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Calcineurin/Nfatc1 signaling links skin stem cell quiescence to hormonal signaling during pregnancy and lactation

ABSTRACT: Cyclosporine A (CSA) leads to the precocious onset of hair follicle growth, which is driven by premature activation and proliferation of hair follicle stem cells. Here, we identify gene expression changes associated with CSA treatment in hair follicle stem cells prior to the onset of proliferation as a readout for the early events in stem cell actvation.

ORGANISM(S): Mus musculus

PROVIDER: GSE51194 | GEO | 2013/09/27

SECONDARY ACCESSION(S): PRJNA221572

REPOSITORIES: GEO

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Calcineurin/Nfatc1 links skin stem cell quiescence to the endocrine hormone prolactin

Project description:Cyclosporine A (CSA) leads to the precocious onset of hair follicle growth, which is driven by premature activation and proliferation of hair follicle stem cells. Here, we identify gene expression changes associated with CSA treatment in hair follicle stem cells prior to the onset of proliferation as a readout for the early events in stem cell actvation. Hair follicle bulge stem cells were FACS-isolated from mouse skin during the 2nd telogen. Two biological replicated were performed.

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Calcineurin/Nfatc1 signaling links skin stem cell quiescence to hormonal signaling during pregnancy and lactation.

Project description:In most tissues, the prevailing view is that stem cell (SC) niches are generated by signals from within the nearby tissue environment. Here, we define genetic changes altered in hair follicle (HF) SCs in mice treated with a potent SC activator, cyclosporine A (CSA), which inhibits the phosphatase calcineurin (CN) and the activity of the transcription factor nuclear factor of activated T cells c1 (Nfatc1). We show that CN/Nfatc1 regulates expression of prolactin receptor (Prlr) and that canonical activation of Prlr and its downstream signaling via Jak/Stat5 drives quiescence of HF SCs during pregnancy and lactation, when serum prolactin (Prl) levels are highly elevated. Using Prl injections and genetic/pharmacological loss-of-function experiments in mice, we show that Prl signaling stalls follicular SC activation through its activity in the skin epithelium. Our findings define a unique CN-Nfatc1-Prlr-Stat5 molecular circuitry that promotes persistent SC quiescence in the skin.

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2013-11-14 | GSE52328 | GEO

Genome-wide analysis of gene expression regulated by calcineurin-NFAT signaling in mouse embryonic stem cells

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Expression data from human hair follicles (ex vivo) incubated with cyclosporine A and vehicle control

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SOX9: a Stem Cell Transcriptional Regulator of Secreted Niche Signaling Factors

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