Igf1r signalling acts on the anagen-to-catagen transition in the hair cycle.
Identifieur interne : 004171 ( Ncbi/Curation ); précédent : 004170; suivant : 004172Igf1r signalling acts on the anagen-to-catagen transition in the hair cycle.
Auteurs : Mathieu Castela [France] ; Fabien Linay [France] ; Edwige Roy [France] ; Philippe Moguelet [France] ; Jie Xu [France] ; Martin Holzenberger [France] ; Kiarash Khosrotehrani [Australie] ; Selim Aractingi [France]Source :
- Experimental dermatology [ 1600-0625 ] ; 2017.
Abstract
Insulin-like growth factor 1 (Igf1) is important for skin development and homoeostasis. However, overexpression and inactivation studies have produced variable findings regarding its role in hair follicle (HF) biology. Here, we studied a conditional and inducible knockout of the Igf1 receptor (Igf1r) in keratin 15-expressing bulge cells. Deletion of Igf1r after the development of the skin appendages in K15-Igf1r(KO) mice showed no abnormalities in epidermal homoeostasis. Numbers of bulge cells were lower in K15-Igf1r(KO) mice than in controls, without consequences on wound healing, at least in young mice. K15-Igf1r(KO) HFs entered anagen phase earlier than controls and showed a delay in the anagen/catagen switch. The expression of Bmp-4 mRNA was inhibited in HFs from K15-Igf1r(KO) . MED1 transcription was impaired in the epidermis of K15-Igf1r(KO) mice. These findings suggest that Igf1r controls the hair cycle, partly through Bmp-4 activation.
DOI: 10.1111/exd.13287
PubMed: 28094870
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<front><div type="abstract" xml:lang="en">Insulin-like growth factor 1 (Igf1) is important for skin development and homoeostasis. However, overexpression and inactivation studies have produced variable findings regarding its role in hair follicle (HF) biology. Here, we studied a conditional and inducible knockout of the Igf1 receptor (Igf1r) in keratin 15-expressing bulge cells. Deletion of Igf1r after the development of the skin appendages in K15-Igf1r(KO) mice showed no abnormalities in epidermal homoeostasis. Numbers of bulge cells were lower in K15-Igf1r(KO) mice than in controls, without consequences on wound healing, at least in young mice. K15-Igf1r(KO) HFs entered anagen phase earlier than controls and showed a delay in the anagen/catagen switch. The expression of Bmp-4 mRNA was inhibited in HFs from K15-Igf1r(KO) . MED1 transcription was impaired in the epidermis of K15-Igf1r(KO) mice. These findings suggest that Igf1r controls the hair cycle, partly through Bmp-4 activation.</div>
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