Evidence map›Paper›PMID 34697142›Full record

ArticleIn vivo (Athens, Greece)

Contribution of Glucosylceramide Synthase to the Proliferation of Mouse Osteoblasts.

Yoshitaka Mishima, Kazunori Hamamura, Hanami Kato, Koichi Furukawa, Yuko Tashima, Tetsuya Okajima, Hisataka Kondo, Takuma Sato, Ken Miyazawa, Shigemi Goto and 1 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Regulation of Glycosylation in Bone Metabolism.International journal of molecular sciences · 2024
    Review
  2. 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

11 authors at 3 institutions in 1 country.

Yoshitaka MishimaDepartment of Pharmacology, 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.
Hanami KatoDepartment 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.
Yuko TashimaDepartment of Molecular Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Tetsuya OkajimaDepartment of Molecular Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hisataka KondoDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, 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.
Shigemi GotoDepartment of Orthodontics, School of Dentistry, Aichi Gakuin University, Nagoya, Japan.
Akifumi TogariDepartment of Pharmacology, School of Dentistry, Aichi Gakuin University, Nagoya, Japan.
Aichi Gakuin University · JPNagoya University · JPChubu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimGlycosphingolipids are known to be involved in bone metabolism. However, their roles and regulatory mechanisms in osteoblast proliferation are largely unknown. In this study, we examined the effects of inhibitors of glucosylceramide synthase (GCS), which is responsible for the generation of all glycosphingolipids, on osteoblast proliferation. MATERIALS AND

methodsWe analyzed the expression of glycosphingolipids and cell growth in MC3T3-E1 mouse osteoblast cells treated with the GCS inhibitors miglustat, D-PDMP and D-PPMP. We also conducted microarray analysis and RNA interference to identify genes involved in cell growth regulated by GCS.

resultsGlycosphingolipids GD1a and Gb4 expressed in MC3T3-E1 cells, were suppressed by GCS inhibitors. Furthermore, the proliferation of MC3T3-E1 cells was suppressed by the inhibitors. Using microarray analysis, we predicted nine genes (Fndc1, Acta2, Igfbp5, Cox6a2, Cth, Mymk, Angptl6, Mab21l2, and Igsf10) suppressed by all three inhibitors. Furthermore, partial silencing of Angptl6 by RNA interference reduced MC3T3-E1 cell growth.

conclusionThese results show that GCS regulates proliferation through Angptl6 in osteoblasts.

Indexed as

GlucosyltransferasesOsteoblastsAngiopoietin-Like Protein 6Angiopoietin-like ProteinsAnimalsCell DifferentiationCell ProliferationEye ProteinsIntracellular Signaling Peptides and ProteinsMiceAngiopoietin-Like Protein 6Angiopoietin-like ProteinsAngptl6 protein, mouseceramide glucosyltransferaseEye ProteinsGlucosyltransferasesIntracellular Signaling Peptides and ProteinsMab21l2 protein, mousecell proliferationglucosylceramide synthaseGlycosphingolipidsosteoblasts

Identifiers

PMID34697142
PMCPMC8627765
OpenAlexW3210235787

What OpenQuestion holds

Textmetadata
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.