Evidence map›Paper›PMID 31185614›Full record

ArticleInternational journal of molecular sciences2019

Deficiency of GD3 Synthase in Mice Resulting in the Attenuation of Bone Loss with Aging.

Shoyoku Yo, Kazunori Hamamura, Yoshitaka Mishima, Kosuke Hamajima, Hironori Mori, Koichi Furukawa, Hisataka Kondo, Kenjiro Tanaka, Takuma Sato, Ken Miyazawa and 2 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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Regulation of Glycosylation in Bone Metabolism.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Recent Advances in Osteoclast Biological Behavior.Frontiers in cell and developmental biology · 2021
    Review
  9. Editorial for Special Issue "Gangliosides: Modes of Action and Cell Fates".International journal of molecular sciences · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. 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

12 authors at 2 institutions in 1 country.

Shoyoku YoDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan. ag163d13@dpc.agu.ac.jp.
Kazunori HamamuraDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan. hamak@dpc.agu.ac.jp.ORCID 0000-0002-8143-338X
Yoshitaka MishimaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan. lb_hidenori@yahoo.co.jp.
Kosuke HamajimaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan. Hamajima.k0329@gmail.com.
Hironori MoriDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan. hironori128@gmail.com.
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
Hisataka KondoDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan. KondoH@dpc.agu.ac.jp.
Kenjiro TanakaDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan. kenjiro1@dpc.agu.ac.jp.
Takuma SatoDepartment of Orthodontics, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan. tk-mail@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, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan. togariaf@dpc.aichi-gakuin.ac.jp.
Aichi Gakuin University · JPChubu University · JP

Funding

JSPS KAKENHI JP17K11657
6 · The paper itself

Abstract

Gangliosides are widely expressed in almost all tissues and cells and are also considered to be essential in the development and maintenance of various organs and tissues. However, little is known about their roles in bone metabolism. In this study, we investigated the effects of genetic deletion of ganglioside D3 (GD3) synthase, which is responsible for the generation of all b-series gangliosides, on bone metabolism. Although b-series gangliosides were not expressed in osteoblasts, these gangliosides were expressed in pre-osteoclasts. However, the expression of these gangliosides was decreased after induction of osteoclastogenesis by receptor activator of nuclear factor kappa-B ligand (RANKL). Three-dimensional micro-computed tomography (3D-μCT) analysis revealed that femoral cancellous bone mass in GD3 synthase-knockout (GD3S KO) mice was higher than that in wild type (WT) mice at the age of 40 weeks, although there were no differences in that between GD3S KO and WT mice at 15 weeks old. Whereas bone formation parameters (osteoblast numbers/bone surface and osteoblast surface/bone surface) in GD3S KO mice did not differ from WT mice, bone resorption parameters (osteoclast numbers/bone surface and osteoclast surface/bone surface) in GD3S KO mice became significantly lower than those in WT mice at 40 weeks of age. Collectively, this study demonstrates that deletion of GD3 synthase attenuates bone loss that emerges with aging.

Indexed as

AgingAnimalsBone ResorptionCells, CulturedGangliosidesMiceOsteoclastsOsteogenesisRANK LigandRAW 264.7 CellsSialyltransferasesalpha-N-acetylneuraminate alpha-2,8-sialyltransferaseGangliosidesRANK LigandSialyltransferasesbone metabolismgangliosidesglycosphingolipidsglycosylation

Identifiers

PMID31185614
PMCPMC6600367
OpenAlexW2948213651

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.