Evidence map›Paper›PMID 21471214›Full record

ArticleThe Journal of biological chemistry2011

Differential use of chondroitin sulfate to regulate hyaluronan binding by receptor CD44 in Inflammatory and Interleukin 4-activated Macrophages.

Brian Ruffell, Grace F T Poon, Sally S M Lee, Kelly L Brown, Sie-Lung Tjew, Jessie Cooper, Pauline Johnson

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. CD44 signaling in skin wound healing and regeneration.Journal of translational medicine · 2025
    Review
  4. Review
  5. Review
  6. X-linked genes exhibit miR6891-5p-regulated skewing in Sjögren's syndrome.Journal of molecular medicine (Berlin, Germany) · 2022
    Article
  7. Review
  8. Article
  9. Effect of mesenchymal stem cells combined with chondroitin sulfate in anAmerican journal of translational research · 2021
    Article
  10. A Novel Splice Variant of HYAL-4 Drives Malignant Transformation and Predicts Outcome in Patients with Bladder Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  11. Review
  12. The CD44-HA axis and inflammation in atherosclerosis: A temporal perspective.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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.

Brian RuffellDepartment of Microbiology and Immunology, Life Sciences Institute, University of British Columbia, Vancouver, British Columbia, Canada.
Grace F T Poon
Sally S M Lee
Kelly L Brown
Sie-Lung Tjew
Jessie Cooper
Pauline Johnson
University of British Columbia · CA

Funding

Canadian Institutes of Health Research 81314
6 · The paper itself

Abstract

CD44 is a cell surface receptor for the extracellular matrix glycosaminoglycan hyaluronan and is involved in processes ranging from leukocyte recruitment to wound healing. In the immune system, the binding of hyaluronan to CD44 is tightly regulated, and exposure of human peripheral blood monocytes to inflammatory stimuli increases CD44 expression and induces hyaluronan binding. Here we sought to understand how mouse macrophages regulate hyaluronan binding upon inflammatory and anti-inflammatory stimuli. Mouse bone marrow-derived macrophages stimulated with tumor necrosis factor α or lipopolysaccharide and interferon-γ (LPS/IFNγ) induced hyaluronan binding by up-regulating CD44 and down-regulating chondroitin sulfation on CD44. Hyaluronan binding was induced to a lesser extent in interleukin-4 (IL-4)-activated macrophages despite increased CD44 expression, and this was attributable to increased chondroitin sulfation on CD44, as treatment with β-d-xyloside to prevent chondroitin sulfate addition significantly enhanced hyaluronan binding. These changes in the chondroitin sulfation of CD44 were associated with changes in mRNA expression of two chondroitin sulfotransferases, CHST3 and CHST7, which were decreased in LPS/IFNγ-stimulated macrophages and increased in IL-4-stimulated macrophages. Thus, inflammatory and anti-inflammatory stimuli differentially regulate the chondroitin sulfation of CD44, which is a dynamic physiological regulator of hyaluronan binding by CD44 in mouse macrophages.

Indexed as

Macrophage ActivationAnimalsCarbohydrate SulfotransferasesCell Line, TumorChondroitin SulfatesGene Expression RegulationHumansHyaluronan ReceptorsHyaluronic AcidInflammationInterferon-gammaInterleukin-4LipopolysaccharidesMacrophagesMiceMice, KnockoutCarbohydrate SulfotransferasesCD44 protein, humanCd44 protein, mouseChondroitin SulfatesHyaluronan ReceptorsHyaluronic AcidIL4 protein, humanInterferon-gammaInterleukin-4LipopolysaccharidesSulfotransferasesTumor Necrosis Factor-alpha

Identifiers

PMID21471214
PMCPMC3103297
OpenAlexW2009503126

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.