Evidence map›Paper›PMID 19609315›Full record

ArticleThe Journal of investigative dermatology2010

Metalloproteinase-mediated, context-dependent function of amphiregulin and HB-EGF in human keratinocytes and skin.

Stefan W Stoll, Jessica L Johnson, Ajay Bhasin, Andrew Johnston, Johann E Gudjonsson, Laure Rittié, James T Elder

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025
    Review
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  20. Rhbdf2 mutations increase its protein stability and drive EGFR hyperactivation through enhanced secretion of amphiregulin.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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.

Stefan W StollDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA. sstoll@umich.edu
Jessica L Johnson
Ajay Bhasin
Andrew Johnston
Johann E Gudjonsson
Laure Rittié
James T Elder
University of Michigan–Ann Arbor · US

Funding

Amphiregulin in Psoriatic Epidermal HyperplasiaR01AR052889 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 2006 to 2010
$1.4M
Metalloproteinase regulation of ErbB signaling in skinK01AR050462 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STOLL, STEFAN W · 2006 to 2010
$489k
Metalloproteinase regulation of ErbB signaling in skinR03AR049420 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STOLL, STEFAN W · 2004 to 2006
$227k
NIAMS NIH HHS K01 AR050462NIAMS NIH HHS R01 AR 052889NIAMS NIH HHS R01 AR052889NIAMS NIH HHS R03 AR049420
6 · The paper itself

Abstract

Human keratinocytes (KCs) express multiple EGF receptor (EGFR) ligands; however, their functions in specific cellular contexts remain largely undefined. To address this issue, first we measured mRNA and protein levels for multiple EGFR ligands in KCs and skin. Amphiregulin (AREG) was by far the most abundant EGFR ligand in cultured KCs, with >19 times more mRNA and >7.5 times more shed protein than any other family member. EGFR ligand expression in normal skin was low (<8 per thousand of RPLP0/36B4); however, HB-EGF and AREG mRNAs were strongly induced in human skin organ culture. KC migration in scratch wound assays was highly metalloproteinase (MP)- and EGFR dependent, and was markedly inhibited by EGFR ligand antibodies. However, lentivirus-mediated expression of soluble HB-EGF, but not soluble AREG, strongly enhanced KC migration, even in the presence of MP inhibitors. Lysophosphatidic acid (LPA)-induced ERK phosphorylation was also strongly EGFR and MP dependent and markedly inhibited by neutralization of HB-EGF. In contrast, autocrine KC proliferation and ERK phosphorylation were selectively blocked by neutralization of AREG. These data show that distinct EGFR ligands stimulate KC behavior in different cellular contexts, and in an MP-dependent fashion.

Indexed as

AmphiregulinAutocrine CommunicationCell DivisionCell MovementCells, CulturedEGF Family of ProteinsErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGlycoproteinsHeparin-binding EGF-like Growth FactorHumansIntercellular Signaling Peptides and ProteinsKeratinocytesLentivirusLigandsLipopolysaccharidesAmphiregulinAREG protein, humanEGF Family of ProteinsErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGlycoproteinsHBEGF protein, humanHeparin-binding EGF-like Growth FactorIntercellular Signaling Peptides and ProteinsLigandsLipopolysaccharidesMetalloproteasesRNA, Messenger

Identifiers

PMID19609315
PMCPMC2795126
OpenAlexW2030005349

What OpenQuestion holds

Textmetadata
LicenceTDM
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.