Evidence map›Paper›PMID 31540393›Full record

ArticleInternational journal of molecular sciences2019

Deletion of Gb3 Synthase in Mice Resulted in the Attenuation of Bone Formation via Decrease in Osteoblasts.

Kazunori Hamamura, Kosuke Hamajima, Shoyoku Yo, Yoshitaka Mishima, Koichi Furukawa, Makoto Uchikawa, Yuji Kondo, Hironori Mori, Hisataka Kondo, Kenjiro Tanaka and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Regulation of Glycosylation in Bone Metabolism.International journal of molecular sciences · 2024
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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 1 country.

Kazunori HamamuraDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. hamak@dpc.agu.ac.jp.ORCID 0000-0002-8143-338X
Kosuke HamajimaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. Hamajima.k0329@gmail.com.
Shoyoku YoDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. ag163d13@dpc.agu.ac.jp.
Yoshitaka MishimaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. lb_hidenori@yahoo.co.jp.
Koichi FurukawaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Aichi 487-8501, Japan. koichi@isc.chubu.ac.jp.ORCID 0000-0002-3321-9784
Makoto UchikawaJapanese Red Cross Tokyo Blood Center, Tokyo 162-8639, Japan. m-uchikawa@ktks.bbc.jrc.or.jp.
Yuji KondoDepartment of Biochemistry II, Nagoya University Graduate School of Medicine, Nagoya 464-8650, Japan. Yuji-Kondo@omrf.org.
Hironori MoriDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. hironori128@gmail.com.
Hisataka KondoDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. KondoH@dpc.agu.ac.jp.
Kenjiro TanakaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. kenjiro1@dpc.agu.ac.jp.
Ken MiyazawaDepartment of Orthodontics, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. miyaken@dpc.aichi-gakuin.ac.jp.
Shigemi GotoDepartment of Orthodontics, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. shig@dpc.agu.ac.jp.
Akifumi TogariDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. togariaf@dpc.aichi-gakuin.ac.jp.
Aichi Gakuin University · JPChubu University · JPJapanese Red Cross Society, Japan · JPNagoya University · JP

Funding

JSPS KAKENHI JP17K11657
6 · The paper itself

Abstract

Glycosphingolipids are known to play a role in developing and maintaining the integrity of various organs and tissues. Among glycosphingolipids, there are several reports on the involvement of gangliosides in bone metabolism. However, there have been no reports on the presence or absence of expression of globo-series glycosphingolipids in osteoblasts and osteoclasts, and the involvement of their glycosphingolipids in bone metabolism. In the present study, we investigated the presence or absence of globo-series glycosphingolipids such as Gb3 (globotriaosylceramide), Gb4 (globoside), and Gb5 (galactosyl globoside) in osteoblasts and osteoclasts, and the effects of genetic deletion of Gb3 synthase, which initiates the synthesis of globo-series glycosphingolipids on bone metabolism. Among Gb3, Gb4, and Gb5, only Gb4 was expressed in osteoblasts. However, these glycosphingolipids were not expressed in pre-osteoclasts and osteoclasts. Three-dimensional micro-computed tomography (3D-μCT) analysis revealed that femoral cancellous bone mass in Gb3 synthase-knockout (Gb3S KO) mice was lower than that in wild type (WT) mice. Calcein double labeling also revealed that bone formation in Gb3S KO mice was significantly lower than that in WT mice. Consistent with these results, the deficiency of Gb3 synthase in mice decreased the number of osteoblasts on the bone surface, and suppressed mRNA levels of osteogenic differentiation markers. On the other hand, osteoclast numbers on the bone surface and mRNA levels of osteoclast differentiation markers in Gb3S KO mice did not differ from WT mice. This study demonstrated that deletion of Gb3 synthase in mice decreases bone mass via attenuation of bone formation.

Indexed as

Gene DeletionOsteogenesisAnimalsCell LineCells, CulturedGalactosyltransferasesGlycosphingolipidsMaleMiceMice, KnockoutOsteoblastsOsteoclastsRAW 264.7 CellsGalactosyltransferasesGlycosphingolipidsUDP-galactose-lactosylceramide alpha 1-4-galactosyltransferasebone metabolismgloboside (Gb4)glycosphingolipidsosteoblasts

Identifiers

PMID31540393
PMCPMC6769804
OpenAlexW2974875164

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.