Evidence map›Paper›PMID 20812867›Full record

ArticleAntioxidants & redox signaling2011

Pathophysiologically relevant levels of hydrogen peroxide induce glutamate-independent neurodegeneration that involves activation of transient receptor potential melastatin 7 channels.

Emily Coombes, Jie Jiang, Xiang-Ping Chu, Koichi Inoue, Joshua Seeds, Deborah Branigan, Roger P Simon, Zhi-Gang Xiong

Open access · greenAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 60 citations in OpenAlex.

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  12. Roles of TRP Channels in Neurological Diseases.Oxidative medicine and cellular longevity · 2020
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Emily CoombesRobert S. Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon, USA.
Jie Jiang
Xiang-Ping Chu
Koichi Inoue
Joshua Seeds
Deborah Branigan
Roger P Simon
Zhi-Gang Xiong
Legacy Health · USGuangdong General Hospital · CN

Funding

Acid-sensing channels as novel target for brain ischemiaR01NS047506 · NINDS · MOREHOUSE SCHOOL OF MEDICINE · PI XIONG, ZHIGANG · 2004 to 2010
$1.7M
A novel cation channel in excitatory neuronal injuryR01NS049470 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI XIONG, ZHIGANG · 2005 to 2008
$1.2M
Acid-sensing channels as novel target for brain ischemiaR56NS047506 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI XIONG, ZHIGANG · 2009 to 2009
$394k
NINDS NIH HHS R01 NS047506NINDS NIH HHS R01 NS049470NINDS NIH HHS R01NS47506NINDS NIH HHS R01NS49470NINDS NIH HHS R56 NS047506
6 · The paper itself

Abstract

Stroke/brain ischemia is a leading cause of death and long-term disabilities. Increased oxidative stress plays an important role in the pathology of brain ischemia. Hydrogen peroxide (H(2)O(2)) is a major oxidant known to cause neuronal injury; however, the detailed mechanism remains unclear. Previous studies have suggested that H(2)O(2)-induced injury is associated with increased intracellular Ca(2+), mediated by glutamate receptors or voltage-gated Ca(2+) channels. Here, we demonstrate that, at concentrations relevant to stroke, H(2)O(2) induces a Ca(2+)-dependent injury of mouse cortical neurons in the absence of activation of these receptors/channels. With the culture medium containing blockers of glutamate receptors and voltage-gated Ca(2+) channels, brief exposure of neurons to H(2)O(2) induced a dose-dependent injury. Reducing [Ca(2+)](e) inhibited whereas increasing [Ca(2+)](e) potentiated the H(2)O(2) injury. Fluorescent Ca(2+) imaging confirmed the increase of [Ca(2+)](i) by H(2)O(2) in the presence of the blockers of glutamate receptors and voltage-gated Ca(2+) channels. Addition of 2-aminoethoxydiphenyl borate, an inhibitor of transient receptor potential melastatin 7 (TRPM7) channels, or the use of TRPM7-small interference RNA, protected the neurons from H(2)O(2) injury. In contrast, overexpressing TRPM7 channels in human embryonic kidney 293 cells increased H(2)O(2) injury. Our findings indicate that H(2)O(2) can induce Ca(2+) toxicity independent of glutamate receptors and voltage-gated Ca(2+) channels. Activation of TRPM7 channels is involved in such toxicity.

Indexed as

AnimalsCalcium ChannelsCells, CulturedCerebral CortexGlutamic AcidHydrogen PeroxideMiceNerve DegenerationNeuronsReceptors, GlutamateRNA, Small InterferingTRPM Cation ChannelsCalcium ChannelsGlutamic AcidHydrogen PeroxideReceptors, GlutamateRNA, Small InterferingTrpm7 protein, mouseTRPM Cation Channels

Identifiers

PMID20812867
PMCPMC3078500
OpenAlexW2065748878

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.