Evidence map›Paper›PMID 29808713›Full record

ArticleCell transplantation2018

Age-related Beta-synuclein Alters the p53/Mdm2 Pathway and Induces the Apoptosis of Brain Microvascular Endothelial Cells In Vitro.

Katrin Brockhaus, Michael R R Böhm, Harutyun Melkonyan, Solon Thanos

Open access · goldAbstract read
In one paragraph

Article in Cell transplantation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Hydrogen Sulfide andJournal of ophthalmology · 2020
    Article
  11. Considering the Role of Murine Double Minute 2 in the Cardiovascular System?Frontiers in cell and developmental biology · 2019
    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

4 authors at 2 institutions in 1 country.

Katrin Brockhaus1 Institute of Experimental Ophthalmology, School of Medicine, Westphalian Wilhelm University of Münster, Münster, Germany.
Michael R R Böhm1 Institute of Experimental Ophthalmology, School of Medicine, Westphalian Wilhelm University of Münster, Münster, Germany.
Harutyun Melkonyan2 Department of Ophthalmology, Essen University Hospital, Essen, Germany.
Solon Thanos2 Department of Ophthalmology, Essen University Hospital, Essen, Germany.
Essen University Hospital · DEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased β-synuclein (Sncb) expression has been described in the aging visual system. Sncb functions as the physiological antagonist of α-synuclein (Snca), which is involved in the development of neurodegenerative diseases, such as Parkinson's and Alzheimer's diseases. However, the exact function of Sncb remains unknown. The aim of this study was to elucidate the age-dependent role of Sncb in brain microvascular endothelial cells (BMECs). BMECs were isolated from the cortices of 5- to 9-d-old Sprague-Dawley rats and were cultured with different concentrations of recombinant Sncb (rSncb) up to 72 h resembling to some degree age-related as well as pathophysiological conditions. Viability, apoptosis, expression levels of Snca, and the members of phospholipase D2 (Pld2)/ p53/ Mouse double minute 2 homolog (Mdm2)/p19(Arf) pathway, response in RAC-alpha serine/threonine-protein kinase (Akt), and stress-mediating factors such as heme oxygenase (decycling) 1 (Hmox) and Nicotinamide adenine dinucleotide phosphate oxygenase 4 (Nox4) were examined. rSncb-induced effects were confirmed through Sncb small interfering RNA (siRNA) knockdown in BMECs. We demonstrated that the viability decreases, while the rate of apoptosis underly dose-dependent alterations. For example, apoptosis increases in BMECs following the treatment with higher dosed rSncb. Furthermore, we observed a decrease in Snca immunostaining and messenger RNA (mRNA) levels following the exposure to higher rScnb concentrations. Akt was shown to be downregulated and pAkt upregulated by this treatment, which was accompanied by a dose-independent increase in p19(Arf) levels and enhanced intracellular Mdm2 translocation in contrast to a dose-dependent p53 activation. Moreover, Pld2 activity was shown to be induced in rSncb-treated BMECs. The expression of Hmox and Nox4 after Sncb treatment was altered on BEMCs. The obtained results demonstrate dose-dependent effects of Sncb on BMECs in vitro. For example, the p53-mediated and Akt-independent apoptosis together with the stress-mediated response of BMECs related to exposure of higher SNCB concentrations may reflect the increase in Sncb with duration of culture as well as its impact on cell decay. Further studies, expanding on the role of Sncb, may help understand its role in the neurodegenerative diseases.

Indexed as

ApoptosisSignal TransductionAgingalpha-SynucleinAnimalsbeta-SynucleinBrainCell SurvivalCyclin-Dependent Kinase Inhibitor p19Endothelial CellsFemaleHeme Oxygenase-1MicrovesselsNADPH Oxidase 4Phospholipase DPhosphorylationalpha-Synucleinbeta-SynucleinCyclin-Dependent Kinase Inhibitor p19Heme Oxygenase-1NADPH Oxidase 4Phospholipase Dphospholipase D2Proto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mdm2Recombinant ProteinsTumor Suppressor Protein p53agingbrain microvascular endothelial cellMdm2p53synucleins

Identifiers

PMID29808713
PMCPMC6047277
OpenAlexW2806765446

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.