Evidence map›Paper›PMID 24703506›Full record

ArticleThe Journal of surgical research2014

Heparin-binding EGF-like growth factor (HB-EGF) promotes cell migration and adhesion via focal adhesion kinase.

Yanwei Su, Gail E Besner

Abstract read
In one paragraph

Article in The Journal of surgical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.8field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  9. Necrotizing enterocolitis: It's not all in the gut.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
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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

2 authors at 1 institution in 2 countries.

Yanwei SuDepartment of Cardiovascular and Respiratory Medicine, Wuhan Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China; Department of Pediatric Surgery, Nationwide Children's Hospital, Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital, The Ohio State University College of Medicine, Columbus, Ohio. Electronic address: yanweisu@126.com.
Gail E BesnerDepartment of Pediatric Surgery, Nationwide Children's Hospital, Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital, The Ohio State University College of Medicine, Columbus, Ohio. Electronic address: gail.besner@nationwidechildrens.org.
Nationwide Children's Hospital · US

Funding

HB-EGF and Intestinal Ischemia/ReperfusionR01GM061193 · NIGMS · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI BESNER, GAIL E · 2002 to 2014
$3.6M
HB-EGF Therapy for Necrotizing EntercolitisR01DK074611 · NIDDK · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI BESNER, GAIL E · 2007 to 2011
$1.4M
NIDDK NIH HHS R01 DK074611NIDDK NIH HHS R01 DK74611NIGMS NIH HHS R01 GM061193NIGMS NIH HHS R01 GM61193
6 · The paper itself

Abstract

backgroundCell migration and adhesion are essential in intestinal epithelial wound healing and recovery from injury. Focal adhesion kinase (FAK) plays an important role in cell-extracellular matrix signal transduction. We have previously shown that heparin-binding EGF-like growth factor (HB-EGF) promotes intestinal epithelial cell (IEC) migration and adhesion in vitro. The present study was designed to determine whether FAK is involved in HB-EGF-induced IEC migration and adhesion. MATERIALS AND

methodsA scrape wound healing model of rat IECs was used to examine the effect of HB-EGF on FAK-dependent cell migration in vitro. Immunofluorescence and Western blot analyses were performed to evaluate the effect of HB-EGF on the expression of phosphorylated FAK (p-FAK). Cell adhesion assays were performed to determine the role of FAK in HB-EGF-induced cell adhesion on fibronectin (FN).

resultsHB-EGF significantly increased healing after scrape wounding, an effect that was reversed in the presence of an FAK inhibitor 14 (both with P < 0.05). HB-EGF increased p-FAK expression and induced p-FAK redistribution and actin reorganization in migrating rat IECs. Cell adhesion and spreading on FN were significantly increased by HB-EGF (P < 0.05). FAK inhibitor 14 significantly inhibited both intrinsic and HB-EGF-induced cell adhesion and spreading on FN (both with P < 0.05).

conclusionsFAK phosphorylation and FAK-mediated signal transduction play essential roles in HB-EGF-mediated IEC migration and adhesion.

Indexed as

Cell MovementAnimalsCell AdhesionCell LineEpithelial CellsFibronectinsFocal Adhesion Protein-Tyrosine KinasesHeparin-binding EGF-like Growth FactorIntercellular Signaling Peptides and ProteinsIntestinal MucosaRatsWound HealingFibronectinsFocal Adhesion Protein-Tyrosine KinasesHbegf protein, ratHeparin-binding EGF-like Growth FactorIntercellular Signaling Peptides and ProteinsCell adhesionCell migrationFocal adhesion kinaseHB-EGFWound healing

Identifiers

PMID24703506
PMCPMC4028394
OpenAlexW2099866135

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.