Evidence map›Paper›PMID 24948534›Full record

ArticleNeuromolecular medicine2014

The Aβ peptides-activated calcium-sensing receptor stimulates the production and secretion of vascular endothelial growth factor-A by normoxic adult human cortical astrocytes.

Ilaria Dal Prà, Ubaldo Armato, Franco Chioffi, Raffaella Pacchiana, James F Whitfield, Balu Chakravarthy, Li Gui, Anna Chiarini

Abstract read
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In one paragraph

Article in Neuromolecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  8. Renal CaInternational journal of molecular sciences · 2019
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  15. Pathogenic role of calcium-sensing receptors in the development and progression of pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
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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

8 authors at 4 institutions in 3 countries.

Ilaria Dal PràHistology and Embryology Section, Department of Life and Reproduction Sciences, University of Verona Medical School, 8 Strada Le Grazie, 37134, Verona, Italy, ippdalpra@gmail.com.
Ubaldo Armato
Franco Chioffi
Raffaella Pacchiana
James F Whitfield
Balu Chakravarthy
Li Gui
Anna Chiarini
University of Verona · ITNational Research Council Canada · CAOspedale Santa Chiara · ITSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The excess vascular endothelial growth factor (VEGF) produced in the Alzheimer's disease (AD) brain can harm neurons, blood vessels, and other components of the neurovascular units (NVUs). But could astrocytes partaking in networks of astrocyte-neuron teams and connected to blood vessels of NVUs contribute to VEGF production? We have shown with cultured cerebral cortical normal (i.e., untransformed) adult human astrocytes (NAHAs) that exogenous amyloid-β peptides (Aβs) stimulate the astrocytes to make and secrete large amounts of Aβs and nitric oxide by a mechanism mediated through the calcium-sensing receptor (CaSR). Here, we report that exogenous Aβs stimulate the NAHAs to produce and secrete even VEGF-A through a CaSR-mediated mechanism. This is indicated by the ability of Aβs to specifically bind the CaSR, and the capability of a CaSR activator, the "calcimimetic" NPS R-568, to imitate, and of the CaSR antagonist, "calcilytic" NPS 2143, to inhibit, the Aβs stimulation of VEGF-A production and secretion by the NAHAs. Thus, Aβs that accumulate in the AD brain may make the astrocytes that envelop and functionally collaborate with neurons into multi-agent AD-driving "machines" via a CaSR signaling mechanism(s). These observations suggest the possibility that CaSR allosteric antagonists such as NPS 2143 might impede AD progression.

Indexed as

AdultAllosteric RegulationAlzheimer DiseaseAmyloid beta-PeptidesAniline CompoundsAstrocytesCalciumCell CommunicationCells, CulturedHumansHypoxia-Inducible Factor 1, alpha SubunitNaphthalenesNeuronsNitric OxidePeptide FragmentsPhenethylaminesAmyloid beta-Peptidesamyloid beta-protein (1-42)amyloid beta-protein (25-35)Aniline CompoundsCalciumCASR protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitN-(2-chlorophenylpropyl)-1-(3-methoxyphenyl)ethylamineN-(2-hydroxy-3-(2-cyano-3-chlorophenoxy)propyl)-1,1-dimethyl-2-(2-nephthyl)ethylamineNaphthalenesNitric OxidePeptide FragmentsPhenethylaminesPropylaminesReceptors, Calcium-SensingVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID24948534
OpenAlexW2006558268

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.