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IL-31 targets the hair follicle bulge across species and restrains hair regeneration in mice

ABSTRACT: IL-31 is a type 2 cytokine best known for actions on sensory neurons, whereas its targets within skin epithelium remain incompletely defined. Here, reanalysis of public single-cell RNA-sequencing datasets and RNAscope identified Il31ra expression predominantly in the bulge and secondary hair germ (sHG) of mouse hair follicles and in the bulge compartment of human hair follicles. In isolated mouse keratinocytes, recombinant IL-31 (rIL-31) induced a bulge-enriched JAK-STAT–associated transcriptional response. In vivo rIL-31 administration activated STAT3, STAT5, and ERK1/2 in mouse bulge/sHG cells, and these responses were lost in keratinocyte-specific Il31ra-deficient mice. In a hair plucking–induced anagen model, continuous rIL-31 administration delayed anagen progression in control mice but not in keratinocyte-specific Il31ra-deficient mice. Parallel analyses of human scalp skin demonstrated that IL31RA is similarly enriched in the bulge compartment. In human skin explants, rIL-31 induced pSTAT5 in KRT15+ bulge cells. Together, these data identify the hair follicle bulge as a conserved epithelial target of IL-31 and support a role for IL-31 signaling in restraining hair regeneration in mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE326083 | GEO | 2026/09/23

REPOSITORIES: GEO

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Project description:Hair follicles undergo recurrent cycling of controlled growth (anagen), regression (catagen), and relative quiescence (telogen) with a defined periodicity. Taking a genomics approach to study gene expression during synchronized mouse hair follicle cycling, we discovered that, in addition to circadian fluctuation, CLOCK-regulated genes are also modulated in phase with the hair growth cycle. During telogen and early anagen, circadian clock genes are prominently expressed in the secondary hair germ, which contains precursor cells for the growing follicle. Analysis of Clock and Bmal1 mutant mice reveals a delay in anagen progression, and the secondary hair germ cells show decreased levels of phosphorylated Rb and lack mitotic cells, suggesting that circadian clock genes regulate anagen progression via their effect on the cell cycle. Consistent with a block at the G1 phase of the cell cycle, we show a significant upregulation of p21 in Bmal1 mutant skin. While circadian clock mechanisms have been implicated in a variety of diurnal biological processes, our findings indicate that circadian clock genes may be utilized to modulate the progression of non-diurnal cyclic processes. To investigate the molecular control of hair follicle cycling, we profiled mRNA expression in mouse dorsal skin at multiple representative time points in the synchronized second postnatal hair growth cycle and in a depilation-induced hair growth cycle. For profiling of second synchronized and depilation-induced hair growth cycle, the same upper-mid region of dorsal skin was excised from C57BL/6 mice at representative postnatal days (P). The time points for second hair growth cycle are classified into different phases of the hair growth cycle based on established morphological guidelines as follow: early anagen (P23, P25), mid anagen (P27), late anagen (P29, P34), early catagen (P37, P39), mid catagen (P41), and telogen (P44). Depilation-induced hair growth cycle by applying wax/rosin mixture on the dorsal skin of seven-week old mice (all follicles in telogen) was performed on mice. The corresponding phases of the hair growth cycle at number of days following depilation (D) is as follow: early anagen (D3), mid anagen (D5), late anagen (D8, D12), and early catagen (D17). For each time point, multiple biological replicates were profiled, with each mouse dorsal skin separately hybridized to an Affymetrix array.

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IL-31 targets the hair follicle bulge across species and restrains hair regeneration in mice

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