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Transcriptomic profiles of type I/III interferon-responsive hair follicle subsets from ROSA26YFP_Mx1 and ADAM10;ROSA26YFP_Mx1mice

ABSTRACT: Inflammation triggered by viral infections can obscure tissue function. We utilized a model of systemic anti-viral immunity and found that the ADAM10-Notch signaling axis in type I/III interferon-responsive upper hair follicles (HF) was crucial for the expression of genes that regulated skin microbiota and protected HFs and its stem cell niche from inflammatory destruction.

ORGANISM(S): Mus musculus

PROVIDER: GSE180798 | GEO | 2021/07/26

REPOSITORIES: GEO

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Single-cell transcriptomic profiles of CD45-negative cells from Mx1Cre-Rbpjf/f mice

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Genome-wide maps of histone modifications unwind in vivo chromatin states of the hair follicle lineage

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β-cateinin activation in hair follicle dermal sheath induces ectopic hair outgrowth and skin fibrosis

Project description:Dermal sheath (DS) shows potent hair inducing capability and high plasticity without leading to immuno rejection. A recent study showed a subset of DS cells, identified as hair follicle (HF) dermal stem cells, can be mobilized to regenerate DS, maintain/supply the cell number of dermal papilla (DP) and modulate hair type. However, it is unclear how Wnt/β-catenin signaling regulates DS cells behaviors. Here we report that activation of β-catenin in DS, to some extent, endows it with hair inducing ability, reprogramming HF epidermal cells to generate new outgrowth. The new formed dermal condensates (DC)/DP lying adjacent the outgrowth derives from DS and/or its progeny, and homeostasis of pre-existing HFs is disturbed. Additionally, progressive skin fibrosis is prominent in hypodermis, where the excessive activated fibroblasts at least partially originate from DS and/or its progeny. Gene expression analysis of purified DS cells revealed that 44% DC signature genes are regulated, most of which are up-regulated. We found elevated expression of several growth factors, including Noggin, Fgf7 and Fgf10, which were previously implicated in HF induction. In summary, we confirm the high plasticity of DS cells by in vivo assays and report a mechanism by which Wnt/β-catenin signaling controls DS cells behaviors.

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