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Role of Vitamin D receptor in adult hair follicle cycling

Hair follicle cycling describes rhythmically re‐occurring phases of growth, regression and tissue re‐modelling events in a complex neuroectodermal‐mesodermal interaction system. Hunting the oscillator mechanism that drives these hair follicle transformations is one of the pre‐eminent challenges of basic and clinically applied hair research. Among the large number of molecules playing a role in the control of this oscillator system, one of the most interesting is the vitamin D receptor (VDR). Lack or alteration of VDR in both human and mouse lead to an absence of adult hair follicle cycling, with a defect in anagen re‐initiation. However lack of VDR does not affect embryonic hair development and differentiation of epidermal keratinocytes, showing the specificity of VDR action in adult hair follicle cycling. The study objective is to identify the target genes of VDR in the control of hair follicle cycling in mice. Our studies using qRTPCR and Immunohistochemistry show that VDR −/ − mouse hair follicles lack induction of two key regulators of the anagen/catagen transition: transforming growth factor‐beta receptor 2 and noggin. These changes are accompanied by decreased expression of versican, thought to be involved with the initiation of hair follicle cycling, an increase in filaggrin but a decrease in keratin krt2–16 suggesting a disruption in hair follicle differentiation, and an increase in PCNA staining indicating an increased cell proliferation. These properties suggest that the normal balance of cell proliferation and differentiation is disrupted in VDR −/ − skin, supporting a model in which VDR regulates this balance.