Evidence map›Paper›PMID 39740874›Full record

ArticleIn vivo (Athens, Greece)

Suppression of Bone Formation and Resorption by the Deletion of Complex Gangliosides.

Shota Ichikawa, Yoshitaka Mishima, Mayu Nagao, Gyosuke Sakashita, Koichi Furukawa, Takuma Sato, Ken Miyazawa, Kazunori Hamamura

Abstract read
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Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Shota IchikawaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, Japan.
Yoshitaka MishimaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, Japan.
Mayu NagaoDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, Japan.
Gyosuke SakashitaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, Japan.
Koichi FurukawaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.
Takuma SatoDepartment of Orthodontics, School of Dentistry, Aichi Gakuin University, Nagoya, Japan.
Ken MiyazawaDepartment of Orthodontics, School of Dentistry, Aichi Gakuin University, Nagoya, Japan.
Kazunori HamamuraDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, Japan; hamak@dpc.agu.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimGangliosides regulate bone formation and resorption. Bone formation is reduced in mice lacking ganglioside GM2/GD2 synthase due to a decrease in osteoblasts. However, the effects of the loss of complex gangliosides by the deletion of both GM2/GD2 and GD3 synthases are unknown. Therefore, we investigated whether deletion of complex gangliosides in mice affected bone metabolism. MATERIALS AND

methodsTwenty-six double-knockout mice lacking both GM2/GD2 and GD3 synthases (dKO) and 30 wild-type (WT) mice as controls were used. The mass of cancellous bone and bone strength in femurs were determined using three-dimensional micro-computed tomography and three-point bending test, respectively. Bone formation and resorption were assessed using histomorphometrical analysis with hematoxylin and eosin, and tartrate-resistant acid phosphatase (TRAP), respectively. Osteoblast proliferation was determined by bromodeoxyuridine assay and the differentiation into osteoclasts by TRAP staining; mRNA levels of osteoclast differentiation markers [nuclear factor of activated T-cells, cytoplasmic 1 (Nfatc1); Trap; and cathepsin K (Ctsk)] were also determined.

resultsBone mass increased in dKO mice, while bone formation and resorption decrease. In terms of bone strength, breaking displacement significantly increased in dKO mice. Furthermore, the proliferation of osteoblasts was suppressed, and the number of TRAP-positive multinucleated cells was reduced in dKO mice. Treatment with receptor activator of NF-[Formula: see text]B ligand significantly reduced Nfatc1, Trap and Ctsk mRNA levels in macrophages from dKO mice.

conclusionBone formation and resorption were reduced by the deletion of genes for complex gangliosides. The slight increase in bone strength in dKO mice may be due to the cancellous bone volume increase in these mice.

Indexed as

Bone ResorptionCell DifferentiationGangliosidesMice, KnockoutOsteoblastsOsteoclastsOsteogenesisAnimalsBone and BonesCell ProliferationFemurMiceNFATC Transcription FactorsSialyltransferasesTartrate-Resistant Acid PhosphataseX-Ray Microtomographyalpha-N-acetylneuraminate alpha-2,8-sialyltransferaseGangliosidesNFATC Transcription FactorsSialyltransferasesTartrate-Resistant Acid Phosphatasebone metabolismGangliosidesganglioside synthase knockout miceglycosyltransferase

Identifiers

PMID39740874
PMCPMC11705114

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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.