Evidence map›Paper›PMID 31331074›Full record

ArticleInternational journal of molecular sciences2019

Alteration of the Total Cellular Glycome during Late Differentiation of Chondrocytes.

Kentaro Homan, Hisatoshi Hanamatsu, Jun-Ichi Furukawa, Kazue Okada, Ikuko Yokota, Tomohiro Onodera, Norimasa Iwasaki

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Molecular Processes in Chondrocyte Biology.International journal of molecular sciences · 2020
    Article
  10. 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

7 authors at 1 institution in 1 country.

Kentaro HomanDepartment of Orthopaedic Surgery, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-ku, Sapporo 060-8638, Japan.ORCID 0000-0002-0288-7691
Hisatoshi HanamatsuDepartment of Advanced Clinical Glycobiology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Kita 21, Nishi 11, Kita-ku, Sapporo 001-0021, Japan.ORCID 0000-0002-8461-2164
Jun-Ichi FurukawaDepartment of Advanced Clinical Glycobiology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Kita 21, Nishi 11, Kita-ku, Sapporo 001-0021, Japan. j_furu@med.hokudai.ac.jp.ORCID 0000-0002-7284-2261
Kazue OkadaDepartment of Advanced Clinical Glycobiology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Kita 21, Nishi 11, Kita-ku, Sapporo 001-0021, Japan.
Ikuko YokotaDepartment of Advanced Clinical Glycobiology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Kita 21, Nishi 11, Kita-ku, Sapporo 001-0021, Japan.
Tomohiro OnoderaDepartment of Orthopaedic Surgery, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-ku, Sapporo 060-8638, Japan. tomozou@med.hokudai.ac.jp.ORCID 0000-0002-4308-174X
Norimasa IwasakiDepartment of Orthopaedic Surgery, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-ku, Sapporo 060-8638, Japan.
Hokkaido University · JP

Funding

Japan Agency for Medical Research and Development JP17ae0101023Sumitomo Electric Industries Group Corporate Social Responsibility Foundation Grants-in-Aid for the Regional R&D Proposal-Based Program
6 · The paper itself

Abstract

In normal articular cartilage, chondrocytes do not readily proliferate or terminally differentiate, and exhibit a low level of metabolism. Hypertrophy-like changes of chondrocytes have been proposed to play a role in the pathogenesis of osteoarthritis by inducing protease-mediated cartilage degradation and calcification; however, the molecular mechanisms underlying these changes are unclear. Glycans are located on the outermost cell surface. Dynamic cellular differentiation can be monitored and quantitatively characterized by profiling the glycan structures of total cellular glycoproteins. This study aimed to clarify the alterations in glycans upon late differentiation of chondrocytes, during which hypertrophy-like changes occur. Primary mouse chondrocytes were differentiated using an insulin-induced chondro-osteogenic differentiation model. Comprehensive glycomics, including N-glycans, O-glycans, free oligosaccharides, glycosaminoglycan, and glycosphingolipid, were analyzed for the chondrocytes after 0-, 10- and 20-days cultivation. The comparison and clustering of the alteration of glycans upon hypertrophy-like changes of primary chondrocytes were performed. Comprehensive glycomic analyses provided complementary alterations in the levels of various glycans derived from glycoconjugates during hypertrophic differentiation. In addition, expression of genes related to glycan biosynthesis and metabolic processes was significantly correlated with glycan alterations. Our results indicate that total cellular glycan alterations are closely associated with chondrocyte hypertrophy and help to describe the glycophenotype by chondrocytes and their hypertrophic differentiation. our results will assist the identification of diagnostic and differentiation biomarkers in the future.

Indexed as

Cell DifferentiationAnimalsBiomarkersCells, CulturedChondrocytesGlycoproteinsGlycosylationHypertrophyMetabolomicsMiceOsteogenesisPolysaccharidesProteomicsBiomarkersGlycoproteinsPolysaccharideschondrocyte hypertrophyglycoconjugateglycomicsglycosaminoglycanglycosphingolipid

Identifiers

PMID31331074
PMCPMC6678350
OpenAlexW2963550110

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.