Evidence map›Paper›PMID 26266487›Full record

ArticleJournal of molecular neuroscience : MN2015

The Interplay of Akt and ERK in Aβ Toxicity and Insulin-Mediated Protection in Primary Hippocampal Cell Culture.

Rasoul Ghasemi, Maryam Moosavi, Asadollah Zarifkar, Karim Rastegar, Nader Maghsoudi

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-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

18 citing papers in PubMed, 30 citations in OpenAlex.

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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 2 institutions in 1 country.

Rasoul GhasemiDepartment of Physiology and Neurophysiology Research Center, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Maryam MoosaviDepartment of Physiology and Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Zand Street, Shiraz, Iran. marmoosavi@sums.ac.ir.
Asadollah ZarifkarDepartment of Physiology and Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Zand Street, Shiraz, Iran. zarifkara@sums.ac.ir.
Karim RastegarDepartment of Physiology and Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Zand Street, Shiraz, Iran.
Nader MaghsoudiNeurobiology Research Center and Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Shiraz University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is not known if insulin prevents Aβ-induced cell death, MAPK, and Akt activity in isolated hippocampal cell culture. This study was aimed to explore the effect of insulin on Aβ-induced cell death and ERK and Akt signaling alteration in isolated hippocampal cell culture. Additionally, it was desirable to assess if there is any interaction between these two pathways. The hippocampal cells were derived from fetuses at the embryonic day 18-19. The cells were treated with different drugs, and MTT assay, morphological assessments, and Western blot were done. Insulin prevented Aβ-induced cell death and caspase-3 cleavage. Aβ-induced toxicity was aligned with decrement of the phosphorylated Akt (pAkt) which was prevented by insulin. The PI3 kinase inhibitor, LY294002, decreased pAkt and abolished the protective effect of insulin. Aβ exposure increased phosphorylated ERK (pERK) in parallel with cell death and apoptosis. Insulin-inhibited ERK activation (phosphorylation) induced by Aβ and PD98059 (as ERK inhibitor) did not affect the protective effect of insulin. One of the interesting finding of this study was the interplay of Akt and ERK in Aβ toxicity and insulin-mediated protection; meaning that there is an inverse relation between pERK and pAkt, in a way that PI3-Akt pathway inhibition leads to pERK increment while ERK inhibition causes Akt phosphorylation (activation). This study showed, for the first time, that insulin protects against Aβ toxicity in isolated hippocampal cell culture via modulating Akt and ERK phosphorylation and also revealed an interaction between those signals in Aβ toxicity and insulin-mediated protection.

Indexed as

Amyloid beta-PeptidesAnimalsApoptosisCaspase 3Cells, CulturedChromonesEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFlavonoidsHippocampusInsulinMAP Kinase Signaling SystemMorpholinesNerve Tissue ProteinsNeuroprotective AgentsPeptide Fragments2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAmyloid beta-Peptidesamyloid beta-protein (25-35)Caspase 3ChromonesExtracellular Signal-Regulated MAP KinasesFlavonoidsInsulinMorpholinesNerve Tissue ProteinsNeuroprotective AgentsPeptide FragmentsPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktAktAlzheimer’s diseaseBeta amyloidCaspase-3ERKHippocampal cell culture

Identifiers

PMID26266487
OpenAlexW1200555839

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.