@entity10898 / @entity17777 signaling is required in @entity864 -induced XXXX and differentiation of hair follicle melanocytes for @entity2118 .

@entity10898 @entity4222 @entity19 @entity17777 @entity1358 @entity2118 @entity865 @entity864
UNASSIGNED: Hair follicle @entity1358 ( @entity1358 ) are responsible for hair pigmentation and also function as a major melanocyte reservoir for @entity2118 . However, the molecular mechanism promoting @entity1358 for @entity2118 remains elusive. @entity864 ( @entity865 ) mimics key signaling involved in melanocyte growth, @entity4222 and differentiation. We therefore investigated the molecular basis for the contribution of hair follicle @entity1358 to @entity2118 using the @entity865 induction model. We found that repetitive @entity865 treatment of female C57BL/6 @entity19 dorsal skin induced @entity2118 by increasing the number of epidermal melanocytes. Particularly, @entity865 treatment induced @entity1358 to initiate proliferation, exit the stem cell niche and differentiate. We also demonstrated that @entity865 promotes melanoblast @entity4222 and differentiation in vitro. At the molecular level, @entity865 treatment induced robust expression of @entity10898 ( @entity10898 ) in keratinocytes and @entity17777 in melanoblasts and melanocytes. Administration of ACK2, a neutralizing antibody against the Kit receptor, suppressed @entity19 @entity2118 , decreased the number of epidermal melanocytes, and inhibited melanoblast @entity4222 . Taken together, our data demonstrate that @entity865 promotes the expansion, @entity4222 and differentiation of hair follicle @entity1358 for @entity19 @entity2118 . @entity10898 / @entity17777 signaling was required for @entity865 -induced @entity4222 and differentiation of hair follicle melanocytes. Our findings may provide an excellent model to investigate the signaling mechanisms regulating @entity2118 from @entity19 hair follicle @entity1358 , and a potential therapeutic option for @entity2118 .
