Evidence map›Paper›PMID 2193100›Full record

ArticleThe Journal of experimental medicine1990

Hyaluronate can function as a cell adhesion molecule and CD44 participates in hyaluronate recognition.

K Miyake, C B Underhill, J Lesley, P W Kincade

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
24.7field-weighted citation impact, top 1% 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

162 citing papers in PubMed, 623 citations in OpenAlex.

  1. Article
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  5. Enzymatic Modulation of the Pulmonary Glycocalyx Enhances Susceptibility toAmerican journal of respiratory cell and molecular biology · 2024
    Article
  6. Review
  7. Review
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  9. Article
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  11. Article
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  14. The Receptor for Hyaluronan-Mediated Motility (CD168) promotes inflammation and fibrosis after acute lung injury.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

102 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

K MiyakeImmunobiology & Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City 73104.
C B Underhill
J Lesley
P W Kincade
Oklahoma Medical Research Foundation · US

Funding

EARLY EVENTS IN MAMMALIAN B-CELL DIFFERENTIATION.R01AI020069 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI KINCADE, PAUL WAYNE · 1985 to 2012
$5.2M
DEVELOPMENTAL DEFECTS AFFECTING HUMORAL IMMUNITYR01AI019884 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI KINCADE, PAUL WAYNE · 1985 to 1991
–
ROLE OF HYALURANOTE RECEPTORS IN LUNG PHYSIOLOGYR01HL041565 · NHLBI · GEORGETOWN UNIVERSITY · PI UNDERHILL, CHARLES B · 1989 to 1991
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EARLY EVENTS IN MAMMALIAN B-CELL DIFFERENTIATIONR37AI020069 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI KINCADE, PAUL WAYNE · 1989 to 1996
–
NHLBI NIH HHS HL-41565NIAID NIH HHS AI-19884NIAID NIH HHS AI-20069
6 · The paper itself

Abstract

A cell adhesion model was previously used to select a series of monoclonal antibodies (mAbs), which were subsequently found to recognize CD44/Pgp-1. Interest in these reagents increased with the finding that they totally inhibited production of lymphoid or myeloid cells in long-term bone marrow cultures. Further investigation has now revealed that hyaluronate is a potential ligand for CD44 and that hyaluronate recognition accounts for the adhesion between B lineage hybridoma and stromal cells. The hybridoma cells adhered to hyaluronate-coated plastic wells as well as to monolayers of stromal cells. The adhesion in both cases was inhibited by treatment with hyaluronidases, and did not require divalent cations. Addition of exogenous hyaluronate also diminished binding of lymphoid cells to stromal cells. One of several mAbs to Pgp-1/CD44 was particularly effective at blocking these interactions. Since hyaluronate and Pgp-1/CD44 were present on both cell types, experiments were done to determine the cellular location of interacting molecules required for the adhesion process. Treatment of lymphoid cells with an anti-Pgp-1/CD44 antibody was more inhibitory than antibody treatment of the stromal cells. Conversely, hyaluronidase treatment of stromal cells reduced subsequent binding more than treatment of the lymphoid cells. Adhesive interactions that involve hyaluronate and CD44 could contribute to a number of cell recognition processes, including ones required for normal lympho-hemopoiesis.

Indexed as

Cell Adhesion MoleculesAnimalsAntibodies, MonoclonalAntigens, DifferentiationAntigens, SurfaceB-LymphocytesBone MarrowBone Marrow CellsCell AdhesionCell LineCell MembraneFlow CytometryGlycosaminoglycansHyaluronic AcidHyaluronoglucosaminidaseHybridomasAntibodies, MonoclonalAntigens, DifferentiationAntigens, SurfaceCell Adhesion MoleculesGlycosaminoglycansHyaluronic AcidHyaluronoglucosaminidaseReceptors, Lymphocyte Homing

Identifiers

PMID2193100
PMCPMC2188161
OpenAlexW2097863314

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.