Evidence map›Paper›PMID 27546824›Full record

ArticleNeuroscience letters2016

Neuroprotective effects of LMW and HMW FGF2 against amyloid beta toxicity in primary cultured hippocampal neurons.

Yong Cheng, Zhaojin Li, Elissavet Kardami, Y Peng Loh

Abstract read
In one paragraph

Article in Neuroscience letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Heliyon · 2021
    Article
  4. Article
  5. Inhibition of FGF Receptor-1 Suppresses Alcohol Consumption: Role of PI3 Kinase Signaling in Dorsomedial Striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  6. Article
  7. Review
  8. 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

4 authors at 2 institutions in 2 countries.

Yong ChengSection on Cellular Neurobiology, Program on Developmental Neuroscience, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Zhaojin LiSection on Cellular Neurobiology, Program on Developmental Neuroscience, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Elissavet KardamiInstitute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, University of Manitoba, Winnipeg, Manitoba, Canada.
Y Peng LohSection on Cellular Neurobiology, Program on Developmental Neuroscience, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: lohp@mail.nih.gov.
National Institutes of Health · USUniversity of Manitoba · CA

Funding

Neuropeptides and Carboxypeptidase E/ Neurotrophic Factor-alpha1 in Neural and Cognitive FunctionsZIAHD000056 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI LOH, Y. PENG · 2009 to 2025
$21.3M
BIOSYNTHESIS, PROCESSING &SECRETION OF NEUROPEPTIDES &PITUITARY PEPTIDE HORMONEZ01HD000056 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI LOH, YOKE P · 1985 to 2008
$2.6M
Intramural NIH HHS Z01 HD000056
6 · The paper itself

Abstract

Basic Fibroblast growth factor (FGF2) is important in development and maintenance of central nervous system function. Studies have demonstrated that low molecular weight (LMW) FGF2 is a neuroprotective factor against various insults in vivo and in vitro. In the present study we investigated the neuroprotective effects of high molecular weight (HMW) and LMW FGF2 against amyloid beta-induced neurotoxicity. The results showed that both LMW and HMW FGF2 attenuated the amyloid beta toxicity in the primary cultured hippocampal neurons as measured by WST and LDH release assay. Moreover, the analysis suggested that HMW FGF2 had stronger neuroprotective effect than LMW FGF2. We then demonstrated that LMW and HMW FGF2 activated the ERK and AKT signaling pathways in a similar way. Furthermore, using the ERK inhibitor and AKT inhibitor, we found that the AKT signaling but not ERK signaling pathway was required for the neuroprotective effects of FGF2. Taken together, these results showed the neuroprotective effects of different forms of FGF2 in an AD model and the mechanism underlying the neuroprotection.

Indexed as

Amyloid beta-PeptidesAnimalsCells, CulturedFibroblast Growth Factor 2HippocampusMolecular WeightNeuronsNeuroprotective AgentsPhosphorylationProtein IsoformsProto-Oncogene Proteins c-aktSignal TransductionAmyloid beta-PeptidesFibroblast Growth Factor 2Neuroprotective AgentsProtein IsoformsProto-Oncogene Proteins c-aktAKTAmyloid betaHippocampal neuronHMW FGF2LMW FGF2

Identifiers

PMID27546824
PMCPMC5042867
OpenAlexW2510312461

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.