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Micro RNA ‐23b‐3p regulates human keratinocyte differentiation through repression of TGIF 1 and activation of the TGF ‐ß– SMAD 2 signalling pathway
Author(s) -
BarbollatBoutrand Laetitia,
JolyTonetti Nicolas,
Dos Santos Morgan,
Metral Elodie,
Boher Aurélie,
Masse Ingrid,
BerthierVergnes Odile,
Bertolino Philippe,
Damour Odile,
Lamartine Jérôme
Publication year - 2017
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13119
Subject(s) - smad , gene silencing , corepressor , microbiology and biotechnology , psychological repression , rna , keratinocyte , biology , rna interference , gene expression , cellular differentiation , regulation of gene expression , signal transduction , gene , genetics , cell culture
Micro RNA s (mi RNA s) are a class of short non‐coding RNA s capable of repressing gene expression at the post‐transcriptional level. mi RNA s participate in the control of numerous cellular mechanisms, including skin homeostasis and epidermal differentiation. However, few mi RNA s involved in these processes have been identified so far in human skin, and the gene networks they control remain largely unknown. Here, we focused on mi R ‐23b‐3p, a mi RNA that is expressed during the late step of human keratinocyte differentiation. We report that mi R ‐23b‐3p silencing modulates epidermal differentiation in human skin reconstructs. The SMAD transcriptional corepressor TGIF 1 was identified on bioinformatic analysis as a potential target of mi R ‐23b‐3p. Expression analysis and reporter gene assays confirmed direct regulation of TGIF 1 expression by mi R ‐23b‐3p. Finally, we showed that mi R ‐23‐3p was able to activate TGF ‐ß signalling in human keratinocytes by increasing SMAD 2 phosphorylation through TGIF 1 repression. Taken together, these data identify mi R ‐23b‐3p as a new regulator of human epidermal differentiation in line with TGF ‐ß signalling.