Evidence map›Paper›PMID 28349987›Full record

ArticleScientific reports2017

Conditional Deletion of the Phd2 Gene in Articular Chondrocytes Accelerates Differentiation and Reduces Articular Cartilage Thickness.

Shaohong Cheng, Sheila Pourteymoor, Catrina Alarcon, Subburaman Mohan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. PHD1-3 oxygen sensors in vivo-lessons learned from gene deletions.Pflugers Archiv : European journal of physiology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Targeted Deletion of theFrontiers in endocrinology · 2022
    Article
  14. Review
  15. Article
  16. Article
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.

Shaohong ChengMusculoskeletal Disease Center, Veterans Affairs Loma Linda Healthcare System, 11201 Benton Street, Loma Linda, CA 92357, USA.
Sheila PourteymoorMusculoskeletal Disease Center, Veterans Affairs Loma Linda Healthcare System, 11201 Benton Street, Loma Linda, CA 92357, USA.
Catrina AlarconMusculoskeletal Disease Center, Veterans Affairs Loma Linda Healthcare System, 11201 Benton Street, Loma Linda, CA 92357, USA.
Subburaman MohanMusculoskeletal Disease Center, Veterans Affairs Loma Linda Healthcare System, 11201 Benton Street, Loma Linda, CA 92357, USA.
VA Loma Linda Healthcare System · USLoma Linda University · US

Funding

Transgenic Approaches to Evaluate IGF-I Role in Peak BMDR01AR048139 · NIAMS · LOMA LINDA VETERANS ASSN RESEARCH &EDUC · PI MOHAN, SUBBURAMAN · 2003 to 2025
$4.7M
Transgenic Approaches to Evalute IGF-1 Role in Peak BMDR56AR048139 · NIAMS · LOMA LINDA VETERANS ASSN RESEARCH & EDUC · PI MOHAN, SUBBURAMAN · 2008 to 2008
$258k
BLRD VA I01 BX001396NIAMS NIH HHS R01 AR048139NIAMS NIH HHS R56 AR048139
6 · The paper itself

Abstract

Based on our findings that PHD2 is a negative regulator of chondrocyte differentiation and that hypoxia signaling is implicated in the pathogenesis of osteoarthritis, we investigated the consequence of disruption of the Phd2 gene in chondrocytes on the articular cartilage phenotype in mice. Immunohistochemistry detected high expression of PHD2 in the superficial zone (SZ), while PHD3 and HIF-1α (target of PHD2) are mainly expressed in the middle-deep zone (MDZ). Conditional deletion of the Phd2 gene (cKO) in chondrocytes accelerated the transition of progenitors to hypertrophic (differentiating) chondrocytes as revealed by reduced SZ thickness, and increased MDZ thickness, as well as increased chondrocyte hypertrophy. Immunohistochemistry further revealed decreased levels of progenitor markers but increased levels of hypertrophy markers in the articular cartilage of the cKO mice. Treatment of primary articular chondrocytes, in vitro, with IOX2, a specific inhibitor of PHD2, promoted articular chondrocyte differentiation. Knockdown of Hif-1α expression in primary articular chondrocytes using lentiviral vectors containing Hif-1α shRNA resulted in reduced expression levels of Vegf, Glut1, Pgk1, and Col10 compared to control shRNA. We conclude that Phd2 is a key regulator of articular cartilage development that acts by inhibiting the differentiation of articular cartilage progenitors via modulating HIF-1α signaling.

Indexed as

AnimalsCartilage, ArticularCell DifferentiationCells, CulturedChondrocytesChondrogenesisCollagen Type XGlucose Transporter Type 1Hypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesMiceMice, Inbred C57BLMice, KnockoutPhosphoglycerate KinaseRNA InterferenceRNA, Small InterferingCol10a1 protein, mouseCollagen Type XEgln1 protein, mouseGlucose Transporter Type 1Hif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesPgk1 protein, mousePhosphoglycerate KinaseRNA, Small InterferingSlc2a1 protein, mouseVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID28349987
PMCPMC5368651
OpenAlexW2598484011

What OpenQuestion holds

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LicenceCC BY
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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.