TY  - JOUR
A1  - Naeem, Zumer
A1  - Zukunft, Sven
A1  - Günther, Stephan
A1  - Liebner, Stefan
A1  - Weigert, Andreas
A1  - Hammock, Bruce D.
A1  - Frömel, Timo
A1  - Fleming, Ingrid
T1  - Role of the soluble epoxide hydrolase in the hair follicle stem cell homeostasis and hair growth
T2  - Pflügers Archiv : European journal of physiology
N2  - Polyunsaturated fatty acids (PUFAs) are used as traditional remedies to treat hair loss, but the mechanisms underlying their beneficial effects are not well understood. Here, we explored the role of PUFA metabolites generated by the cytochrome P450/soluble epoxide hydrolase (sEH) pathway in the regulation of the hair follicle cycle. Histological analysis of the skin from wild-type and sEH−/− mice revealed that sEH deletion delayed telogen to anagen transition, and the associated activation of hair follicle stem cells. Interestingly, EdU labeling during the late anagen stage revealed that hair matrix cells from sEH−/− mice proliferated at a greater rate which translated into increased hair growth. Similar effects were observed in in vitro studies using hair follicle explants, where a sEH inhibitor was also able to augment whisker growth in follicles from wild-type mice. sEH activity in the dorsal skin was not constant but altered with the cell cycle, having the most prominent effects on levels of the linoleic acid derivatives 12,13-epoxyoctadecenoic acid (12,13-EpOME), and 12,13-dihydroxyoctadecenoic acid (12,13-DiHOME). Fitting with this, the sEH substrate 12,13-EpOME significantly increased hair shaft growth in isolated anagen stage hair follicles, while its diol; 12,13-DiHOME, had no effect. RNA sequencing of isolated hair matrix cells implicated altered Wnt signaling in the changes associated with sEH deletion. Taken together, our data indicate that the activity of the sEH in hair follicle changes during the hair follicle cycle and impacts on two stem cell populations, i.e., hair follicle stem cells and matrix cells to affect telogen to anagen transition and hair growth.
Y1  - 2022
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/69562
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-695624
SN  - 1432-2013
N1  - Open Access funding enabled and organized by Projekt DEAL. This work was supported by the Deutsche Forschungsgemeinschaft (SFB1039/3 B6 – Project ID 204083920, GRK 2336 TP5—Project ID 321115009 and the CardioPulmonary Institute, EXC 2026, Project ID: 390649896). Partial support was provided by Deutsche Forschungsgemeinschaft grant LI 911/7–1, NIH – NIEHS (RIVER Award) R35 ES030443-01 and NIH – NIEHS (Superfund Award) P42 ES004699.
VL  - 474
IS  - 9
SP  - 1021
EP  - 1035
PB  - Springer
CY  - Berlin ; Heidelberg
ER  -