Fibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process

Abstract In the wound healing process, the morphology of keratinocytes at the wound edge temporarily changes to a spindle morphology, which is thought to occur due to an epithelial–mesenchymal transition (EMT). Fibroblast growth factor (FGF) 2, also called basic FGF, has the potential to accelerate...

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Autores principales:	Yuta Koike, Mariko Yozaki, Atsushi Utani, Hiroyuki Murota
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/657a7d6686ff4b44b893cab9629aa1fb
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spelling	oai:doaj.org-article:657a7d6686ff4b44b893cab9629aa1fb2021-12-02T15:10:05ZFibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process10.1038/s41598-020-75584-72045-2322https://doaj.org/article/657a7d6686ff4b44b893cab9629aa1fb2020-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-75584-7https://doaj.org/toc/2045-2322Abstract In the wound healing process, the morphology of keratinocytes at the wound edge temporarily changes to a spindle morphology, which is thought to occur due to an epithelial–mesenchymal transition (EMT). Fibroblast growth factor (FGF) 2, also called basic FGF, has the potential to accelerate wound closure by activating vascular endothelial cells and fibroblasts. We examined the effects of FGF2 on keratinocyte morphology and EMT in wounded skin. Histological examination of murine wounds treated with FGF2 revealed that wound edge keratinocytes formed thickened and multilayered epithelia. In addition, we detected wound edge keratinocytes migrating individually toward the wound center. These migrating keratinocytes exhibited not only spindle morphology but also down-regulated E-cadherin and up-regulated vimentin expression, which is characteristic of EMT. In FGF2-treated wounds, a PCR array revealed the upregulation of genes related to EMT, including transforming growth factor (TGF) signaling. Further, FGF2-treated wound edge keratinocytes expressed EMT-associated transcription factors, including Snai2, and showed translocation of β-catenin from the cell membrane to the cytoplasm/nucleus. However, in vitro examination of keratinocytes revealed that FGF2 alone did not activate EMT in keratinocytes, but that FGF2 might promote EMT in combination with TGFβ1. These findings suggest that FGF2 treatment of wounds could promote keratinocyte EMT, accelerating wound closure.Yuta KoikeMariko YozakiAtsushi UtaniHiroyuki MurotaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-13 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yuta Koike Mariko Yozaki Atsushi Utani Hiroyuki Murota Fibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process
description	Abstract In the wound healing process, the morphology of keratinocytes at the wound edge temporarily changes to a spindle morphology, which is thought to occur due to an epithelial–mesenchymal transition (EMT). Fibroblast growth factor (FGF) 2, also called basic FGF, has the potential to accelerate wound closure by activating vascular endothelial cells and fibroblasts. We examined the effects of FGF2 on keratinocyte morphology and EMT in wounded skin. Histological examination of murine wounds treated with FGF2 revealed that wound edge keratinocytes formed thickened and multilayered epithelia. In addition, we detected wound edge keratinocytes migrating individually toward the wound center. These migrating keratinocytes exhibited not only spindle morphology but also down-regulated E-cadherin and up-regulated vimentin expression, which is characteristic of EMT. In FGF2-treated wounds, a PCR array revealed the upregulation of genes related to EMT, including transforming growth factor (TGF) signaling. Further, FGF2-treated wound edge keratinocytes expressed EMT-associated transcription factors, including Snai2, and showed translocation of β-catenin from the cell membrane to the cytoplasm/nucleus. However, in vitro examination of keratinocytes revealed that FGF2 alone did not activate EMT in keratinocytes, but that FGF2 might promote EMT in combination with TGFβ1. These findings suggest that FGF2 treatment of wounds could promote keratinocyte EMT, accelerating wound closure.
format	article
author	Yuta Koike Mariko Yozaki Atsushi Utani Hiroyuki Murota
author_facet	Yuta Koike Mariko Yozaki Atsushi Utani Hiroyuki Murota
author_sort	Yuta Koike
title	Fibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process
title_short	Fibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process
title_full	Fibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process
title_fullStr	Fibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process
title_full_unstemmed	Fibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process
title_sort	fibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/657a7d6686ff4b44b893cab9629aa1fb
work_keys_str_mv	AT yutakoike fibroblastgrowthfactor2acceleratestheepithelialmesenchymaltransitioninkeratinocytesduringwoundhealingprocess AT marikoyozaki fibroblastgrowthfactor2acceleratestheepithelialmesenchymaltransitioninkeratinocytesduringwoundhealingprocess AT atsushiutani fibroblastgrowthfactor2acceleratestheepithelialmesenchymaltransitioninkeratinocytesduringwoundhealingprocess AT hiroyukimurota fibroblastgrowthfactor2acceleratestheepithelialmesenchymaltransitioninkeratinocytesduringwoundhealingprocess
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Fibroblast growth factor 2 accelerates the epithelial–mesenchymal transition in keratinocytes during wound healing process

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