Evidence map›Paper›PMID 25122137›Full record

ArticlePloS one2014

Alteration of skin wound healing in keratinocyte-specific mediator complex subunit 1 null mice.

Fumihito Noguchi, Takeshi Nakajima, Shigeki Inui, Janardan K Reddy, Satoshi Itami

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Genetically Engineered Mice Unveil In Vivo Roles of the Mediator Complex.International journal of molecular sciences · 2023
    Review
  4. MED1 Ablation Promotes Oral Mucosal Wound Healing via JNK Signaling Pathway.International journal of molecular sciences · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Celery (Veterinary world · 2020
    Article
  10. Article
  11. Article
  12. IL-17R-EGFR axis links wound healing to tumorigenesis in Lrig1The Journal of experimental medicine · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
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

5 authors.

Fumihito NoguchiDepartment of Regenerative Dermatology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Takeshi NakajimaDepartment of Dermatology, Osaka General Medical Center, Osaka, Japan.
Shigeki InuiDepartment of Regenerative Dermatology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Janardan K ReddyDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States of America.
Satoshi ItamiDepartment of Regenerative Dermatology, Graduate School of Medicine, Osaka University, Osaka, Japan.

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Med1 in Liver Metabolism, Regeneration and CancerR01DK097249 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI JIA, YUZHI, REDDY, JANARDAN K. · 2013 to 2017
$1.7M
NCI NIH HHS P30 CA060553
6 · The paper itself

Abstract

MED1 (Mediator complex subunit 1) is a co-activator of various transcription factors that function in multiple transcriptional pathways. We have already established keratinocyte-specific MED1 null mice (Med1(epi-/-)) that develop epidermal hyperplasia. Herein, to investigate the function(s) of MED1 in skin wound healing, full-thickness skin wounds were generated in Med1(epi-/-) and age-matched wild-type mice and the healing process was analyzed. Macroscopic wound closure and the re-epithelialization rate were accelerated in 8-week-old Med1(epi-/-) mice compared with age-matched wild-type mice. Increased lengths of migrating epithelial tongues and numbers of Ki67-positive cells at the wounded epidermis were observed in 8-week-old Med1(epi-/-) mice, whereas wound contraction and the area of α-SMA-positive myofibroblasts in the granulation tissue were unaffected. Migration was enhanced in Med1(epi-/-) keratinocytes compared with wild-type keratinocytes in vitro. Immunoblotting revealed that the expression of follistatin was significantly decreased in Med1(epi-/-) keratinocytes. Moreover, the mitogen-activated protein kinase pathway was enhanced before and after treatment of Med1(epi-/-) keratinocytes with activin A in vitro. Cell-cycle analysis showed an increased ratio of S phase cells after activin A treatment of Med1(epi-/-) keratinocytes compared with wild-type keratinocytes. These findings indicate that the activin-follistatin system is involved in this acceleration of skin wound healing in 8-week-old Med1(epi-/-) mice. On the other hand, skin wound healing in 6-month-old Med1(epi-/-) mice was significantly delayed with decreased numbers of Ki67-positive cells at the wounded epidermis as well as BrdU-positive label retaining cells in hair follicles compared with age-matched wild-type mice. These results agree with our previous observation that hair follicle bulge stem cells are reduced in older Med1(epi-/-) mice, indicating a decreased contribution of hair follicle stem cells to epidermal regeneration after wounding in 6-month-old Med1(epi-/-) mice. This study sheds light on the novel function of MED1 in keratinocytes and suggests a possible new therapeutic approach for skin wound healing and aging.

Indexed as

ActinsActivinsAnimalsCell MovementFollistatinHair FollicleKeratinocytesKi-67 AntigenMediator Complex Subunit 1MiceMice, KnockoutMitogen-Activated Protein KinasesRe-EpithelializationSignal TransductionSkinS PhaseActinsActivinsalpha-smooth muscle actin, mouseFollistatinKi-67 AntigenMed1 protein, mouseMediator Complex Subunit 1Mitogen-Activated Protein Kinases

Identifiers

PMID25122137
PMCPMC4133190

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Registered trials

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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.