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Obesity accelerates hair thinning in stem cell-centric converging mechanism

ABSTRACT: Obesity accelerates hair thinning in stem cell-centric converging mechanism

PROVIDER: PRJNA545462 | ENA |

REPOSITORIES: ENA

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Obesity accelerates hair thinning by stem cell-centric converging mechanism [RNA-seq]

Project description:Obesity accelerates hair thinning by stem cell-centric converging mechanism [RNA-seq]

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Obesity accelerates hair thinning in stem cell-centric converging mechanism

Project description:Obesity, a worldwide epidemic, predisposes to many ageing-associated diseases, yet its exact impact on organ dysfunction is largely unknown. Hair follicles, mini-epithelial organs that grow hair, miniaturize by ageing to cause hair loss through the depletion of hair follicle stem cells (HFSCs). Here, we report that obesity-induced stress such as by high-fat diet (HFD) feeding primarily targets HFSCs to accelerate hair thinning. Chronological gene expression analysis revealed that HFD feeding for four consecutive days directs activated HFSCs toward epidermal keratinization by generating excessive reactive oxygen species yet retains HFSC pools in young mice. Integrative analysis with stem cell fate tracing, epigenetic analysis and reverse genetics revealed that further feeding of HFD subsequently induces lipid droplets and NF-κB activation within HFSCs via autocrine/paracrine IL1R signaling. Those integrated factors converge on the profound inhibition of Sonic hedgehog (Shh) signal transduction in HFSCs, thereby further depleting lipid-laden HFSCs from the skin surface and inducing hair follicle miniaturization and eventual hair loss. Conversely, Shh activation by transgenes or compounds rescues HFD-induced hair loss. These data collectively demonstrate that stem cell inflammageing induced by obesity robustly represses organ regeneration signals to accelerate the mini-organ miniaturization, and indicates suggests the importance of daily prevention of organ dysfunction.

2021-04-14 | GSE131958 | GEO

Obesity accelerates hair thinning by stem cell-centric converging mechanism [RNA-seq]

Project description:Obesity, a worldwide epidemic, predisposes to many ageing-associated diseases, yet its exact impact on organ dysfunction is largely unknown. Hair follicles, mini-epithelial organs that grow hair, miniaturize by ageing to cause hair loss through the depletion of hair follicle stem cells (HFSCs). Here, we report that obesity-induced stress such as by high-fat diet (HFD) feeding primarily targets HFSCs to accelerate hair thinning. Chronological gene expression analysis revealed that HFD feeding for four consecutive days directs activated HFSCs toward epidermal keratinization by generating excessive reactive oxygen species yet retains HFSC pools in young mice. Integrative analysis with stem cell fate tracing, epigenetic analysis and reverse genetics revealed that further feeding of HFD subsequently induces lipid droplets and NF-B activation within HFSCs via autocrine/paracrine IL1R signaling. Those integrated factors converge on the profound inhibition of Sonic hedgehog (Shh) signal transduction in HFSCs, thereby further depleting lipid-laden HFSCs through their aberrant differentiation and inducing hair follicle miniaturization and eventual hair loss. Conversely, Shh activation by transgenes or compounds rescues HFD-induced hair loss. These data collectively demonstrate that stem cell inflammageing induced by obesity robustly represses organ regeneration signals to accelerate the mini-organ miniaturization, and suggests the importance of daily prevention of organ dysfunction.

2021-04-14 | GSE169173 | GEO

Obesity accelerates hair thinning by stem cell-centric converging mechanisms.

Project description: Not available

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Thyroid hormone augmentation accelerates hair cell maturation in human cochlear organoids

Project description:Thyroid hormone augmentation accelerates hair cell maturation in human cochlear organoids

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Thyroid hormone augmentation accelerates hair cell maturation in human cochlear organoids

Project description:Outer and inner hair cells in the cochlea are essential for hearing, but are vulnerable to damage by genetic mutations and environmental insults, resulting in irreversible sensorineural hearing loss. Investigating these processes requires access to large numbers of human cochlear hair cells and the ability to precisely control genetic, biochemical, and environmental conditions. We recently established a new organoid system that recapitulates human cochlear differentiation. However, maturation of cochlear organoid cultures is inefficient, requiring several months to express the mature outer hair cell marker Prestin. To efficiently obtain fully functional outer hair cells, we tested the effects of the thyroid hormone thyroxine on hair cell maturation in human cochlear organoids. Thyroxine supplementation significantly increased the percentages of Prestin-positive hair cells in an age-dependent manner. Additionally, transcriptomic analyses revealed upregulation of mature outer hair cell genes and downregulation of immature hair cell genes in thyroxine-treated hair cells. Furthermore, some of the treated hair cells exhibited electromotility, a functional hallmark of mature outer hair cells. These results suggest that thyroid hormones accelerate the maturation of hair cells in human cochlear organoids, thereby useful for establishing an improved in vitro model for pre-clinical investigation on sensorineural hearing loss.

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