Injury-activated glial cells promote wound healing of the adult skin in mice

Vadims Parfejevs, Julien Debbache, Olga Shakhova, Simon M. Schaefer, Mareen Glausch, Michael Wegner, Ueli Suter, Una Riekstina, Sabine Werner and Lukas Sommer ()
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Vadims Parfejevs: Institute of Anatomy, University of Zürich
Julien Debbache: Institute of Anatomy, University of Zürich
Olga Shakhova: University Hospital Zürich
Simon M. Schaefer: Institute of Anatomy, University of Zürich
Mareen Glausch: Institute of Anatomy, University of Zürich
Michael Wegner: Institute of Biochemistry, Friedrich-Alexander-Universität Erlangen-Nürnberg
Ueli Suter: Institute of Molecular Health Sciences, ETH
Una Riekstina: Faculty of Medicine, University of Latvia
Sabine Werner: Institute of Molecular Health Sciences, ETH
Lukas Sommer: Institute of Anatomy, University of Zürich

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously associated with wound healing and promote myofibroblast differentiation by paracrine modulation of TGF-β signalling. Accordingly, depletion of these cells impairs epithelial proliferation and wound closure through contraction, while their expansion promotes myofibroblast formation. Thus, injury-activated glia and/or their secretome might have therapeutic potential in human wound healing disorders.

Date: 2018
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DOI: 10.1038/s41467-017-01488-2

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