Evidence map›Paper›PMID 21075175›Full record

ArticleNeuroscience2011

Novel mechanism of increased Ca2+ release following oxidative stress in neuronal cells involves type 2 inositol-1,4,5-trisphosphate receptors.

S Kaja, R S Duncan, S Longoria, J D Hilgenberg, A J Payne, N M Desai, R A Parikh, S L Burroughs, E V Gregg, D L Goad and 1 more

Abstract read
In one paragraph

Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Dietary Alcohol Consumption Elicits Corneal Toxicity Through the Generation of Cellular Oxidative Stress.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2023
    Article
  3. Frontiers in cellular neuroscience · 2022
    Article
  4. Article
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  19. Article
  20. Polycystin-2 expression and function in adult mouse lacrimal acinar cells.Investigative ophthalmology & visual science · 2011
    Article
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

11 authors at 1 institution in 1 country.

S KajaDepartment of Ophthalmology and BasicMedical Science, University of Missouri, Kansas City, MO 64108, USA. kajas@umkc.edu
R S Duncan
S Longoria
J D Hilgenberg
A J Payne
N M Desai
R A Parikh
S L Burroughs
E V Gregg
D L Goad
P Koulen
University of Missouri–Kansas City · US

Funding

Protein Targets of Oxidative Brain AgingP01AG022550 · NIA · WEST VIRGINIA UNIVERSITY · PI SIMPKINS, JAMES W. · 2003 to 2013
$15.7M
System Gene Delivery for Alzheimer's Disease- SupplementP01AG010485 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI ZOLOTUKHIN, SERGEI · 1991 to 2009
$11.3M
ROLE OF MITHOCHONDRIAL ERB IN NEURONAL VULNDERABILITY TO NEUROTOXIC STRESSP01AG027956 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI SINGH, MEHARVAN · 2007 to 2017
$11.3M
Visceral Fat & Lipid & Inflammatory Risk factors: Role of EthnicityP20MD001633 · NIMHD · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI GONZALEZ, ADELA · 2005 to 2009
$7.1M
Mechanisms of calcium signaling in retinal neuronsR01EY014227 · NEI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI KOULEN, PETER · 2003 to 2006
$1.6M
Confocal Laser Scanning MicroscopeS10RR027093 · NCRR · UNIVERSITY OF MISSOURI KANSAS CITY · PI KOULEN, PETER · 2010 to 2010
$497k
CONFOCAL MICROSCOPE FOR CAMPUS EXPANSION IN THE CBH BUILDING: NEUROSCIENCES10RR022570 · NCRR · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI KOULEN, PETER · 2006 to 2006
$356k
NCRR NIH HHS RR022570NCRR NIH HHS RR027093NCRR NIH HHS S10 RR022570NCRR NIH HHS S10 RR027093NEI NIH HHS EY014227NEI NIH HHS R01 EY014227NIA NIH HHS AG010485NIA NIH HHS AG022550NIA NIH HHS AG027956NIA NIH HHS P01 AG010485NIA NIH HHS P01 AG022550NIA NIH HHS P01 AG027956NIMHD NIH HHS P20 MD001633NIMHD NIH HHS P20-MD001633
6 · The paper itself

Abstract

Dysregulation of Ca(2+) signaling following oxidative stress is an important pathophysiological mechanism of many chronic neurodegenerative disorders, including Alzheimer's disease, age-related macular degeneration, glaucomatous and diabetic retinopathies. However, the underlying mechanisms of disturbed intracellular Ca(2+) signaling remain largely unknown. We here describe a novel mechanism for increased intracellular Ca(2+) release following oxidative stress in a neuronal cell line. Using an experimental approach that included quantitative polymerase chain reaction, quantitative immunoblotting, microfluorimetry and the optical imaging of intracellular Ca(2+) release, we show that sub-lethal tert-butyl hydroperoxide-mediated oxidative stress result in a selective up-regulation of type-2 inositol-1,4,5,-trisphophate receptors. This oxidative stress mediated change was detected both at the transcriptional and translational level and functionally resulted in increased Ca(2+) release into the nucleoplasm from the membranes of the nuclear envelope at a given receptor-specific stimulus. Our data describe a novel source of Ca(2+) dysregulation induced by oxidative stress with potential relevance for differential subcellular Ca(2+) signaling specifically within the nucleus and the development of novel neuroprotective strategies in neurodegenerative disorders.

Indexed as

AnimalsCalciumCalcium SignalingCell LineInositol 1,4,5-Trisphosphate ReceptorsIntracellular FluidIntracellular SpaceMiceModels, NeurologicalNerve DegenerationNeuronsOxidative Stresstert-ButylhydroperoxideUp-RegulationCalciumInositol 1,4,5-Trisphosphate Receptorstert-Butylhydroperoxide

Identifiers

PMID21075175
PMCPMC3038464
OpenAlexW2023682415

What OpenQuestion holds

Textmetadata
LicenceTDM
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.