Evidence map›Paper›PMID 24777663›Full record

ArticleJournal of cellular physiology2014

The paracrine feedback loop between vitamin D₃ (1,25(OH)₂D₃) and PTHrP in prehypertrophic chondrocytes.

Frances C Bach, Kirsten Rutten, Kristyanne Hendriks, Frank M Riemers, Peter Cornelissen, Alain de Bruin, Ger J Arkesteijn, Richard Wubbolts, William A Horton, Louis C Penning and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. miR-195 contributes to human osteoarthritis via targeting PTHrP.Journal of bone and mineral metabolism · 2019
    Article
  9. Article
  10. Article
  11. Vitamin D and Its Effects on Articular Cartilage and Osteoarthritis.Orthopaedic journal of sports medicine · 2017
    Review
  12. Review
  13. Review
  14. Article
  15. 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

11 authors at 2 institutions in 2 countries.

Frances C BachFaculty of Veterinary Medicine, Department of Clinical Sciences of Companion Animals, Utrecht University, Utrecht, The Netherlands.
Kirsten Rutten
Kristyanne Hendriks
Frank M Riemers
Peter Cornelissen
Alain de Bruin
Ger J Arkesteijn
Richard Wubbolts
William A Horton
Louis C Penning
Marianna A Tryfonidou
Utrecht University · NLOregon Health & Science University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endocrine feedback loop between vitamin D3(1,25(OH)2D3) and parathyroid hormone (PTH) plays a central role in skeletal development. PTH-related protein (PTHrP) shares homology and its receptor (PTHR1) with PTH. The aim of this study was to investigate whether there is a functional paracrine feedback loop between 1,25(OH)2D3 and PTHrP in the growth plate, in parallel with the endocrine feedback loop between 1,25(OH)2D3 and PTH. This was investigated in ATDC5 cells treated with 10(-8) M 1,25(OH)2D3 or PTHrP, Col2-pd2EGFP transgenic mice, and primary Col2-pd2EGFP growth plate chondrocytes isolated by FACS, using RT-qPCR, Western blot, PTHrP ELISA, chromatin immunoprecipitation (ChIP) assay, silencing of the 1,25(OH)2D3 receptor (VDR), immunofluorescent staining, immunohistochemistry, and histomorphometric analysis of the growth plate. The ChIP assay confirmed functional binding of the VDR to the PTHrP promoter, but not to the PTHR1 promoter. Treatment with 1,25(OH)2D3 decreased PTHrP protein production, an effect which was prevented by silencing of the VDR. Treatment with PTHrP significantly induced VDR production, but did not affect 1α- and 24-hydroxylase expression. Hypertrophic differentiation was inhibited by PTHrP and 1,25(OH)2D3 treatment. Taken together, these findings indicate that there is a functional paracrine feedback loop between 1,25(OH)2D3 and PTHrP in the growth plate. 1,25(OH)2D3 decreases PTHrP production, while PTHrP increases chondrocyte sensitivity to 1,25(OH)2D3 by increasing VDR production. In light of the role of 1,25(OH)2D3 and PTHrP in modulating chondrocyte differentiation, 1,25(OH)2D3 in addition to PTHrP could potentially be used to prevent undesirable hypertrophic chondrocyte differentiation during cartilage repair or regeneration.

Indexed as

AnimalsCell DifferentiationCholecalciferolChondrocytesFeedback, PhysiologicalGene Expression Regulation, DevelopmentalGrowth PlateHumansMiceParacrine CommunicationParathyroid Hormone-Related ProteinReceptor, Parathyroid Hormone, Type 1CholecalciferolParathyroid Hormone-Related ProteinPTH1R protein, humanReceptor, Parathyroid Hormone, Type 1

Identifiers

PMID24777663
PMCPMC4298802
OpenAlexW1571140927

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.