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Hair follicles (HF) undergo precisely regulated recurrent cycles of growth, cessation, and rest. The transitions from anagen (growth), to catagen (regression), to telogen (rest) involve a physiological involution of the HF. This process is likely coordinated by a variety of mechanisms including apoptosis and loss of growth factor signaling. However, the precise molecular mechanisms underlying follicle involution after hair keratinocyte differentiation and hair shaft assembly remain poorly understood. Here we demonstrate that a highly conserved microRNA,  miR-22  is markedly upregulated during catagen and peaks in telogen. Using gain- and loss-of-function approaches  in vivo , we find that  miR-22  overexpression leads to hair loss by promoting anagen-to-catagen transition of the HF, and that deletion of  miR-22  delays entry to catagen and accelerates the transition from telogen to anagen. Ectopic activation of  miR-22  results in hair loss due to the repression a hair keratinocyte differentiation program and keratinocyte progenitor expansion, as well as promotion of apoptosis. At the molecular level, we demonstrate that  miR-22  directly represses numerous transcription factors upstream of phenotypic keratin genes, including  Dlx3 ,  Foxn1 , and  Hoxc13 . We conclude that  miR-22  is a critical post-transcriptional regulator of the hair cycle and may represent a novel target for therapeutic modulation of hair growth.

Post-transcriptional Regulation of Keratinocyte Progenitor Cell Expansion, Differentiation and Hair Follicle Regression by miR-22