Evidence map›Paper›PMID 39033138›Full record

ArticleBMC musculoskeletal disorders2024

Depletion of b-series ganglioside prevents limb length discrepancy after growth plate injury.

Yoshiaki Hosokawa, Masatake Matsuoka, Yuko Sakai, Ryuichi Fukuda, Keizumi Matsugasaki, Kentaro Homan, Jun-Ichi Furukawa, Tomohiro Onodera, Norimasa Iwasaki

Abstract read
In one paragraph

Article in BMC musculoskeletal disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

9 authors.

Yoshiaki HosokawaDepartment of Orthopaedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-Ku, Sapporo, Hokkaido, 060-8638, Japan.
Masatake MatsuokaDepartment of Orthopaedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-Ku, Sapporo, Hokkaido, 060-8638, Japan. masatakem@pop.med.hokudai.ac.jp.
Yuko SakaiDepartment of Orthopaedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-Ku, Sapporo, Hokkaido, 060-8638, Japan.
Ryuichi FukudaDepartment of Orthopaedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-Ku, Sapporo, Hokkaido, 060-8638, Japan.
Keizumi MatsugasakiDepartment of Orthopaedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-Ku, Sapporo, Hokkaido, 060-8638, Japan.
Kentaro HomanDepartment of Orthopaedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-Ku, Sapporo, Hokkaido, 060-8638, Japan.
Jun-Ichi FurukawaInstitute for Glyco-core Research (iGCORE), Nagoya University, Nagoya, 464-8601, Japan.
Tomohiro OnoderaDepartment of Orthopaedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-Ku, Sapporo, Hokkaido, 060-8638, Japan.
Norimasa IwasakiDepartment of Orthopaedic Surgery, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, North 15 West 7, Kita-Ku, Sapporo, Hokkaido, 060-8638, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGrowth plate damage in long bones often results in progressive skeletal growth imbalance and deformity, leading to significant physical problems. Gangliosides, key glycosphingolipids in cartilage, are notably abundant in articular cartilage and regulate chondrocyte homeostasis. This suggests their significant roles in regulating growth plate cartilage repair.

methodsChondrocytes from 3 to 5 day-old C57BL/6 mice underwent glycoblotting and mass spectrometry. Based on the results of the glycoblotting analysis, we employed GD3 synthase knockout mice (GD3-/-), which lack b-series gangliosides. In 3-week-old mice, physeal injuries were induced in the left tibiae, with right tibiae sham operated. Tibiae were analyzed at 5 weeks postoperatively for length and micro-CT for growth plate height and bone volume at injury sites. Tibial shortening ratio and bone mineral density were measured by micro-CT.

resultsGlycoblotting analysis indicated that b-series gangliosides were the most prevalent in physeal chondrocytes among ganglioside series. At 3 weeks, GD3-/- exhibited reduced tibial shortening (14.7 ± 0.2 mm) compared to WT (15.0 ± 0.1 mm, P = 0.03). By 5 weeks, the tibial lengths in GD3-/- (16.0 ± 0.4 mm) closely aligned with sham-operated lengths (P = 0.70). Micro-CT showed delayed physeal bridge formation in GD3-/-, with bone volume measuring 168.9 ± 5.8 HU at 3 weeks (WT: 180.2 ± 3.2 HU, P = 0.09), but normalizing by 5 weeks.

conclusionThis study highlights that GD3 synthase knockout mice inhibit physeal bridge formation after growth plate injury, proposing a new non-invasive approach for treating skeletal growth disorders.

Indexed as

ChondrocytesGangliosidesGrowth PlateMice, Inbred C57BLMice, KnockoutAnimalsDisease Models, AnimalLeg Length InequalityMiceSialyltransferasesTibiaX-Ray Microtomographyalpha-N-acetylneuraminate alpha-2,8-sialyltransferaseGangliosidesSialyltransferasesGangliosideGlycosphingolipidGrowth plateGrowth plate cartilageOrthopedic surgery

Identifiers

PMID39033138
PMCPMC11264953

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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.