GDNF promotes hair formation and cutaneous wound healing by targeting bulge stem cells.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 32566252.
- Also identified by DOI 10.1038/s41536-020-0098-z and PMC identifier 7293257.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Glial-cell-derived neurotrophic factor (GDNF) is a well-studied neuroregenerative factor; however, the degree to which it supports hair formation and skin wound repair is not known. By using a <i>Gfra1</i> (GDNF family receptor alpha 1) knock-in reporter mouse line, GDNF signaling was found to occur within hair bulge stem cells (BSCs) during the initiation of the hair cycle and early stages of hair formation after depilation. Both recombinant and transgene overexpression of GDNF promoted BSC colony growth, hair formation, and skin repair after wounding through enhanced self-renewal of BSCs and commitment of BSC-derived progenitors into becoming epidermal cells at the injury site. Conditional ablation of <i>Gfra1</i> among BSCs impaired the onset of the hair cycle, while conditional ablation of the GDNF family member signal transducer, <i>Ret</i>, within BSCs prevented the onset of the hair cycle and depilation-induced anagen development of hair follicles. Our findings reveal that GDNF promotes hair formation and wound repair and that bulge stem cells are critical mediators of both.