Evidence map›Paper›PMID 25579226›Full record

ArticleMolecular and cellular neurosciences2015

Release of mitochondrial Opa1 following oxidative stress in HT22 cells.

Thomas H Sanderson, Sarita Raghunayakula, Rita Kumar

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

  1. Mitochondrial membrane potential and oxidative stress interact to regulate Oma1-dependent processing of Opa1 and mitochondrial dynamics.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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  18. Decreased ceramide underlies mitochondrial dysfunction in Charcot-Marie-Tooth 2F.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
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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

3 authors at 1 institution in 1 country.

Thomas H SandersonDepartment of Emergency Medicine, Wayne State University School of Medicine, 550 E. Canfield, Detroit, MI, USA; Cardiovascular Research Institute, Wayne State University School of Medicine, 540 E. Canfield, Detroit, MI, USA; Department of Physiology, Wayne State University School of Medicine, 550 E. Canfield, Detroit, MI, USA.
Sarita RaghunayakulaDepartment of Emergency Medicine, Wayne State University School of Medicine, 550 E. Canfield, Detroit, MI, USA.
Rita KumarDepartment of Emergency Medicine, Wayne State University School of Medicine, 550 E. Canfield, Detroit, MI, USA; Cardiovascular Research Institute, Wayne State University School of Medicine, 540 E. Canfield, Detroit, MI, USA; Department of Physiology, Wayne State University School of Medicine, 550 E. Canfield, Detroit, MI, USA. Electronic address: rkumar@med.wayne.edu.
Wayne State University · US

Funding

Mitochondrial Integrity Regulates Cerebral Reperfusion InjuryR01NS076715 · NINDS · WAYNE STATE UNIVERSITY · PI KUMAR, RITA, SANDERSON, THOMAS HUDSON · 2013 to 2017
$1.7M
NINDS NIH HHS NS076715NINDS NIH HHS R01 NS076715
6 · The paper itself

Abstract

Cellular mechanisms involved in multiple neurodegenerative diseases converge on mitochondria to induce overproduction of reactive oxygen species, damage to mitochondria, and subsequent cytochrome c release. Little is currently known regarding the contribution mitochondrial dynamics play in cytochrome c release following oxidative stress in neurodegenerative disease. Here we induced oxidative stress in the HT22 cell line with glutamate and investigated key mediators of mitochondrial dynamics to determine the role this process may play in oxidative stress induced neuronal death. We report that glutamate treatment in HT22 cells induces increase in reactive oxygen species (ROS), release of the mitochondrial fusion protein Opa1 into the cytosol, with concomitant release of cytochrome c. Furthermore, following the glutamate treatment alterations in cell signaling coincide with mitochondrial fragmentation which culminates in significant cell death in HT22 cells. Finally, we report that treatment with the antioxidant tocopherol attenuates glutamate induced-ROS increase, release of mitochondrial Opa1 and cytochrome c, and prevents cell death.

Indexed as

Oxidative StressAnimalsAntioxidantsCell LineGTP PhosphohydrolasesMiceMitochondriaTocopherolsAntioxidantsGTP PhosphohydrolasesOpa1 protein, mouseTocopherolsCytochrome cGlutamateHT22Mitochondrial dynamics: mitochondriaNeurodegenerationOxidative stress

Identifiers

PMID25579226
PMCPMC4429534
OpenAlexW2016239388

What OpenQuestion holds

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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.