Evidence map›Paper›PMID 27184385›Full record

ArticleScientific reports2016

Vitamin-D receptor agonist calcitriol reduces calcification in vitro through selective upregulation of SLC20A2 but not SLC20A1 or XPR1.

M P Keasey, R R Lemos, T Hagg, J R M Oliveira

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 30 citations in OpenAlex.

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  10. Intracranial Calcification and Seizure with Down Syndrome: A Case Report.JNMA; journal of the Nepal Medical Association · 2022
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  12. Developmental Changes in Phosphate Homeostasis.Reviews of physiology, biochemistry and pharmacology · 2021
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  13. Frontiers in genetics · 2021
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  15. Review
  16. A likely pathogenic variant in theAnnals of clinical and translational neurology · 2019
    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

4 authors at 2 institutions in 2 countries.

M P KeaseyDepartment of Biomedical Sciences - Quillen College of Medicine, East Tennessee State University, Johnson City, USA.
R R LemosKeizo Asami Laboratory - Federal University of Pernambuco, Recife-PE, Brazil.
T HaggDepartment of Biomedical Sciences - Quillen College of Medicine, East Tennessee State University, Johnson City, USA.
J R M OliveiraKeizo Asami Laboratory - Federal University of Pernambuco, Recife-PE, Brazil.
East Tennessee State University · USUniversidade Federal de Pernambuco · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vitamin D deficiency (hypovitaminosis D) causes osteomalacia and poor long bone mineralization. In apparent contrast, hypovitaminosis D has been reported in patients with primary brain calcifications ("Fahr's disease"). We evaluated the expression of two phosphate transporters which we have found to be associated with primary brain calcification (SLC20A2, whose promoter has a predicted vitamin D receptor binding site, and XPR1), and one unassociated (SLC20A1), in an in vitro model of calcification. Expression of all three genes was significantly decreased in calcifying human bone osteosarcoma (SaOs-2) cells. Further, we confirmed that vitamin D (calcitriol) reduced calcification as measured by Alizarin Red staining. Cells incubated with calcitriol under calcifying conditions specifically maintained expression of the phosphate transporter SLC20A2 at higher levels relative to controls, by RT-qPCR. Neither SLC20A1 nor XPR1 were affected by calcitriol treatment and remained suppressed. Critically, knockdown of SLC20A2 gene and protein with CRISPR technology in SaOs2 cells significantly ablated vitamin D mediated inhibition of calcification. This study elucidates the mechanistic importance of SLC20A2 in suppressing the calcification process. It also suggests that vitamin D might be used to regulate SLC20A2 gene expression, as well as reduce brain calcification which occurs in Fahr's disease and normal aging.

Indexed as

Ascorbic AcidCalcinosisCalcitriolCell DifferentiationCell Line, TumorCRISPR-Cas SystemsGene Knockdown TechniquesGlycerophosphatesHumansModels, BiologicalPhosphate Transport ProteinsReceptors, CalcitriolReceptors, G-Protein-CoupledReceptors, VirusRNA, MessengerSodium-Phosphate Cotransporter Proteins, Type IIIAscorbic Acidbeta-glycerophosphoric acidCalcitriolGlycerophosphatesPhosphate Transport ProteinsReceptors, CalcitriolReceptors, G-Protein-CoupledReceptors, VirusRNA, MessengerSLC20A1 protein, humanSLC20A2 protein, humanSodium-Phosphate Cotransporter Proteins, Type IIIXenotropic and Polytropic Retrovirus ReceptorXPR1 protein, human

Identifiers

PMID27184385
PMCPMC4868979
OpenAlexW2401543637

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.