Corticosterone inhibits GAS6 to govern hair follicle stem-cell quiescence

Sekyu Choi, Bing Zhang, Sai Ma, Meryem Gonzalez-Celeiro, Daniel Stein, Xin Jin, Seung Tea Kim, Yuan-Lin Kang, Antoine Besnard, Amelie Rezza, Laura Grisanti, Jason D. Buenrostro, Michael Rendl, Matthias Nahrendorf, Amar Sahay and Ya-Chieh Hsu ()
Additional contact information
Sekyu Choi: Harvard University
Bing Zhang: Harvard University
Sai Ma: Harvard University
Meryem Gonzalez-Celeiro: Harvard University
Daniel Stein: Harvard University
Xin Jin: Harvard University
Seung Tea Kim: Harvard University
Yuan-Lin Kang: Harvard University
Antoine Besnard: Harvard Stem Cell Institute
Amelie Rezza: Icahn School of Medicine at Mount Sinai
Laura Grisanti: Icahn School of Medicine at Mount Sinai
Jason D. Buenrostro: Harvard University
Michael Rendl: Icahn School of Medicine at Mount Sinai
Matthias Nahrendorf: Massachusetts General Hospital Research Institute, Harvard Medical School
Amar Sahay: Harvard Stem Cell Institute
Ya-Chieh Hsu: Harvard University

Nature, 2021, vol. 592, issue 7854, 428-432

Abstract: Abstract Chronic, sustained exposure to stressors can profoundly affect tissue homeostasis, although the mechanisms by which these changes occur are largely unknown. Here we report that the stress hormone corticosterone—which is derived from the adrenal gland and is the rodent equivalent of cortisol in humans—regulates hair follicle stem cell (HFSC) quiescence and hair growth in mice. In the absence of systemic corticosterone, HFSCs enter substantially more rounds of the regeneration cycle throughout life. Conversely, under chronic stress, increased levels of corticosterone prolong HFSC quiescence and maintain hair follicles in an extended resting phase. Mechanistically, corticosterone acts on the dermal papillae to suppress the expression of Gas6, a gene that encodes the secreted factor growth arrest specific 6. Restoring Gas6 expression overcomes the stress-induced inhibition of HFSC activation and hair growth. Our work identifies corticosterone as a systemic inhibitor of HFSC activity through its effect on the niche, and demonstrates that the removal of such inhibition drives HFSCs into frequent regeneration cycles, with no observable defects in the long-term.

Date: 2021
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DOI: 10.1038/s41586-021-03417-2

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