Evidence map›Paper›PMID 27793180›Full record

ArticleStem cell research & therapy2016

Specific disruption of Lnk in murine endothelial progenitor cells promotes dermal wound healing via enhanced vasculogenesis, activation of myofibroblasts, and suppression of inflammatory cell recruitment.

Jun Hee Lee, Seung Taek Ji, Jaeho Kim, Satoshi Takaki, Takayuki Asahara, Young-Joon Hong, Sang-Mo Kwon

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 19% 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

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

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
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  7. Review
  8. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 3 countries.

Jun Hee LeeDepartment of Pharmacology and Toxicology, University of Alabama at Birmingham School of Medicine, Birmingham, AL, 35294, USA.
Seung Taek JiDepartment of Physiology, Laboratory for Vascular Medicine and Stem Cell Biology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 626-870, Republic of Korea.
Jaeho KimResearch Institute of Convergence Biomedical Science and Technology, Pusan National University School of Medicine, Yangsan, Republic of Korea.
Satoshi TakakiDepartment of Immune Regulation, Research Centre for Hepatitis and Immunology, Research Institute, National Centre for Global Health and Medicine, Chiba, Japan.
Takayuki AsaharaDepartment of Regenerative Medicine Science, Tokai University School of Medicine, Kanagawa, Japan.
Young-Joon HongDivision of Cardiology of Chonnam National University Hospital, Cardiovascular Convergence Research Center Nominated by Korea Ministry of Health and Welfare, Gwangju, 501-757, Republic of Korea. hyj200@hanmail.net.
Sang-Mo KwonDepartment of Physiology, Laboratory for Vascular Medicine and Stem Cell Biology, Medical Research Institute, School of Medicine, Pusan National University, Yangsan, 626-870, Republic of Korea. smkwon323@hotmail.com.
Pusan National University · KRChonnam National University Hospital · KRNational Center for Global Health and Medicine · JPTokai University · JPUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough endothelial progenitor cells (EPCs) contribute to wound repair by promoting neovascularization, the mechanism of EPC-mediated wound healing remains poorly understood due to the lack of pivotal molecular targets of dermal wound repair. METHODS AND

resultsWe found that genetic targeting of the Lnk gene in EPCs dramatically enhances the vasculogenic potential including cell proliferation, migration, and tubule-like formation as well as accelerates in vivo wound healing, with a reduction in fibrotic tissue and improved neovascularization via significant suppression of inflammatory cell recruitment. When injected into wound sites, Lnk

conclusionsThe specific targeting of Lnk may be a promising EPC-based therapeutic strategy for dermal wound healing via improvement of neovascularization but inhibition of excessive inflammation as well as activation of myofibroblasts during dermal tissue remodeling.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell MovementCell ProliferationDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Disease Models, AnimalEndothelial Progenitor CellsFibroblastsInflammationIntracellular Signaling Peptides and ProteinsMacrophagesMaleMembrane ProteinsMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingIntracellular Signaling Peptides and ProteinsLnk protein, mouseMembrane ProteinsAnti-inflammatoryCell-based therapyEndothelial progenitor cellNeovascularizationWound healing

Identifiers

PMID27793180
PMCPMC5084514
OpenAlexW2545154697

What OpenQuestion holds

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LicenceCC BY
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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.