Evidence map›Paper›PMID 22495178›Full record

ArticleThe Journal of investigative dermatology2012

β2AR antagonists and β2AR gene deletion both promote skin wound repair processes.

Christine E Pullar, Gabrielle S Le Provost, Andrew P O'Leary, Sian E Evans, Brian S Baier, R Rivkah Isseroff

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 74 citations in OpenAlex.

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  17. [Mechanisms of adrenergic β-antagonist for wounds and its application prospect in diabetic foot ulcers].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2020
    Review
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  19. Catecholamines in the regulation of angiogenesis in cutaneous wound healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 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

6 authors at 2 institutions in 2 countries.

Christine E PullarDeparment of Cell Physiology and Pharmacology, University of Leicester, Leicester, UK. cp161@le.ac.uk
Gabrielle S Le Provost
Andrew P O'Leary
Sian E Evans
Brian S Baier
R Rivkah Isseroff
University of California, Davis · USUniversity of Leicester · GB

Funding

Supplement: Keratinocyte Galvanotaxis and Wound HealingR01AR044518 · NIAMS · UNIVERSITY OF CALIFORNIA DAVIS · PI ISSEROFF, ROSLYN R · 1998 to 2006
$2.5M
Beta2 Adrenergic Receptor in Keratinocyte MigrationK01AR048827 · NIAMS · UNIVERSITY OF CALIFORNIA DAVIS · PI PULLAR, CHRISTINE E · 2003 to 2006
$375k
Medical Research Council G0901844Medical Research Council G0901844(93675)NIAMS NIH HHS AR44518NIAMS NIH HHS AR48827NIAMS NIH HHS K01 AR048827NIAMS NIH HHS R01 AR044518Wellcome Trust 082586Wellcome Trust 85586
6 · The paper itself

Abstract

Skin wound healing is a complex process requiring the coordinated, temporal orchestration of numerous cell types and biological processes to regenerate damaged tissue. Previous work has demonstrated that a functional β-adrenergic receptor autocrine/paracrine network exists in skin, but the role of β2-adrenergic receptor (β2AR) in wound healing is unknown. A range of in vitro (single-cell migration, immunoblotting, ELISA, enzyme immunoassay), ex vivo (rat aortic ring assay), and in vivo (chick chorioallantoic membrane assay, zebrafish, murine wild-type, and β2AR knockout excisional skin wound models) models were used to demonstrate that blockade or loss of β2AR gene deletion promoted wound repair, a finding that is, to our knowledge, previously unreported. Compared with vehicle-only controls, β2AR antagonism increased angiogenesis, dermal fibroblast function, and re-epithelialization, but had no effect on wound inflammation in vivo. Skin wounds in β2AR knockout mice contracted and re-epithelialized faster in the first few days of wound repair in vivo. β2AR antagonism enhanced cell motility through distinct intracellular signalling mechanisms and increased vascular endothelial growth factor secretion from keratinocytes. β2AR antagonism promoted wound repair processes in the early stages of wound repair, revealing a possible new avenue for therapeutic intervention.

Indexed as

Gene DeletionAdrenergic beta-2 Receptor AntagonistsAnimalsAortaChick EmbryoEnzyme-Linked Immunosorbent AssayFibroblastsInflammationKeratinocytesMiceNeovascularization, PathologicRatsReceptors, Adrenergic, beta-2SkinTime FactorsVascular Endothelial Growth Factor AAdrenergic beta-2 Receptor AntagonistsReceptors, Adrenergic, beta-2Vascular Endothelial Growth Factor A

Identifiers

PMID22495178
PMCPMC3396744
OpenAlexW2016074728

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.