Evidence map›Paper›PMID 28002442›Full record

ArticlePloS one2016

Overexpression of TIMP-3 in Chondrocytes Produces Transient Reduction in Growth Plate Length but Permanently Reduces Adult Bone Quality and Quantity.

Blandine Poulet, Ke Liu, Darren Plumb, Phoung Vo, Mittal Shah, Katherine Staines, Alexandra Sampson, Hiroyuki Nakamura, Hideaki Nagase, Alessandra Carriero and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

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  9. Poor bone matrix quality: What can be done about it?Current osteoporosis reports · 2021
    Review
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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

13 authors at 4 institutions in 2 countries.

Blandine PouletDepartment of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Apex building, Liverpool, United Kingdom.ORCID http://orcid.org/0000-0002-9224-5253
Ke LiuDepartment of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Apex building, Liverpool, United Kingdom.ORCID http://orcid.org/0000-0003-3769-1653
Darren PlumbDepartment of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Apex building, Liverpool, United Kingdom.
Phoung VoKennedy Institute of Rheumatology, Oxford, United Kingdom.
Mittal ShahComparative Biomedical Sciences, The Royal Veterinary College, London, United Kingdom.
Katherine StainesComparative Biomedical Sciences, The Royal Veterinary College, London, United Kingdom.
Alexandra SampsonComparative Biomedical Sciences, The Royal Veterinary College, London, United Kingdom.
Hiroyuki NakamuraKennedy Institute of Rheumatology, Oxford, United Kingdom.ORCID http://orcid.org/0000-0002-2524-3063
Hideaki NagaseKennedy Institute of Rheumatology, Oxford, United Kingdom.ORCID http://orcid.org/0000-0002-8563-2263
Alessandra CarrieroDepartment of Biomedical Engineering, Florida Institute of Technology, Melbourne, FL, United States of America.ORCID http://orcid.org/0000-0001-8103-4795
Sandra ShefelbineCollege of Engineering, Northeastern University, Boston, MA, United States of America.
Andrew A PitsillidesComparative Biomedical Sciences, The Royal Veterinary College, London, United Kingdom.
George Bou-GhariosDepartment of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Apex building, Liverpool, United Kingdom.
Royal Veterinary College · GBUniversity of Liverpool · GBFlorida Institute of Technology · USNortheastern University · US

Funding

Versus Arthritis 18768Versus Arthritis 20039Versus Arthritis 20581Versus Arthritis 20859
6 · The paper itself

Abstract

Bone development and length relies on the growth plate formation, which is dependent on degradative enzymes such as MMPs. Indeed, deletion of specific members of this enzyme family in mice results in important joint and bone abnormalities, suggesting a role in skeletal development. As such, the control of MMP activity is vital in the complex process of bone formation and growth. We generated a transgenic mouse line to overexpress TIMP3 in mouse chondrocytes using the Col2a1-chondrocyte promoter. This overexpression in cartilage resulted in a transient shortening of growth plate in homozygote mice but bone length was restored at eight weeks of age. However, tibial bone structure and mechanical properties remained compromised. Despite no transgene expression in adult osteoblasts from transgenic mice in vitro, their differentiation capacity was decreased. Neonates, however, did show transgene expression in a subset of bone cells. Our data demonstrate for the first time that transgene function persists in the chondro-osseous lineage continuum and exert influence upon bone quantity and quality.

Indexed as

AnimalsBone and BonesCartilageCells, CulturedCollagen Type IIFemurGrowth PlateHumansMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicOsteoblastsOsteogenesisPromoter Regions, GeneticCollagen Type IITIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3

Identifiers

PMID28002442
PMCPMC5176305
OpenAlexW2570036828

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.