Leptin of dermal adipose tissue is differentially expressed during the hair cycle and contributes to adipocyte-mediated growth inhibition of anagen-phase vibrissa hair

Adipose tissue encircles the lower portion of anagen hair follicles and may regulate hair cycle progression. As leptin is a major adipokine, its level of expression from the dermal white adipose tissue during hair cycle progression was studied. The result shows that leptin level is differentially ex...

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Bibliographic Details
Published in:Experimental dermatology 2015-01, Vol.24 (1), p.57-60
Main Authors: Yang, Chao-Chun, Sheu, Hamm-Ming, Chung, Pei-Lun, Chang, Chung-Hsing, Tsai, Yau-Sheng, Hughes, Michael W., Tuan, Tai-Lan, Huang, Lynn L. H.
Format: Article
Language:English
Subjects:
adipocytes
Adipocytes - cytology
adipokines
Adipose Tissue - metabolism
Animals
Coculture Techniques
Dermis - metabolism
Female
Gene Expression Profiling
Gene Expression Regulation
Hair - physiology
hair follicles
Humans
leptin
Leptin - physiology
Mice
Organ Culture Techniques
Skin - metabolism
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Summary:Adipose tissue encircles the lower portion of anagen hair follicles and may regulate hair cycle progression. As leptin is a major adipokine, its level of expression from the dermal white adipose tissue during hair cycle progression was studied. The result shows that leptin level is differentially expressed during hair cycle, the lowest in early anagen phase, upregulated in late anagen phase and the highest in the telogen phase. On the other hand, leptin receptor is detected in keratin 15‐positive hair bulge epithelium of both anagen‐ and telogen‐phase hair follicles of mice pelage and vibrissa hair, and hair from human scalp. Leptin contributes to adipocyte‐mediated growth inhibition of anagen‐phase vibrissa hair as demonstrated in organ culture and coculture system. Our data suggest that leptin of dermal white adipose tissue might regulate hair growth and, therefore, hair cycle progression via leptin receptor on the hair follicle epithelium.
ISSN:0906-6705
1600-0625
DOI:10.1111/exd.12566