ◽  
Zucker Diabetic Fatty Rats ◽  
Brainstem Response ◽  
Zdf Rats ◽  
Nadph Oxidase 2

Clinical data has confirmed that auditory impairment may be a secondary symptom of type 2 diabetes mellitus (T2DM). However, mechanisms underlying pathologic changes that occur in the auditory system, especially in the central auditory system (CAS), remain poorly understood. In this study, Zucker diabetic fatty (ZDF) rats were used as a T2DM rat model to observe ultrastructural alterations in the auditory cortex and investigate possible mechanisms underlying CAS damage in T2DM. The auditory brainstem response (ABR) of ZDF rats was found to be markedly elevated in low (8 kHz) and high (32 kHz) frequencies. Protein expression of NADPH oxidase 2 (NOX2) and its matching subunits P22phox, P47phox, and P67phox was increased in the auditory cortex of ZDF rats. Expression of 8-hydroxy-2-deoxyguanosine (8-OHdG), a marker of DNA oxidative damage, was also increased in the neuronal mitochondria of the auditory cortex of ZDF rats. Additionally, decreases in the mitochondrial total antioxidant capabilities (T-AOC), adenosine triphosphate (ATP) production, and mitochondrial membrane potential (MMP) were detected in the auditory cortex of ZDF rats, suggesting mitochondrial dysfunction. Transmission electron microscopy results indicated that ultrastructural damage had occurred to neurovascular units and mitochondria in the auditory cortex of ZDF rats. Furthermore, cytochrome c (Cyt c) translocation from mitochondria to cytoplasm and caspase 3-dependent apoptosis were also detected in the auditory cortex of ZDF rats. Consequently, the study demonstrated that T2DM may cause morphological damage to the CAS and that NOX2-associated mitochondrial oxidative damage and apoptosis may be partly responsible for this insult.

scholarly journals Intermittent Hypoxia Affects the Spontaneous DifferentiationIn Vitroof Human Neutrophils into Long-Lived Giant Phagocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Larissa Dyugovskaya ◽  
Slava Berger ◽  
Andrey Polyakov ◽  
Peretz Lavie ◽  
Lena Lavie
Keyword(s):  
Nadph Oxidase ◽  
Intermittent Hypoxia ◽  
Oxidase Inhibitor ◽  
Human Neutrophils ◽  
Hypoxic Conditions ◽  
Oxygen Conditions ◽  
Extended Lifespan ◽  
First Time ◽  
Dose Dependent

Previously we identified, for the first time, a new small-size subset of neutrophil-derived giant phagocytes (Gϕ) which spontaneously developin vitrowithout additional growth factors or cytokines. Gϕare CD66b+/CD63+/MPO+/LC3B+and are characterized by extended lifespan, large phagolysosomes, active phagocytosis, and reactive oxygen species (ROS) production, and autophagy largely controls their formation. Hypoxia, and particularly hypoxia/reoxygenation, is a prominent feature of many pathological processes. Herein we investigated Gϕformation by applying various hypoxic conditions. Chronic intermittent hypoxia (IH) (29 cycles/day for 5 days) completely abolished Gϕformation, while acute IH had dose-dependent effects. Exposure to 24 h (56 IH cycles) decreased their size, yield, phagocytic ability, autophagy, mitophagy, and gp91-phox/p22-phoxexpression, whereas under 24 h sustained hypoxia (SH) the size and expression of LC3B and gp91-phox/p22-phoxresembled Gϕformed in normoxia. Diphenyl iodide (DPI), a NADPH oxidase inhibitor, as well as the PI3K/Akt and autophagy inhibitor LY294002 abolished Gϕformation at all oxygen conditions. However, the potent antioxidant, N-acetylcysteine (NAC) abrogated the effects of IH by inducing large CD66b+/LC3B+Gϕand increased both NADPH oxidase expression and phagocytosis. These findings suggest that NADPH oxidase, autophagy, and the PI3K/Akt pathway are involved in Gϕdevelopment.

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