Evidence map›Paper›PMID 18386027›Full record

ArticleArchives of dermatological research2008

SERPINE1 (PAI-1) is deposited into keratinocyte migration "trails" and required for optimal monolayer wound repair.

Kirwin M Providence, Stephen P Higgins, Andrew Mullen, Ashley Battista, Rohan Samarakoon, Craig E Higgins, Cynthia E Wilkins-Port, Paul J Higgins

Open access · greenAbstract read
In one paragraph

Article in Archives of dermatological research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 73 citations in OpenAlex.

  1. Plasminogen activator inhibitor-1 promotes the proliferation and blocks TGF-β1-dependent growth inhibition of cholesteatoma keratinocytes by ERK signaling.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026
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  13. Regulation of anoikis by extrinsic death receptor pathways.Cell communication and signaling : CCS · 2023
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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

8 authors at 2 institutions in 1 country.

Kirwin M ProvidenceDepartment of Biology, Ithaca College, Ithaca, NY 14850, USA.
Stephen P Higgins
Andrew Mullen
Ashley Battista
Rohan Samarakoon
Craig E Higgins
Cynthia E Wilkins-Port
Paul J Higgins
Albany Medical Center Hospital · USIthaca College · US

Funding

MATRIX MEDIATORS OF WOUND HEALINGR01GM057242 · NIGMS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI HIGGINS, PAUL J. · 1998 to 2010
$3.2M
NIGMS NIH HHS GM57242NIGMS NIH HHS R01 GM057242
6 · The paper itself

Abstract

Cutaneous tissue injury, both in vivo and in vitro, initiates activation of a "wound repair" transcriptional program. One such highly induced gene encodes plasminogen activator inhibitor type-1 (PAI-1, SERPINE1). PAI-1-GFP, expressed as a fusion protein under inducible control of +800 bp of the wound-activated PAI-1 promoter, prominently "marked" keratinocyte migration trails during the real-time of monolayer scrape-injury repair. Addition of active recombinant PAI-1 to wounded wild-type keratinocyte monolayers as well as to PAI-1(-/-) MEFs and PAI-1(-/-) keratinocytes significantly stimulated directional motility above basal levels in all cell types. PAI-1 expression knockdown or antibody-mediated functional inhibition, in contrast, effectively attenuated injury repair. The defect in wound-associated migratory activity as a consequence of antisense-mediated PAI-1 down-regulation was effectively reversed by addition of recombinant PAI-1 immediately after scrape injury. One possible mechanism underlying the PAI-1-dependent motile response may involve fine control of the keratinocyte substrate detachment/re-attachment process. Exogenous PAI-1 significantly enhanced keratinocyte spread cell "footprint" area while PAI-1 neutralizing antibodies, but not control non-immune IgG, effectively inhibited spreading with apoptotic hallmarks evident within 24 h. Importantly, PAI-1 not only stimulated keratinocyte adhesion and wound-initiated planar migration but also rescued keratinocytes from plasminogen-induced substrate detachment/anoikis. The early transcriptional response of the PAI-1 gene to monolayer trauma and its prominence in the injury repair genetic signature are consistent with its function as both a survival factor and regulator of the time course of epithelial migration as part of the cutaneous injury response program.

Indexed as

Wound HealingAnimalsAnoikisAntibodies, BlockingCell AdhesionCell LineCell MovementCell Surface ExtensionsGreen Fluorescent ProteinsHumansKeratinocytesMiceMice, KnockoutPlasminogen Activator Inhibitor 1RatsRecombinant Fusion ProteinsAntibodies, BlockingGreen Fluorescent ProteinsPlasminogen Activator Inhibitor 1Recombinant Fusion ProteinsRNA, Small Interfering

Identifiers

PMID18386027
PMCPMC2628461
OpenAlexW2100867448

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.