Presentation Radioresistance of the Hair Follicles Caused by FGF18

Nakayama, Fumiaki  ,  Umeda, Sachiko  ,  Yasuda, Takeshi  ,  Imamura, Toru  ,  Imai, Takashi

Hair cycle resting phase (telogen) hair follicles are known to be more radioresistant than growth phase (anagen) hair follicles. Recently, FGF18 signaling has been reported to maintain the telogen phase of the hair cycle, and also the quiescence of hair follicle stem cells. In contrast, several FGFs can exert radioprotective effects to reduce and improve radiation-induced tissue damage. This study focuses on clarifying the contribution of FGF18 to radioresistance of telogen hair follicles. Irradiation of anagen hair follicles of BALB/c mice with gamma-rays at 6 Gy caused hair follicle dystrophy, resulting in the prominent delay of hair regeneration, whereas irradiation of telogen hair follicles at 6 Gy did not induce the dystrophy even after the post-irradiation plucking. In addition, K15+ stem cells did not decrease in the telogen hair follicles after irradiation, although they prominently decreased in the anagen hair follicles after irradiation. In contrast, FGF receptor inhibitor treatment induced radiation-induced hair follicle dystrophy in the telogen phase, suggesting that FGF signaling plays an important role in the radioresistance of telogen hair follicles. Actually, administration of recombinant FGF18 inhibited the proliferation of hair follicle cells and radiation-induced apoptosis in the hair bulbs, and maintained the number of K15+ stem cells in the bulge after irradiation, so that hair was successfully regenerated after irradiation at 6 Gy in the anagen phase. Moreover, FGF18 treatment drastically reduced DNA double strand breaks in the anagen hair follicle cells 4 h after irradiation, and also decreased the transcript levels of CDK1 and Cyclin B, which play a critical role in the G2/M transition of cell cycle. These findings suggest that FGF18 signaling for hair cycle resting phase causes radioresistance in the telogen hair follicles through the enhancement of DNA repair by the cell-cycle arrest.
15th International Congress of Radiation Research (ICRR 2015)

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