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Cited by 14Wound Healing and TreatmentsTGF-β signaling in diseasesLiver physiology and pathology

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Smad4 disruption accelerates keratinocyte reepithelialization in murine cutaneous wound repair

Yang, Leilei, Li, Wenlong, Wang, Shaoxia, Wang, Lijuan, Li, Yang, Yang, Xiao, Peng, Ruiyun·2012·Histochemistry and Cell Biology
DOI 10.1007/s00418-012-0974-8
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Abstract

Keratinocyte reepithelialization is a rate-limiting event in cutaneous wound repair, which involves the migration and proliferation of keratinocytes to cover the denuded dermal surface. Transforming growth factor-β1 (TGF-β1) has the ability to induce epithelial cell migration while inhibiting proliferation, and controversial results have been generated regarding the effect of TGF-β signaling on reepithelialization. In this study, full-thickness skin wounds were made in keratinocyte-specific Smad4 knockout and the control mice. The wound closure, reepithelialization, keratinocyte proliferation, myofibroblast numbers and collagen deposition of were assessed. The results showed that the proliferation of keratinocytes increased, which accelerated the reepithelialization, and led to faster wound repair in the epidermis of Smad4 mutant mice. Upregulation of keratin 17, 14-3-3 sigma and phosphorylated AKT in the hyperproliferative epidermis may be correlated with the accelerated reepithelialization. We conclude that Smad4 plays an inhibitory role in the keratinocyte-mediated reepithelialization of wound healing.

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Crossref · 10.1007/s00418-012-0974-8

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  • Specific deletion of Smad4 in epidermal keratinocytes showed enhanced re-epithelialisation mainly due to increased keratinocyte proliferation.

    “specific deletion of Smad4 in epidermal keratinocytes and showed enhanced re-epithelialisation of wounds, which was mainly due to increased keratinocyte proliferation [164].”

    From Transition from inflammation to proliferation: a critical step during wound healing (2016) · cites this paper as [164]

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References 29 · Cited by 14

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Metadata

Authors
Yang, L., Li, W., Wang, S., Wang, L., Li, Y., Yang, X., & Peng, R.
Affiliations
State Key Laboratory of Proteomics (CN)
Corresponding author
  • Yang, Xiao
  • Peng, Ruiyun
ORCID
Venue
Histochemistry and Cell Biology
Publisher
Springer Science and Business Media LLC
Published
2012-05-30
Volume
138
Issue
4
Pages
573-582
ISSN
  • 0948-6143 (ISSN-L)
  • 1432-119X
DOI
10.1007/s00418-012-0974-8
OpenAlex
W2090999292
Cited by
14
References
29
Citations by year
2021: 1 · 2019: 3 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 2 · 2013: 4
FWCI
2.36
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Histochemistry and Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Health Sciences › Medicine › Surgery › Wound Healing and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
SMAD4, skin wound healing, keratinocyte proliferation, keratinocyte migration, TGF-beta signaling, keratin 17, 14-3-3 sigma, Akt phosphorylation, myofibroblasts, collagen deposition, full-thickness skin wounds, epidermis
MeSH terms
Animals, Cell Count, Epithelial Cells, Genotype, Skin, Wound Healing, Blotting, Western, Keratinocytes, Up-Regulation, Mice, Knockout, 14-3-3 Proteins, Cell Proliferation, Mice, Smad4 Protein, Keratin-17, Myofibroblasts

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