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Anatomical and functional landscapes of hair regeneration across the body
Author(s) -
Plikus Maksim,
Wang Qixuan,
Oh Ji Won,
Nie Qing
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.232.1
Subject(s) - regeneration (biology) , wnt signaling pathway , activator (genetics) , neuroscience , anatomy , microbiology and biotechnology , chemistry , biology , signal transduction , receptor , genetics
Hair follicles (HFs) in the skin show robust cyclic regeneration. Yet, since skin contains many thousands of HFs, control principles of collective hair regeneration and hair growth regionalization remain unclear. Using multi‐scale mathematical modeling we shows that coupling inhibitor and activator signals with physical growth of HFs is sufficient to drive periodicity and excitability of hair regeneration. Model simulations and experimental data reveal that the entire skin in mice behaves as a heterogeneous regenerative landscape, composed of anatomical domains where HFs have distinct cycling dynamics. Interactions between fast‐cycling ventral and chin HFs and slow‐cycling dorsal HFs produce prominent bilaterally symmetric patterns. Skin on mouse ears behaves as a hyper‐refractory domain with HFs that remain, in principle, competent to cyclic regeneration, yet that physiologically enter extended rest phase. Ear HF hyper‐refractivity relates to high levels of BMP ligands and WNT antagonists, in part expressed by ear‐specific cartilage and muscle, the novel component of skin signaling macro‐environment. Hair growth stops at the boundaries with hyper‐refractory ears and anatomically discontinuous eyelids, generating wave‐breaking effects. We posit that similar mechanisms for coupled regeneration and large‐scale patterning of growth activities with dominant activator, hyper‐refractory, and wave‐breaker regions can operate in other actively renewing organs. Support or Funding Information MVP is supported by the NIH NIAMS grants R01‐AR067273, R01‐AR069653 and Pew Charitable Trust grant. QN is supported by NSF grants: DMS 1161621, and DMS 1562176 and NIH grants: P50‐GM076516, R01‐GM107264, and R01‐NS095355. JWO is supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (2016R1C1B1015211). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .