Hedgehog stimulates hair follicle neogenesis by creating inductive dermis during murine skin wound healing

Chae Ho Lim, Qi Sun, Karan Ratti, Soung-Hoon Lee, Ying Zheng, Makoto Takeo, Wendy Lee, Piul Rabbani, Maksim V. Plikus, Jason E. Cain, David H. Wang, D. Neil Watkins, Sarah Millar, M. Mark Taketo, Peggy Myung, George Cotsarelis and Mayumi Ito ()
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Chae Ho Lim: New York University School of Medicine
Qi Sun: New York University School of Medicine
Karan Ratti: New York University School of Medicine
Soung-Hoon Lee: New York University School of Medicine
Ying Zheng: University of Pennsylvania
Makoto Takeo: New York University School of Medicine
Wendy Lee: New York University School of Medicine
Piul Rabbani: New York University School of Medicine
Maksim V. Plikus: University of California
Jason E. Cain: Monash University
David H. Wang: University of Texas Southwestern Medical Center
D. Neil Watkins: The Kinghorn Cancer Centre, Garvan Institute of Medical Research
Sarah Millar: University of Pennsylvania
M. Mark Taketo: Kyoto University
Peggy Myung: School of Medicine, Yale University
George Cotsarelis: University of Pennsylvania
Mayumi Ito: New York University School of Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract Mammalian wounds typically heal by fibrotic repair without hair follicle (HF) regeneration. Fibrosis and regeneration are currently considered the opposite end of wound healing. This study sought to determine if scar could be remodeled to promote healing with HF regeneration. Here, we identify that activation of the Sonic hedgehog (Shh) pathway reinstalls a regenerative dermal niche, called dermal papilla, which is required and sufficient for HF neogenesis (HFN). Epidermal Shh overexpression or constitutive Smoothened dermal activation results in extensive HFN in wounds that otherwise end in scarring. While long-term Wnt activation is associated with fibrosis, Shh signal activation in Wnt active cells promotes the dermal papilla fate in scarring wounds. These studies demonstrate that mechanisms of scarring and regeneration are not distant from one another and that wound repair can be redirected to promote regeneration following injury by modifying a key dermal signal.

Date: 2018
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DOI: 10.1038/s41467-018-07142-9

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