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Sci Rep. 2017 Aug 10;7(1):7797. doi: 10.1038/s41598-017-07513-0.

MicroRNA-132 promotes fibroblast migration via regulating RAS p21 protein activator 1 in skin wound healing.

Author information

1
Unit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
2
Unit of Dermatology and Venereology, Karolinska University Hospital, Stockholm, Sweden.
3
Unit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. ning.xu@ki.se.

Abstract

MicroRNA (miR)-132 has been identified as a top up-regulated miRNA during skin wound healing and its inhibition impairs wound repair. In a human in vivo surgical wound model, we showed that miR-132 was induced in epidermal as well as in dermal wound-edge compartments during healing. Moreover, in a panel of cells isolated from human skin wounds, miR-132 was found highly expressed in human dermal fibroblasts (HDFs). In HDFs, miR-132 expression was upregulated by TGF-β1. By overexpression or inhibition of miR-132, we showed that miR-132 promoted HDF migration. Mechanistically, global transcriptome analysis revealed that RAS signaling pathway was regulated by miR-132 in HDFs. We found that RAS p21 protein activator 1 (RASA1), a known target of miR-132, was downregulated in HDFs upon miR-132 overexpression. Silencing of RASA1 phenocopied the pro-migratory effect of miR-132. Collectively, our study reveals an important role for miR-132 in HDFs during wound healing and indicates a therapeutic potential of miR-132 in hard-to-heal skin wounds.

PMID:
28798331
PMCID:
PMC5552762
DOI:
10.1038/s41598-017-07513-0
[Indexed for MEDLINE]
Free PMC Article

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