Evidence map›Paper›PMID 24126843›Full record

ArticleThe Journal of investigative dermatology2014

Bone morphogenetic protein signaling suppresses wound-induced skin repair by inhibiting keratinocyte proliferation and migration.

Christopher J Lewis, Andrei N Mardaryev, Krzysztof Poterlowicz, Tatyana Y Sharova, Ahmar Aziz, David T Sharpe, Natalia V Botchkareva, Andrey A Sharov

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 12% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

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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 2 countries.

Christopher J LewisCentre for Skin Sciences, University of Bradford, Bradford, West Yorkshire, UK; Plastic Surgery and Burns Research Unit, University of Bradford, Bradford, West Yorkshire, UK.
Andrei N MardaryevCentre for Skin Sciences, University of Bradford, Bradford, West Yorkshire, UK.
Krzysztof PoterlowiczCentre for Skin Sciences, University of Bradford, Bradford, West Yorkshire, UK.
Tatyana Y SharovaDepartment of Dermatology, Boston University, Boston, Massachusetts, USA.
Ahmar AzizDepartment of Dermatology, Boston University, Boston, Massachusetts, USA.
David T SharpePlastic Surgery and Burns Research Unit, University of Bradford, Bradford, West Yorkshire, UK.
Natalia V BotchkarevaCentre for Skin Sciences, University of Bradford, Bradford, West Yorkshire, UK. Electronic address: n.botchkareva@bradford.ac.uk.
Andrey A SharovDepartment of Dermatology, Boston University, Boston, Massachusetts, USA. Electronic address: drsharov@bu.edu.
University of Bradford · GBBoston University · US

Funding

FUNCTIONS OF NOGGIN AND SMAD1/5 IN HAIR GROWTH CONTROLR01AR049778 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BOTCHKAREV, VLADIMIR A · 2004 to 2014
$3.5M
Molecular control of normal and neoplastic skin stem cellsK01AR056771 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SHAROV, ANDREY · 2009 to 2013
$621k
Bone Morphogentic Protein signaling in the control of skin development, hair growR56AR049778 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BOTCHKAREV, VLADIMIR A · 2009 to 2009
$406k
Medical Research Council MR/K011324/1NIAMS NIH HHS AR049778NIAMS NIH HHS K01 AR056771NIAMS NIH HHS K01AR056771NIAMS NIH HHS R01 AR049778NIAMS NIH HHS R56 AR049778
6 · The paper itself

Abstract

Bone morphogenetic protein (BMP) signaling plays a key role in the control of skin development and postnatal remodeling by regulating keratinocyte proliferation, differentiation, and apoptosis. To study the role of BMPs in wound-induced epidermal repair, we used transgenic mice overexpressing the BMP downstream component Smad1 under the control of a K14 promoter as an in vivo model, as well as ex vivo and in vitro assays. K14-caSmad1 (transgenic mice overexpressing a constitutively active form of Smad1 under K14 promoter) mice exhibited retarded wound healing associated with significant inhibition of proliferation and increased apoptosis in healing wound epithelium. Furthermore, microarray and quantitative real-time reverse-transcriptase-PCR (qRT-PCR) analyses revealed decreased expression of a number of cytoskeletal/cell motility-associated genes including wound-associated keratins (Krt16, Krt17) and Myosin VA (Myo5a), in the epidermis of K14-caSmad1 mice versus wild-type (WT) controls during wound healing. BMP treatment significantly inhibited keratinocyte migration ex vivo, and primary keratinocytes of K14-caSmad1 mice showed retarded migration compared with WT controls. Finally, small interfering RNA (siRNA)-mediated silencing of BMPR-1B in primary mouse keratinocytes accelerated cell migration and was associated with increased expression of Krt16, Krt17, and Myo5a compared with controls. Thus, this study demonstrates that BMPs inhibit keratinocyte proliferation, cytoskeletal organization, and migration in regenerating skin epithelium during wound healing, and raises a possibility for using BMP antagonists for the management of chronic wounds.

Indexed as

AnimalsApoptosisBone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsCell MovementCell ProliferationCells, CulturedEpidermal CellsEpidermisHumansKeratin-14KeratinocytesMiceMice, Inbred StrainsMice, TransgenicRNA, Small InterferingBmpr1b protein, mouseBone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsKeratin-14KRT14 protein, humanRNA, Small InterferingSmad1 ProteinSmad1 protein, mouse

Identifiers

PMID24126843
PMCPMC3945401
OpenAlexW2087861689

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.