Evidence map›Paper›PMID 24449577›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2014

Protective effects of C-type natriuretic peptide on linear growth and articular cartilage integrity in a mouse model of inflammatory arthritis.

Hülya Bükülmez, Fozia Khan, Cynthia F Bartels, Shunichi Murakami, Adriana Ortiz-Lopez, Abdus Sattar, Tariq M Haqqi, Matthew L Warman

Open access · hybridAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-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

14 citing papers in PubMed, 28 citations in OpenAlex.

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  10. Effects of Sprifermin, IGF1, IGF2, BMP7, or CNP on Bovine Chondrocytes in Monolayer and 3D Culture.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020
    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 3 institutions in 1 country.

Hülya BükülmezMetroHealth Medical Center and Case Western Reserve University, Cleveland, Ohio.
Fozia Khan
Cynthia F Bartels
Shunichi Murakami
Adriana Ortiz-Lopez
Abdus Sattar
Tariq M Haqqi
Matthew L Warman
Case Western Reserve University · USBoston Children's Hospital · USHarvard University · US

Funding

COBRE for Skeletal Health and RepairP20GM104937 · NIGMS · RHODE ISLAND HOSPITAL · PI CHEN, QIAN · 2012 to 2016
$10.8M
Suppression of MMP-13 Expression in Arthritis by PomegranateR01AT005520 · NCCIH · NORTHEAST OHIO MEDICAL UNIVERSITY · PI HAQQI, TARIQ M · 2010 to 2014
$1.9M
MECHANISMS OF CHONDROPROTECTION BY POMEGRANATE FRUIT EXTRACTR01AT003627 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI HAQQI, TARIQ M · 2007 to 2011
$1.7M
C-type natriuretic peptide signaling pathway disruption leading to growth arrestK08AR053943 · NIAMS · CASE WESTERN RESERVE UNIVERSITY · PI BUKULMEZ, HULYA · 2007 to 2011
$618k
CHONDROPROTECTIVE ACTIVITY OF POMEGRANATE EXTRACTR21AT004026 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI HAQQI, TARIQ M · 2009 to 2010
$255k
NCCIH NIH HHS R01-AT-0036227NCCIH NIH HHS R01 AT003627NCCIH NIH HHS R01 AT005520NCCIH NIH HHS R01-AT-005520NCCIH NIH HHS R21-AT-004026NIAMS NIH HHS K08-AR0-53943-01NIGMS NIH HHS P20 GM104937
6 · The paper itself

Abstract

objectiveThe C-type natriuretic peptide (CNP) signaling pathway is a major contributor to postnatal skeletal growth in humans. This study was undertaken to investigate whether CNP signaling could prevent growth delay and cartilage damage in an animal model of inflammatory arthritis.

methodsWe generated transgenic mice that overexpress CNP (B6.SJL-Col2a1-NPPC) in chondrocytes. We introduced the CNP transgene into mice with experimental systemic inflammatory arthritis (K/BxN T cell receptor [TCR]) and determined the effect of CNP overexpression in chondrocytes on the severity of arthritis, cartilage damage, and linear growth. We also examined primary chondrocyte cultures for changes in gene and protein expression resulting from CNP overexpression.

resultsK/BxN TCR mice exhibited linear growth delay (P < 0.01) compared to controls, and this growth delay was correlated with the severity of arthritis. Diminished chondrocyte proliferation and matrix production was also seen in K/BxN TCR mice. Compared to non-CNP-transgenic mice, K/BxN TCR mice with overexpressed CNP had milder arthritis, no growth delay, and less cartilage damage. Primary chondrocytes from mice overexpressing CNP were less sensitive to inflammatory cytokines than wild-type mouse chondrocytes.

conclusionCNP overexpression in chondrocytes can prevent endochondral growth delay and protect against cartilage damage in a mouse model of inflammatory arthritis. Pharmacologic or biologic modulation of the CNP signaling pathway may prevent growth retardation and protect cartilage in patients with inflammatory joint diseases, such as juvenile idiopathic arthritis.

Indexed as

AnimalsArthritis, ExperimentalArthritis, JuvenileBone DevelopmentCartilage, ArticularCell DifferentiationCell ProliferationChondrocytesMiceMice, TransgenicNatriuretic Peptide, C-TypeSignal TransductionNatriuretic Peptide, C-Type

Identifiers

PMID24449577
PMCPMC4034591
OpenAlexW2127718403

What OpenQuestion holds

Textmetadata
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.