Noncoding dsRNA induces retinoic acid synthesis to stimulate hair follicle regeneration via TLR3

Dongwon Kim, Ruosi Chen, Mary Sheu, Noori Kim, Sooah Kim, Nasif Islam, Eric M. Wier, Gaofeng Wang, Ang Li, Angela Park, Wooyang Son, Benjamin Evans, Victoria Yu, Vicky P. Prizmic, Eugene Oh, Zixiao Wang, Jianshi Yu, Weiliang Huang, Nathan K. Archer, Zhiqi HuNashay Clemetson, Amanda M. Nelson, Anna Chien, Ginette A. Okoye, Lloyd S. Miller, Gabriel Ghiaur, Sewon Kang, Jace W. Jones, Maureen A. Kane, Luis A. Garza

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

How developmental programs reactivate in regeneration is a fundamental question in biology. We addressed this question through the study of Wound Induced Hair follicle Neogenesis (WIHN), an adult organogenesis model where stem cells regenerate de novo hair follicles following deep wounding. The exact mechanism is uncertain. Here we show that self-noncoding dsRNA activates the anti-viral receptor toll like receptor 3 (TLR3) to induce intrinsic retinoic acid (RA) synthesis in a pattern that predicts new hair follicle formation after wounding in mice. Additionally, in humans, rejuvenation lasers induce gene expression signatures for dsRNA and RA, with measurable increases in intrinsic RA synthesis. These results demonstrate a potent stimulus for RA synthesis by non-coding dsRNA, relevant to their broad functions in development and immunity.

Original languageEnglish (US)
Article number2811
JournalNature communications
Volume10
Issue number1
DOIs
StatePublished - Dec 1 2019

All Science Journal Classification (ASJC) codes

  • Chemistry(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)

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    Kim, D., Chen, R., Sheu, M., Kim, N., Kim, S., Islam, N., Wier, E. M., Wang, G., Li, A., Park, A., Son, W., Evans, B., Yu, V., Prizmic, V. P., Oh, E., Wang, Z., Yu, J., Huang, W., Archer, N. K., ... Garza, L. A. (2019). Noncoding dsRNA induces retinoic acid synthesis to stimulate hair follicle regeneration via TLR3. Nature communications, 10(1), [2811]. https://doi.org/10.1038/s41467-019-10811-y