GDNF neurotrophic factor signalling determines the fate of dermal fibroblasts in wound-induced hair neogenesis and skin regeneration.

Autor: Vishlaghi N; Biology Department, Cox Science Center, University of Miami, Coral Gables, Florida, USA., Rieger S; Biology Department, Cox Science Center, University of Miami, Coral Gables, Florida, USA.; Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, Florida, USA., McGaughey V; Biology Department, Cox Science Center, University of Miami, Coral Gables, Florida, USA., Lisse TS; Biology Department, Cox Science Center, University of Miami, Coral Gables, Florida, USA.; Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, Florida, USA.
Jazyk: angličtina
Zdroj: Experimental dermatology [Exp Dermatol] 2022 Apr; Vol. 31 (4), pp. 577-581. Date of Electronic Publication: 2022 Jan 22.
DOI: 10.1111/exd.14526
Abstrakt: We propose that GDNF, a glial cell line-derived neurotrophic factor, can promote hair follicle neogenesis and skin regeneration after wounding by directing the fate of dermal fibroblasts. Our hypothesis is largely based on detailed GDNF and receptor analysis during skin regenerative stages, as well as the induction of GDNF receptors after wounding between the pro-regenerative spiny mouse (genus Acomys) and its less-regenerative descendant, the house mouse (Mus musculus). To characterize the GDNF-target cells, we will conduct a series of lineage-tracing experiments in conjunction with single-cell RNA and assay for transposase-accessible chromatin sequencing experiments. The heterogenetic dynamics of skin regeneration have yet to be fully defined, and this research will help to advance the fields of regenerative medicine and biology. Finally, we believe that stimulating the GDNF signalling pathway in fibroblasts from less-regenerative animals, such as humans, will promote skin regeneration, morphogenesis and scarless wound healing.
(© 2022 The Authors. Experimental Dermatology published by John Wiley & Sons Ltd.)
Databáze: MEDLINE
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