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Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth [dataset2]

ABSTRACT: Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth [dataset2]

PROVIDER: PRJNA1105362 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28822111_1.fastq.gz	Fastqsanger.gz
	SRR28822111_2.fastq.gz	Fastqsanger.gz
	SRR28822112_1.fastq.gz	Fastqsanger.gz
	SRR28822112_2.fastq.gz	Fastqsanger.gz
	SRR28822113_1.fastq.gz	Fastqsanger.gz

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Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth [dataset2]

Project description:Pain, detected by nociceptors, is an integral part of injury, yet whether and how it can impact tissue physiology and recovery remain understudied. Here we applied chemogenetics in mice to locally activate dermal TRPV1 innervations in naïve skin and found it triggered new regenerative cycling by dormant hair follicles (HFs).This was preceded by rapid apoptosis of dermal macrophages, mediated by the neuropeptide calcitonin gene-related peptide (CGRP). TRPV1 activation also triggered a macrophage-dependent induction of Spp1-expressing dermal fibroblasts. The neuropeptide CGRP andSpp1were essential for the nociceptor-triggered hair growth. Finally, we show that epidermal abrasion injury induced Spp1-expressing dermal fibroblasts and hair growth via a TRPV1 neuron and CGRP dependent mechanism.Collectively, these data demonstrate a role for TRPV1 nociceptors in orchestrating a macrophage and fibroblast-supported mechanism to promote hair growth, and enabling the efficient restoration of this mechano- and thermo-protective barrier after wounding.

2024-05-10 | GSE266028 | GEO

Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth [dataset1]

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Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth [dataset1]

Project description:Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth [dataset1]

| PRJNA1105363 | ENA

Dermal TRPV1 innervations engage a macrophage- and fibroblast-containing pathway to activate hair growth in mice.

Project description:Pain, detected by nociceptors, is an integral part of injury, yet whether and how it can impact tissue physiology and recovery remain understudied. Here, we applied chemogenetics in mice to locally activate dermal TRPV1 innervations in naive skin and found that it triggered new regenerative cycling by dormant hair follicles (HFs). This was preceded by rapid apoptosis of dermal macrophages, mediated by the neuropeptide calcitonin gene-related peptide (CGRP). TRPV1 activation also triggered a macrophage-dependent induction of osteopontin (Spp1)-expressing dermal fibroblasts. The neuropeptide CGRP and the extracellular matrix protein Spp1 were required for the nociceptor-triggered hair growth. Finally, we showed that epidermal abrasion injury induced Spp1-expressing dermal fibroblasts and hair growth via a TRPV1 neuron and CGRP-dependent mechanism. Collectively, these data demonstrated a role for TRPV1 nociceptors in orchestrating a macrophage and fibroblast-supported mechanism to promote hair growth and enabling the efficient restoration of this mechano- and thermo-protective barrier after wounding.

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TRPV1 SUMOylation suppresses itch by inhibiting TRPV1 interaction with H1 receptors

Project description:To examine the functional significance of TRPV1 SUMOylation in vivo, we created a TRPV1K823R KI transgenic mouse line.We thus performed gene expression profiling analysis using data obtained from RNA-seq of the trigeminal ganglion of TRPV1K823R and control mouse models . Our analyses unveiled a role for TRPV1 SUMOylation in regulating gene networks related to the pain and itch pathway.

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The transcriptome of TRPV1-positive sensory neurons revealed by subgroup-elimination transcriptomics

Project description:We developed an approach to rapidly eliminate the subgroup of sensory neurons expressing the heat-gated cation channel TRPV1 from dissociated rat sensory ganglia using agonist treatment followed by density centrifugation. To identify transcripts predominantly expressed in TRPV1-positive neurons, we compared the transcriptome of all cells within sensory ganglia versus all cells without TRPV1 expressing neurons using RNA-Seq.

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Dermal adipocytes activate hair follicle stem cells through metabolic communication [HFSC]

Project description:The ability of tissue stem cells to sense and respond to their surroundings enables them to adapt their activity to meet the needs of the organism. External irritation has long been observed in humans to cause acquired hypertrichosis, but the mechanism is unknown. We discovered that external irritation activates hair follicle stem cells (HFSCs), leading to substantial hair regeneration in mice. The external irritation is sensed by niche adipocytes, which undergo lipolysis to activate HFSCs, rather than by the HFSCs themselves. Fatty acids released by adipocytes are taken up by HFSCs and activate them by priming them for fatty acid oxidation and increasing the mitochondrial oxidative phosphorylation capacity for ATP production. Inhibiting lipolysis, fatty acid uptake, or fatty acid oxidation restricts irritation-induced hair regeneration. As a result, adipocytes create an injury-sensing niche, allowing HFSCs to respond to external irritation by initiating a new round of hair growth to protect the skin.

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Dermal adipocytes activate hair follicle stem cells through metabolic communication [SDS]

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