Evidence map›Paper›PMID 28285347›Full record

ArticleNeurotoxicity research2017

Endothelin-1 Induces Degeneration of Cultured Motor Neurons Through a Mechanism Mediated by Nitric Oxide and PI3K/Akt Pathway.

S D'Antoni, E Ranno, M Spatuzza, S Cavallaro, M V Catania

Abstract read
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Article in Neurotoxicity research, 2017. 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
1.8field-weighted citation impact, top 16% 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, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Endothelin-1, over-expressed in SOD1Frontiers in cellular neuroscience · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. TheMolecular and cellular biology · 2018
    Article
  17. Article
  18. Review
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.

S D'AntoniInstitute of Neurological Sciences, National Research Council (CNR), Catania, Italy.
E RannoInstitute of Neurological Sciences, National Research Council (CNR), Catania, Italy.
M SpatuzzaInstitute of Neurological Sciences, National Research Council (CNR), Catania, Italy.
S CavallaroInstitute of Neurological Sciences, National Research Council (CNR), Catania, Italy.
M V CataniaInstitute of Neurological Sciences, National Research Council (CNR), Catania, Italy. mariavincenza.catania@cnr.it.ORCID http://orcid.org/0000-0002-9329-8517
Institute of Neurological Sciences · ITOasi Maria SS · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelin-1 (ET-1) is a vasoactive peptide produced by activated astrocytes and microglia and is implicated in initiating and sustaining reactive gliosis in neurodegenerative diseases. We have previously suggested that ET-1 can play a role in the pathophysiology of amyotrophic lateral sclerosis (ALS). Indeed, we reported that this peptide is abundantly expressed in reactive astrocytes in the spinal cord of SOD1-G93A mice and ALS patients and exerts a toxic effect on motor neurons (MNs) in an in vitro model of mixed spinal cord cultures enriched with reactive astrocytes. Here, we explored the possible mechanisms underlying the toxic effect of ET-1 on cultured MNs. We show that ET-1 toxicity is not directly caused by oxidative stress or activation of cyclooxygenase-2 but requires the synthesis of nitric oxide and is mediated by a reduced activation of the phosphoinositide 3-kinase pathway. Furthermore, we observed that ET-1 is also toxic for microglia, although its effect on MNs is independent of the presence of this type of glial cells. Our study confirms that ET-1 may contribute to MN death and corroborates the view that the modulation of ET-1 signaling might be a therapeutic strategy to slow down MN degeneration in ALS.

Indexed as

AnimalsAntioxidantsArabidopsis ProteinsAscorbic AcidCyclooxygenase 2Embryo, MammalianEndothelin-1FemaleGene Expression RegulationImmunoprecipitationMotor NeuronsNerve DegenerationNerve Tissue ProteinsNitric OxideNuclear ProteinsPhosphatidylinositol 3-KinasesAntioxidantsArabidopsis ProteinsAscorbic AcidCyclooxygenase 2Endothelin-1Nerve Tissue ProteinsNitric OxideNuclear ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTIC protein, ArabidopsisAmyotrophic lateral sclerosisAstrocytesEndothelinMotor neuronsNeurodegenerationNitric oxide

Identifiers

PMID28285347
OpenAlexW2594796913

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.