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Sensory neurons accelerate reepithelialization through Substance P release in an innervated tissue‐engineered model of skin wound healing.
Author(s) -
Blais Mathieu,
Mottier Lorène,
Cadau Sébastien,
Bareil Rémi Parenteau,
Berthod François
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.193.3
Subject(s) - substance p , wound healing , epidermis (zoology) , sensory system , dermis , keratinocyte , immunofluorescence , regeneration (biology) , neuroscience , sensory neuron , neuropeptide , receptor , microbiology and biotechnology , biology , chemistry , anatomy , medicine , cell culture , immunology , genetics , antibody
The keratinocytes are responsible for the restoration of the epidermal barrier through reepithelialization during the wound healing process in humans. The influence of sensory neurons on this mechanism is poorly understood. We tested whether sensory neurons influence reepithelialization via a secretion of the neuropeptide substance P (SP). We developed a new tissueengineered model of skin wound healing. It consists of a perforated tissue‐engineered skin made of keratinocytes expressing GFP and that was stacked on a dermis to reconstitute the wound bed. The dermal construct is endothelialized by human endothelial cells and innervated or not by mouse sensory neurons. The migration of keratinocytes was imaged and quantified with GFP fluorescence. Sensory neurons produce SP in the construct as shown with ELISA and immunofluorescence analysis. Keratinocytes were found to express the NK1 cell receptor for SP in the reconstructed epidermis. The rate of reephithelialization was increased in presence of sensory neurons and SP was shown to contribute to this effect using antagonist to NK1 and recombinant SP instead of neurons. We conclude that this new model is promising for the study of the influence of the peripheral nervous system on reepithelialization. Grant Funding Source : N/A