Evidence map›Paper›PMID 22383956›Full record

ArticlePloS one2012

Delayed cutaneous wound healing and aberrant expression of hair follicle stem cell markers in mice selectively lacking Ctip2 in epidermis.

Xiaobo Liang, Shreya Bhattacharya, Gaurav Bajaj, Gunjan Guha, Zhixing Wang, Hyo-Sang Jang, Mark Leid, Arup Kumar Indra, Gitali Ganguli-Indra

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Cell journal · 2023
    Article
  7. Article
  8. Review
  9. The lysosomal trafficking regulator is necessary for normal wound healing.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2022
    Article
  10. Review
  11. Article
  12. Cxcr6-Based Mesenchymal Stem Cell Gene Therapy Potentiates Skin Regeneration in Murine Diabetic Wounds.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  13. Article
  14. A mouse model for vitamin D-induced human cathelicidin antimicrobial peptide gene expression.The Journal of steroid biochemistry and molecular biology · 2020
    Article
  15. Bcl11b/Ctip2 in Skin, Tooth, and Craniofacial System.Frontiers in cell and developmental biology · 2020
    Review
  16. Article
  17. Review
  18. Article
  19. 1α,25-dihydroxyvitamin DNanomedicine (London, England) · 2018
    Article
  20. 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

9 authors at 1 institution in 1 country.

Xiaobo LiangDepartment of Pharmaceutical Sciences, College of Pharmacy, Oregon State University, Corvallis, United States of America.
Shreya Bhattacharya
Gaurav Bajaj
Gunjan Guha
Zhixing Wang
Hyo-Sang Jang
Mark Leid
Arup Kumar Indra
Gitali Ganguli-Indra
Oregon State University · US

Funding

Reducing Susceptibility to Environmental Stress Throughout the Life SpanP30ES000210 · NIEHS · OREGON STATE UNIVERSITY · PI BECKMAN, JOSEPH S · 1985 to 2015
$21.4M
Mechanism of CTIP2 action in mouse epidermal homeostasis and barrier formation, R01AR056008 · NIAMS · OREGON STATE UNIVERSITY · PI INDRA, ARUP K. · 2008 to 2012
$1.5M
NIAMS NIH HHS 5R01AR056008-02NIAMS NIH HHS R01 AR056008NIEHS NIH HHS ES00210NIEHS NIH HHS P30 ES000210
6 · The paper itself

Abstract

backgroundCOUP-TF interacting protein 2 [(Ctip2), also known as Bcl11b] is an important regulator of skin homeostasis, and is overexpressed in head and neck cancer. Ctip2(ep-/-) mice, selectively ablated for Ctip2 in epidermal keratinocytes, exhibited impaired terminal differentiation and delayed epidermal permeability barrier (EPB) establishment during development, similar to what was observed in Ctip2 null (Ctip2(-/-)) mice. Considering that as an important role of Ctip2, and the fact that molecular networks which underlie cancer progression partially overlap with those responsible for tissue remodeling, we sought to determine the role of Ctip2 during cutaneous wound healing. METHODOLOGY/PRINCIPAL

findingsFull thickness excisional wound healing experiments were performed on Ctip2(L2/L2) and Ctip2(ep-/-) animals per time point and used for harvesting samples for histology, immunohistochemistry (IHC) and immunoblotting. Results demonstrated inherent defects in proliferation and migration of Ctip2 lacking keratinocytes during re-epithelialization. Mutant mice exhibited reduced epidermal proliferation, delayed keratinocyte activation, altered cell-cell adhesion and impaired ECM development. Post wounding, Ctip2(ep-/-) mice wounds displayed lack of E-Cadherin suppression in the migratory tongue, insufficient expression of alpha smooth muscle actin (alpha SMA) in the dermis, and robust induction of K8. Importantly, dysregulated expression of several hair follicle (HF) stem cell markers such as K15, NFATc1, CD133, CD34 and Lrig1 was observed in mutant skin during wound repair. CONCLUSIONS/SIGNIFICANCE: Results confirm a cell autonomous role of keratinocytic Ctip2 to modulate cell migration, proliferation and/or differentiation, and to maintain HF stem cells during cutaneous wounding. Furthermore, Ctip2 in a non-cell autonomous manner regulated granulation tissue formation and tissue contraction during wound closure.

Indexed as

Gene Expression RegulationActinsAnimalsAnimals, NewbornCadherinsCell DifferentiationCell MovementDisease ProgressionHair FollicleImmunohistochemistryKeratinocytesMaleMiceMice, Inbred C57BLMice, TransgenicPhalloidineActinsBcl11b protein, mouseCadherinsPhalloidineRepressor ProteinsTretinoinTumor Suppressor Proteins

Identifiers

PMID22383956
PMCPMC3283611
OpenAlexW2119585270

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.