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Malgrange, Brigitte; Rogister, Bernard; Lefèbvre, Philippe; Mazy-Servais, Cécile; Welcher, Andrew A.; Bonnet, Christophe; Hsu, Rou Yin; Rigo, Jean-Michel; Water, Thomas R. Van De; Moonen, Gustave

doi:10.1023/a:1020724506337

Cited by 41 publications

(8 citation statements)

References 19 publications

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“…Expression of NOX3 in Different Parts of the Cochlea-To identify regions of the inner ear that express NOX3, we isolated distinct parts of rat cochlea, such as organ of Corti, stria vascularis, and spiral ganglia, from newborn rats (postnatal day 0 to 4) as described previously (33). As a control tissue, we used dorsal root ganglia.…”

Section: Nox3 Is Predominantly Expressed In the Innermentioning

confidence: 99%

NOX3, a Superoxide-generating NADPH Oxidase of the Inner Ear

Bánfi

Malgrange

Knisz³

et al. 2004

Journal of Biological Chemistry

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398

360

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Reactive oxygen species (ROS) play a major role in drug-, noise-, and age-dependent hearing loss, but the source of ROS in the inner ear remains largely unknown. Herein, we demonstrate that NADPH oxidase (NOX) 3, a member of the NOX/dual domain oxidase family of NADPH oxidases, is highly expressed in specific portions of the inner ear. As assessed by real-time PCR, NOX3 mRNA expression in the inner ear is at least 50-fold higher than in any other tissues where its expression has been observed (e.g. fetal kidney, brain, skull). Microdissection and in situ hybridization studies demonstrated that NOX3 is localized to the vestibular and cochlear sensory epithelia and to the spiral ganglions. Transfection of human embryonic kidney 293 cells with NOX3 revealed that it generates low levels of ROS on its own but produces high levels of ROS upon co-expression with cytoplasmic NOX subunits. NOX3-dependent superoxide production required a stimulus in the absence of subunits and upon co-expression with phagocyte NADPH oxidase subunits p47 phox and p67 phox , but it was stimulus-independent upon co-expression with colon NADPH oxidase subunits NOX organizer 1 and NOX activator 1. Pre-incubation of NOX3-transfected human embryonic kidney 293 cells with the ototoxic drug cisplatin markedly enhanced superoxide production, in both the presence and the absence of subunits. Our data suggest that NOX3 is a relevant source of ROS generation in the cochlear and vestibular systems and that NOX3-dependent ROS generation might contribute to hearing loss and balance problems in response to ototoxic drugs.The inner ear is a highly complex structure involved in hearing and balancing. The conversion of sound into electrical signals occurs within the cochlea, in the organ of Corti, and the electrical signals are conducted by the axons of spiral ganglion neurons to the brain. The linear movement of the head is sensed by the otolith organs (utricle and saccule) and the rotation movements by the ampulla of the semicircular canals. The signals generated in the vestibular system are transmitted by the vestibular ganglion neurons to the central nervous system.Hearing impairment caused by loss of cochlear function occurs frequently, if not invariably, over a lifetime. Noise and ototoxic chemicals may lead to a precocious, rapid hearing loss, whereas aging leads to a more insidious, chronic loss of hearing. Research over the last decades has identified reactive oxygen species (ROS) 1 as the major factor mediating hearing loss (1). ROS is generated within the cochlea after exposure to ototoxic drugs (e.g. cisplatin (2, 3), aminoglycoside antibiotics (3)) or to noise (4). Signs of oxidative stress, such as DNA damage and lipid peroxidation, have been documented in vivo in response to those challenges (5, 6), as well as in cochlear aging (7). The vestibular system is also damaged by ototoxic drugs (8, 9) in a process that includes excessive ROS production (10, 11).Although the role of oxidative stress in inner ear damage is well established, its source ...

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Section: Nox3 Is Predominantly Expressed In the Innermentioning

confidence: 99%

NOX3, a Superoxide-generating NADPH Oxidase of the Inner Ear

Bánfi

Malgrange

Knisz³

et al. 2004

Journal of Biological Chemistry

Self Cite

398

360

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“…For relativistic quantum field theories, Epstein and Glaser [11] have pointed out that ultraviolet divergencies appear because of the improper splitting of operator-valued distributions into retarded and advanced part. They demonstrated that perturbation theory will remain finite if one uses the proper theory of distribution splitting [12] and causality. The details of how CPT is used in relativistic quantum electrodynamics have been explained in Ref.…”

Section: Causal Perturbation Theorymentioning

confidence: 99%

Spontaneous emission and atomic line shift in causal perturbation theory

Marzlin

Fitzgerald

2018

Journal of Mathematical Physics

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We derive spontaneous emission rate and line shift for two-level atoms coupled to the radiation field using causal perturbation theory. In this approach, employing the theory of distribution splitting prevents the occurrence of divergent integrals. Our method confirms the result for atomic decay rate but suggests that the cutoff frequency for the atomic line shift is determined by the atomic mass, rather than Bohr radius or electron mass.

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“…The RT product was amplified in the presence of primers for CNTF (30), CNTFR␣ (30), gp130 (31), and LIFR␤ (32). Control experiments were performed in parallel in the absence of the reverse transcriptase enzyme and did not produce any products.…”

Section: Rna Isolation Microarray Hybridization and Pcrmentioning

confidence: 99%

Co-administration of Ciliary Neurotrophic Factor with Its Soluble Receptor Protects against Neuronal Death and Enhances Neurite Outgrowth

Ozog¹,

Modha

Church

et al. 2008

Journal of Biological Chemistry

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Attempts to promote neuronal survival and repair with ciliary neurotrophic factor (CNTF) have met with limited success. The variability of results obtained with CNTF may, in part, reflect the fact that some of the biological actions of the cytokine are mediated by a complex formed between CNTF and its specific receptor, CNTFR␣, which exists in both membrane-bound and soluble forms. In this study, we compared the actions of CNTF alone and CNTF complexed with soluble CNTFR␣ (hereafter termed "Complex") on neuronal survival and growth. Although CNTF alone produced limited effects, Complex protected against glutamate-mediated excitotoxicity via gap junction-dependent and -independent mechanisms. Further examination revealed that only Complex promoted neurite outgrowth. Differential gene expression analysis revealed that, compared with CNTF alone, Complex differentially regulates several neuroprotective and neurotrophic genes. Collectively, these findings indicate that CNTF exerts more robust effects on neuronal survival and growth when applied in combination with its soluble receptor.

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Untitled

Cited by 41 publications

References 19 publications

NOX3, a Superoxide-generating NADPH Oxidase of the Inner Ear

NOX3, a Superoxide-generating NADPH Oxidase of the Inner Ear

Spontaneous emission and atomic line shift in causal perturbation theory

Co-administration of Ciliary Neurotrophic Factor with Its Soluble Receptor Protects against Neuronal Death and Enhances Neurite Outgrowth

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