Evidence map›Paper›PMID 28252046›Full record

ArticleScientific reports2017

Depletion of Gangliosides Enhances Articular Cartilage Repair in Mice.

Masatake Matsuoka, Tomohiro Onodera, Kentaro Homan, Fumio Sasazawa, Jun-Ichi Furukawa, Daisuke Momma, Rikiya Baba, Kazutoshi Hontani, Zenta Joutoku, Shinji Matsubara and 2 more

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Masatake MatsuokaDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Tomohiro OnoderaDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Kentaro HomanDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Fumio SasazawaDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Jun-Ichi FurukawaDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Daisuke MommaDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Rikiya BabaDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Kazutoshi HontaniDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Zenta JoutokuDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Shinji MatsubaraDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Tadashi YamashitaLaboratory of Biochemistry, Azabu University, Graduate School of Veterinary Medicine, Sagamihara, Japan.
Norimasa IwasakiDepartment of Orthopaedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Hokkaido University · JPAzabu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elucidation of the healing mechanisms in damaged tissues is a critical step for establishing breakthroughs in tissue engineering. Articular cartilage is clinically one of the most successful tissues to be repaired with regenerative medicine because of its homogeneous extracellular matrix and few cell types. However, we only poorly understand cartilage repair mechanisms, and hence, regenerated cartilage remains inferior to the native tissues. Here, we show that glycosylation is an important process for hypertrophic differentiation during articular cartilage repair. GM3, which is a precursor molecule for most gangliosides, was transiently expressed in surrounding damaged tissue, and depletion of GM3 synthase enhanced cartilage repair. Gangliosides also regulated chondrocyte hypertrophy via the Indian hedgehog pathway. These results identify a novel mechanism of cartilage healing through chondrocyte hypertrophy that is regulated by glycosylation. Manipulation of gangliosides and their synthases may have beneficial effects on articular cartilage repair.

Indexed as

Bone RegenerationAnimalsBiomarkersCartilage, ArticularCell DifferentiationChondrocytesChondrogenesisCollagenDisease Models, AnimalFemaleGangliosidesGene ExpressionG(M3) GangliosideHedgehog ProteinsMiceMice, KnockoutBiomarkersCollagenGangliosidesG(M3) GangliosideHedgehog Proteinsihh protein, mouse

Identifiers

PMID28252046
PMCPMC5333092
OpenAlexW2594069310

What OpenQuestion holds

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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.