Evidence map›Paper›PMID 30264903›Full record

ArticleBrain and behavior2018

Protective effect of docosahexaenoic acid on lipotoxicity-mediated cell death in Schwann cells: Implication of PI3K/AKT and mTORC2 pathways.

Magda Descorbeth, Karen Figueroa, Miguel Serrano-Illán, Marino De León

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

19 citing papers in PubMed, 32 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

4 authors at 1 institution in 1 country.

Magda DescorbethCenter for Health Disparities and Molecular Medicine and Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California.
Karen FigueroaCenter for Health Disparities and Molecular Medicine and Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California.
Miguel Serrano-IllánCenter for Health Disparities and Molecular Medicine and Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California.
Marino De LeónCenter for Health Disparities and Molecular Medicine and Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California.ORCID 0000-0001-6576-785X
Loma Linda University · US

Funding

NIH-LLU Initiative for Maximizing Student DiversityR25GM060507 · NIGMS · LOMA LINDA UNIVERSITY · PI DE LEON, MARINO · 2001 to 2022
$11.3M
Research Training/Education CoreP20MD006988 · NIMHD · LOMA LINDA UNIVERSITY · PI DE LEON, MARINO · 2012 to 2016
$6.2M
NIGMS NIH HHS R25 GM060507NIMHD NIH HHS P20 MD006988
6 · The paper itself

Abstract

BACKGROUND AND

aimDocosahexaenoic acid (DHA) exhibits neuroprotective properties and has been shown to preserve nerve cells following trauma and ischemic injury. Recently, we showed that DHA pretreatment improved locomotion and reduced neuropathic pain after acute spinal cord injury in adult rats. These improvements were associated with an increase in the levels of AKT in spinal cord injury neurons. In this study, we investigate the implication of PI3K/AKT and mTOR pathway in DHA-mediated protection of primary cultured Schwann cells (pSC) undergoing palmitic acid-induced lipotoxicity (PA-LTx).

methodsPrimary cultured Schwann cells were treated with PA (PA:BSA, 2:1) in the presence or absence of DHA (1-200 µM) for 24-48 hr. Cell viability was determined by crystal violet staining and nuclear morphology was examined using Hoechst staining.

resultsWe found that pSC cultures exposed to palmitic acid (PA) overload showed chromatin condensation, a decrease in cell viability and an inhibition of AKT phosphorylation in a time-dependent manner. Next, pSC exposed to PA overload were treated with DHA. The data show that co-treatment with DHA inhibited the loss of cell viability and apoptosis caused by PA. Moreover, treatment with DHA inhibited chromatin condensation, significantly stimulated p-AKT phosphorylation under PA-LTx condition, and DHA alone increased AKT phosphorylation. Additionally, when these pSC cultures were treated with PI3K inhibitors LY294002 and, BKM120 and mTOR inhibitors Torin 1 (mTORC1/mTORC2), but not rapamycin (mTORC1), the protective effects of DHA were not observed.

conclusionThese findings suggest PI3K/AKT and mTORC2 kinase pathways are involved in the protective function (s) of DHA in PA-induced Schwann cell death.

Indexed as

AnimalsAnimals, NewbornApoptosisCell DeathCell SurvivalDocosahexaenoic AcidsLocomotionMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2NeuronsNeuroprotective AgentsPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktRatsSchwann CellsDocosahexaenoic AcidsMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Neuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAKT phosphorylationdocosahexaenoic acidPA-induced lipotoxicityprimary cultured Schwann cells

Identifiers

PMID30264903
PMCPMC6236228
OpenAlexW2892648154

What OpenQuestion holds

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LicenceCC BY
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.