Evidence map›Paper›PMID 28543279›Full record

ArticleJournal of neurochemistry2017

Role of AMPA receptors in homocysteine-NMDA receptor-induced crosstalk between ERK and p38 MAPK.

Ranjana Poddar, Alexandria Chen, Lucas Winter, Sathyanarayanan Rajagopal, Surojit Paul

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  14. GluN2A-NMDA receptor-mediated sustained CaThe Journal of biological chemistry · 2019
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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

5 authors at 1 institution in 1 country.

Ranjana PoddarDepartment of Neurology, University of New Mexico Health Sciences Center, University of New Mexico, Albuquerque, New Mexico, USA.ORCID 0000-0002-8459-5560
Alexandria ChenDepartment of Neurology, University of New Mexico Health Sciences Center, University of New Mexico, Albuquerque, New Mexico, USA.
Lucas WinterDepartment of Neurology, University of New Mexico Health Sciences Center, University of New Mexico, Albuquerque, New Mexico, USA.
Sathyanarayanan RajagopalDepartment of Neurology, University of New Mexico Health Sciences Center, University of New Mexico, Albuquerque, New Mexico, USA.
Surojit PaulDepartment of Neurology, University of New Mexico Health Sciences Center, University of New Mexico, Albuquerque, New Mexico, USA.
University of New Mexico · US

Funding

Role of Brain Specific Tyrosne Phosphatase STEP in Neuroprotection and DeathR01NS059962 · NINDS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI PAUL, SUROJIT · 2008 to 2023
$5.9M
Molecular basis of hyperhomocysteinemia induced brain injury in ischemic strokeR01NS083914 · NINDS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI PODDAR, RANJANA · 2014 to 2025
$4.5M
Molecular basis of homocysteine-glutamate receptor mediated neuronal cell deathR21NS065343 · NINDS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI PODDAR, RANJANA · 2011 to 2012
$415k
NINDS NIH HHS R01 NS059962NINDS NIH HHS R01 NS083914NINDS NIH HHS R21 NS065343
6 · The paper itself

Abstract

Homocysteine, a metabolite of the methionine cycle has been reported to play a role in neurotoxicity through activation of N-methyl-d-aspartate receptors (NMDAR)-mediated signaling pathway. The proposed mechanisms associated with homocysteine-NMDAR-induced neurotoxicity involve a unique signaling pathway that triggers a crosstalk between extracellular signal-regulated kinase (ERK) and p38 MAPKs, where activation of p38 MAPK is downstream of and dependent on ERK MAPK. However, the molecular basis of the ERK MAPK-mediated p38 MAPK activation is not understood. This study investigates whether α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) play a role in facilitating the ERK MAPK-mediated p38 MAPK activation. Using surface biotinylation and immunoblotting approaches we show that treatment with homocysteine leads to a decrease in surface expression of GluA2-AMPAR subunit in neurons, but have no effect on the surface expression of GluA1-AMPAR subunit. Inhibition of NMDAR activation with D-AP5 or ERK MAPK phosphorylation with PD98059 attenuates homocysteine-induced decrease in surface expression of GluA2-AMPAR subunit. The decrease in surface expression of GluA2-AMPAR subunit is associated with p38 MAPK phosphorylation, which is inhibited by 1-napthyl acetyl spermine trihydrochloride (NASPM), a selective antagonist of GluA2-lacking Ca

Indexed as

alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsCell DeathExtracellular Signal-Regulated MAP KinasesHippocampusHomocysteineNeuronsN-Methylaspartatep38 Mitogen-Activated Protein KinasesRatsReceptors, AMPAReceptors, N-Methyl-D-AspartateSignal Transductionalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidExtracellular Signal-Regulated MAP KinasesHomocysteineN-Methylaspartatep38 Mitogen-Activated Protein KinasesReceptors, AMPAReceptors, N-Methyl-D-AspartateERK MAPKGluA2-AMPA receptorshomocysteineneurotoxicityNMDA receptorsp38 MAPK

Identifiers

PMID28543279
PMCPMC5554079
OpenAlexW2620020604

What OpenQuestion holds

Textmetadata
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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.