Evidence map›Paper›PMID 9276746›Full record

ArticleThe Journal of clinical investigation1997

Heparin-binding ligands mediate autocrine epidermal growth factor receptor activation In skin organ culture.

S Stoll, W Garner, J Elder

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
9.7field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
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  4. Review
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  11. Pulmonary epithelial barrier function: some new players and mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2015
    Review
  12. Article
  13. Human epidermal growth factor receptor signaling in acute lung injury.American journal of respiratory cell and molecular biology · 2012
    Review
  14. Amphiregulin-dependent mucous cell metaplasia in a model of nonallergic lung injury.American journal of respiratory cell and molecular biology · 2012
    Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

3 authors at 1 institution in 1 country.

S StollDepartment of Dermatology, University of Michigan, Ann Arbor, Michigan 48109, USA.
W Garner
J Elder
University of Michigan–Ann Arbor · US

Funding

POSITIONAL CLONING OF EPIDERMAL DIFFERENTIATION GENESR01AR042248 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 1993 to 1996
–
TGF-ALPHA AND TYROSINE KINASE ACTIVATION IN PSORIASISR29AR040016 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 1989 to 1993
–
NIAMS NIH HHS R01 AR42248NIAMS NIH HHS R29 AR40016
6 · The paper itself

Abstract

Exogenous EGF and TGF-alpha accelerate wound healing, but treatment effects are often modest. Using short-term human skin organ culture, we found that autocrine EGF receptor activation could account for this observation. Amphiregulin and heparin-binding EGF-like growth factor (HB-EGF) transcripts were rapidly and markedly induced, whereas EGF and TGF-alpha mRNAs were undetectable or only slightly increased. Vascular permeability factor and keratin 6 transcripts were also strongly induced, albeit with a >/= 3 h delay relative to HB-EGF and amphiregulin. All four transcripts were upregulated in actual healing skin wounds, HB-EGF and keratin 6 being the most prominent. The highly EGF receptor-specific tyrosine kinase inhibitor PD153035 strongly inhibited induction of all four transcripts in organ culture, as well as release of immunoreactive HB-EGF into the medium. These effects were confirmed using the anti-EGF receptor mAb 225 IgG. Neither PD153035 nor 225 IgG was toxic to keratinocytes, as judged by calcein-AM uptake. PD153035 completely abrogated the proliferative phase of keratinocyte outgrowth in skin explant cultures, whereas it had no effect on the antecedent migratory phase. Based on these results, we conclude that EGF receptor activation by highly inducible, keratinocyte-derived heparin-binding ligands is an important mechanism for amplification and transmission of the cutaneous wound healing signal.

Indexed as

Wound HealingAdultCells, CulturedEpidermal Growth FactorErbB ReceptorsGene ExpressionHeparin-binding EGF-like Growth FactorHumansIntercellular Signaling Peptides and ProteinsOrgan Culture TechniquesQuinazolinesSkin4-((3-bromophenyl)amino)-6,7-dimethoxyquinazolineEpidermal Growth FactorErbB ReceptorsHBEGF protein, humanHeparin-binding EGF-like Growth FactorIntercellular Signaling Peptides and ProteinsQuinazolines

Identifiers

PMID9276746
PMCPMC508305
OpenAlexW2056263610

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.