Hair regeneration in mice was promoted by 3-methyladenine through inhibiting autophagy flux

LI Jing; LUO Fuling; WU Shengwang; WAN Jingyuan; ZHAO Hengguang

doi:10.11665/j.issn.1000-5048.20190412

Journal of China Pharmaceutical University > 2019 > 50(4): 468-474. > DOI: 10.11665/j.issn.1000-5048.20190412

LI Jing, LUO Fuling, WU Shengwang, WAN Jingyuan, ZHAO Hengguang. Hair regeneration in mice was promoted by 3-methyladenine through inhibiting autophagy flux[J]. Journal of China Pharmaceutical University, 2019, 50(4): 468-474. DOI: 10.11665/j.issn.1000-5048.20190412

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Hair regeneration in mice was promoted by 3-methyladenine through inhibiting autophagy flux

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Abstract

To explore the role of autophagy in hair follicle cycle and whether 3-methyladenine(3-MA)could promote hair regeneration in C57BL/6 mice through inhibiting autophagy flux, hair regeneration model of C57BL/6 mice was induced on the dorsal skin by depilation, and 3-MA was intraperitoneally injected to investigate hair regrowth, meanwhile vehicle and rapamycin(RAPA)were used as the controls. Results showed that 3-MA could obviously promote hair regrowth in depilated C57BL/6 mice. Furtherly, haematoxylin-eosin staining, immunohistochemical staining, immunofluorescence and Western blot tests were used to investigate the autophagy signals and the cell proliferation. Results showed that the expression of Beclin1 and LC3B II/I ratio were significantly decreased. Expression of P62 and Ki67 were increased, as well as the CD34 and CD49f double-labeled hair follicle stem cells were obviously increased inside bulge areas in 3-MA group, while contrarily in RAPA group. These results affirmed 3-MA, an autophagy inhibitor, could promote hair regeneration in depilated C57BL/6 mice by facilitating the transformation of hair follicle from telogen to anagen. 3-MA and other analogous autophagy inhibitors probably have a potential usage in future therapy in human telogen effluvium diseases.
- 3-methyladenine,
- autophagy,
- hair regeneration,
- rapamycin

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Hair regeneration in mice was promoted by 3-methyladenine through inhibiting autophagy flux

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