Hydrogen peroxide mediated the neurotoxicity of an antibody against plasmalemmal neuronspecific enolase in primary cortical neurons

Yamamoto, Yasuhiro; Koma, Hiromi; Yagami, Tatsurou

doi:10.1016/j.neuro.2015.05.008

Cited by 16 publications

(22 citation statements)

References 32 publications

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“…30) Briefly, cells were seeded into 24-well plates at a density of 25000 cells/cm 2 . Neurons were treated without or with normal goat IgG (sc-2028) or anti-Hsp70 antibody (sc-1016) in the absence or presence of catalase.…”

Section: Methodsmentioning

confidence: 99%

Anti-heat Shock 70 kDa Protein Antibody Induced Neuronal Cell Death

Yamamoto

Koma

Nishii

et al. 2017

Biological & Pharmaceutical Bulletin

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Section: Methodsmentioning

confidence: 99%

Anti-heat Shock 70 kDa Protein Antibody Induced Neuronal Cell Death

Yamamoto

Koma

Nishii

et al. 2017

Biological & Pharmaceutical Bulletin

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“…DIDS Enhanced the 15d-PGJ 2 -Activated Caspase-3 Caspase-3 activation is known as a biochemical marker of apoptosis. 26) Since DIDS-induced apoptosis is accompanied with the caspase-3 activation in hippocampal neurons, 2) we measured caspase-3 activity to confirm whether DIDS induced neuronal apoptosis in cortical neurons (Fig. 5).…”

Section: Dids Exhibited Neurotoxicity In the Primary Culture Of Corticalmentioning

confidence: 99%

“…DIDS Enhanced the 15d-PGJ 2 -Condensed Chromatin Chromatin condensation is another biochemical marker of apoptosis. 26) To ascertain whether DIDS induced neuronal cell death via apoptosis or not, we stained nuclei by Hoechst33342 (Fig. 6).…”

Section: Dids Exhibited Neurotoxicity In the Primary Culture Of Corticalmentioning

confidence: 99%

4,4-Diisothiocyanatostilbene Disulfonic Acid Enhanced 15-Deoxy-Δ<sup>12,14</sup>-prostaglandin J<sub>2</sub>-Induced Neuronal Apoptosis

Koma

Yamamoto

Kumagai

et al. 2019

Biological & Pharmaceutical Bulletin

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4,4-Diisothiocyanatostilbene disulfonic acid (DIDS), an antagonist of anion channel including voltage-dependent anion channel (VDAC), acts as both neurotoxicant and neuroprotectant, resulting in the controversy. VDAC contributes to neuronal apoptosis and is a candidate target protein of 15-deoxy-Δ 12,14-prostaglandin J 2 (15d-PGJ 2). Caspase-3 is activated during neuronal apoptosis caused by 15d-PGJ 2. In the present study, we ascertained whether DIDS was neuroprotective or neurotoxic in the primary culture of rat cortical neurons. Neuronal cell viabilities were primarily evaluated by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H tetrazolium bromide (MTT) reduction assay. Plasma membrane integrity and apoptosis were detected by the staining of propidium iodide (PI) and Hoechst33342, respectively. Alternatively, apoptosis was also measured by caspase-3 assay kit. DIDS did not prevent neurons from undergoing the 15d-PGJ 2-induced apoptosis. In contrast, DIDS caused neuronal cell death in a concentration-dependent manner by itself, confirming its neurotoxicity. The sublethal application of DIDS did not decrease MTT-reducing activity, increase caspase-3 activity, condense chromatin, allow PI to enter neuron and degenerate neuronal morphology significantly. Interestingly, DIDS enhanced the 15d-PGJ 2-induced neuronal apoptosis markedly under the sublethal condition. To our knowledge, this is the first report of synergistic effects of DIDS on the neurotoxicity of 15d-PGJ 2. Key words primary cortical neuron; 15-deoxy-Δ 12,14-prostaglandin J 2 ; apoptosis; 4,4-diisothiocyanatostilbene disulfonic acid; voltage-dependent anion channel

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“…Vitamin C Harrison and May, 25 Singh et al, 26 Martin et al, 27 Calabrese et al, 29 Heo & Lee, 28 Lewis et al, 30 and Devore et al 34 β Carotenes (vitamin A) Singh et al, 26 Sommer, 32 Yamamoto et al, 33 Devore et al, 34 and Reddy 35…”

Section: And Ulatowski and Manor 22mentioning

confidence: 99%

Neuroprotective effects of antioxidants in the management of neurodegenerative disorders: A literature review

Panahi

Rajaee

Johnston

et al. 2018

J of Cellular Biochemistry

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It is proven that oxidative stress has a pivotal role in the process of neurodegeneration. The use of antioxidants is an attractive method to prevent the incidence of neurodegenerative diseases. We searched major databases (PubMed, Med Line and Google Scholar) using the keywords of neurodegeneration, oxidative stress, and antioxidant for both review and original studies which have reported the various beneficial effects of antioxidants. About 70 studies were identified for this review. Among various antioxidants, 9 antioxidants with the most applications in research investigations were selected and the major findings concerning their protective effects were reviewed. It is concluded that antioxidants can modify and re-adjust the oxidative stress in the biological milieu, elicit neuroprotective effects, and positively impact themanagement of neurodegenerative processes. This article is protected by copyright. All rights reserved.

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Hydrogen peroxide mediated the neurotoxicity of an antibody against plasmalemmal neuronspecific enolase in primary cortical neurons

Cited by 16 publications

References 32 publications

Anti-heat Shock 70 kDa Protein Antibody Induced Neuronal Cell Death

Anti-heat Shock 70 kDa Protein Antibody Induced Neuronal Cell Death

4,4-Diisothiocyanatostilbene Disulfonic Acid Enhanced 15-Deoxy-Δ<sup>12,14</sup>-prostaglandin J<sub>2</sub>-Induced Neuronal Apoptosis

Neuroprotective effects of antioxidants in the management of neurodegenerative disorders: A literature review

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