Autophagy critically controls skin inflammation and apoptosis-induced stem cell activation
- Author
- Lisette Van Hove, Annagiada Toniolo (UGent) , Mohammad Ghiasloo (UGent) , Kim Lecomte (UGent) , Fleur Boone (UGent) , Maarten Ciers (UGent) , Kris Raaijmakers, Niels Vandamme (UGent) , Jana Roels (UGent) , Sophia Maschalidi (UGent) , Kodi Ravichandran (UGent) , Maria Kasper, Geert van Loo (UGent) and Esther Hoste (UGent)
- Organization
- Project
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- Manipulation of fibroblast-mediated proteolytic events in the cutaneous wound and tumour microenvironment
- Design of an acellular pro-survival hydrogel to improve autologous fat grafting
- Molecular mechanisms of cellular crosstalk in skin regeneration and cancer
- Investigating the role and molecular mechanisms of two distinct cell death modalities in cutaneous regenerative and neoplastic inflammation
- The impact of cell death on the cancer stem cell niche in non-melanoma skin cancer
- Abstract
- Macroautophagy/autophagy is a cellular recycling program regulating cell survival and controlling inflammatory responses in a context-dependent manner. Here, we demonstrate that keratinocyte-selective ablation of Atg16l1, an essential autophagy mediator, results in exacerbated inflammatory and neoplastic skin responses. In addition, mice lacking keratinocyte autophagy exhibit precocious onset of hair follicle growth, indicating altered activation kinetics of hair follicle stem cells (HFSCs). These HFSCs also exhibit expanded potencies in an autophagy-deficient context as shown by de novo hair follicle formation and improved healing of abrasion wounds. ATG16L1-deficient keratinocytes are markedly sensitized to apoptosis. Compound deletion of RIPK3-dependent necroptotic and CASP8-dependent apoptotic responses or of TNFRSF1A/TNFR1 reveals that the enhanced sensitivity of autophagy-deficient keratinocytes to TNF-dependent cell death is driving altered activation of HFSCs. Together, our data demonstrate that keratinocyte autophagy dampens skin inflammation and tumorigenesis but curtails HFSC activation by restraining apoptotic responses.
- Keywords
- wound healing, skin cancer, hair follicle stem cells, hair cycling, autophagy, Apoptosis
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-01HDKNFNC6B3D5ERR3J2PQYY9F
- MLA
- Van Hove, Lisette, et al. “Autophagy Critically Controls Skin Inflammation and Apoptosis-Induced Stem Cell Activation.” AUTOPHAGY, vol. 19, no. 11, 2023, pp. 2958–71, doi:10.1080/15548627.2023.2247742.
- APA
- Van Hove, L., Toniolo, A., Ghiasloo, M., Lecomte, K., Boone, F., Ciers, M., … Hoste, E. (2023). Autophagy critically controls skin inflammation and apoptosis-induced stem cell activation. AUTOPHAGY, 19(11), 2958–2971. https://doi.org/10.1080/15548627.2023.2247742
- Chicago author-date
- Van Hove, Lisette, Annagiada Toniolo, Mohammad Ghiasloo, Kim Lecomte, Fleur Boone, Maarten Ciers, Kris Raaijmakers, et al. 2023. “Autophagy Critically Controls Skin Inflammation and Apoptosis-Induced Stem Cell Activation.” AUTOPHAGY 19 (11): 2958–71. https://doi.org/10.1080/15548627.2023.2247742.
- Chicago author-date (all authors)
- Van Hove, Lisette, Annagiada Toniolo, Mohammad Ghiasloo, Kim Lecomte, Fleur Boone, Maarten Ciers, Kris Raaijmakers, Niels Vandamme, Jana Roels, Sophia Maschalidi, Kodi Ravichandran, Maria Kasper, Geert van Loo, and Esther Hoste. 2023. “Autophagy Critically Controls Skin Inflammation and Apoptosis-Induced Stem Cell Activation.” AUTOPHAGY 19 (11): 2958–2971. doi:10.1080/15548627.2023.2247742.
- Vancouver
- 1.Van Hove L, Toniolo A, Ghiasloo M, Lecomte K, Boone F, Ciers M, et al. Autophagy critically controls skin inflammation and apoptosis-induced stem cell activation. AUTOPHAGY. 2023;19(11):2958–71.
- IEEE
- [1]L. Van Hove et al., “Autophagy critically controls skin inflammation and apoptosis-induced stem cell activation,” AUTOPHAGY, vol. 19, no. 11, pp. 2958–2971, 2023.
@article{01HDKNFNC6B3D5ERR3J2PQYY9F,
abstract = {{Macroautophagy/autophagy is a cellular recycling program regulating cell survival and controlling inflammatory responses in a context-dependent manner. Here, we demonstrate that keratinocyte-selective ablation of Atg16l1, an essential autophagy mediator, results in exacerbated inflammatory and neoplastic skin responses. In addition, mice lacking keratinocyte autophagy exhibit precocious onset of hair follicle growth, indicating altered activation kinetics of hair follicle stem cells (HFSCs). These HFSCs also exhibit expanded potencies in an autophagy-deficient context as shown by de novo hair follicle formation and improved healing of abrasion wounds. ATG16L1-deficient keratinocytes are markedly sensitized to apoptosis. Compound deletion of RIPK3-dependent necroptotic and CASP8-dependent apoptotic responses or of TNFRSF1A/TNFR1 reveals that the enhanced sensitivity of autophagy-deficient keratinocytes to TNF-dependent cell death is driving altered activation of HFSCs. Together, our data demonstrate that keratinocyte autophagy dampens skin inflammation and tumorigenesis but curtails HFSC activation by restraining apoptotic responses.}},
author = {{Van Hove, Lisette and Toniolo, Annagiada and Ghiasloo, Mohammad and Lecomte, Kim and Boone, Fleur and Ciers, Maarten and Raaijmakers, Kris and Vandamme, Niels and Roels, Jana and Maschalidi, Sophia and Ravichandran, Kodi and Kasper, Maria and van Loo, Geert and Hoste, Esther}},
issn = {{1554-8627}},
journal = {{AUTOPHAGY}},
keywords = {{wound healing,skin cancer,hair follicle stem cells,hair cycling,autophagy,Apoptosis}},
language = {{eng}},
number = {{11}},
pages = {{2958--2971}},
title = {{Autophagy critically controls skin inflammation and apoptosis-induced stem cell activation}},
url = {{http://doi.org/10.1080/15548627.2023.2247742}},
volume = {{19}},
year = {{2023}},
}
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