ArticleHistochemistry and cell biology2012
Smad4 disruption accelerates keratinocyte reepithelialization in murine cutaneous wound repair.
Article in Histochemistry and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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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.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- SETD2 epidermal deficiency promotes cutaneous wound healing via activation of AKT/mTOR Signalling.Cell proliferation · 2021Article
- Vascular endothelial Cdc42 deficiency delays skin wound-healing processes by increasing IL-1β and TNF-α expression.American journal of translational research · 2019Article
- Cancer Stem Cells in Squamous Cell Carcinoma.The Journal of investigative dermatology · 2017Review
- Transition from inflammation to proliferation: a critical step during wound healing.Cellular and molecular life sciences : CMLS · 2016Review
- Bone Morphogenetic Protein (BMP) signaling in development and human diseases.Genes & diseases · 2014Article
- Bone morphogenetic protein signaling suppresses wound-induced skin repair by inhibiting keratinocyte proliferation and migration.The Journal of investigative dermatology · 2014Article
- Transforming Growth Factor Beta Signaling in Cutaneous Wound Healing: Lessons Learned from Animal Studies.Advances in wound care · 2013Review
- The Histochemistry and Cell Biology compendium: a review of 2012.Histochemistry and cell biology · 2013Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
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.