Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/107371
Title: microRNA-155 inhibition restores Fibroblast Growth Factor 7 expression in diabetic skin and decreases wound inflammation
Authors: Moura, João 
Sørensen, Anja
Leal, Ermelindo 
Svendsen, Rikke
Carvalho, Lina 
Willemoes, Rie Juul
Jørgensen, Per Trolle
Jenssen, Håvard
Wengel, Jesper
Dalgaard, Louise Torp
Carvalho, Eugenia 
Issue Date: 9-Apr-2019
Publisher: Springer Nature
Project: SFRH/BPD/112883/2015 
CENTRO-01-0145-FEDER-000012/HealthyAging2020 
metadata.degois.publication.title: Scientific Reports
metadata.degois.publication.volume: 9
metadata.degois.publication.issue: 1
Abstract: Treatment for chronic diabetic foot ulcers is limited by the inability to simultaneously address the excessive inflammation and impaired re-epithelization and remodeling. Impaired re-epithelization leads to significantly delayed wound closure and excessive inflammation causes tissue destruction, both enhancing wound pathogen colonization. Among many differentially expressed microRNAs, miR-155 is significantly upregulated and fibroblast growth factor 7 (FGF7) mRNA (target of miR-155) and protein are suppressed in diabetic skin, when compared to controls, leading us to hypothesize that topical miR-155 inhibition would improve diabetic wound healing by restoring FGF7 expression. In vitro inhibition of miR-155 increased human keratinocyte scratch closure and topical inhibition of miR-155 in vivo in wounds increased murine FGF7 protein expression and significantly enhanced diabetic wound healing. Moreover, we show that miR-155 inhibition leads to a reduction in wound inflammation, in accordance with known pro-inflammatory actions of miR-155. Our results demonstrate, for the first time, that topical miR-155 inhibition increases diabetic wound fibroblast growth factor 7 expression in diabetic wounds, which, in turn, increases re-epithelization and, consequently, accelerates wound closure. Topical miR-155 inhibition targets both excessive inflammation and impaired re-epithelization and remodeling, being a potentially new and effective treatment for chronic diabetic foot ulcers.
URI: https://hdl.handle.net/10316/107371
ISSN: 2045-2322
DOI: 10.1038/s41598-019-42309-4
Rights: openAccess
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais
I&D CNC - Artigos em Revistas Internacionais

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