Cell death as an architect of adult skin stem cell niches.


Journal

Cell death and differentiation
ISSN: 1476-5403
Titre abrégé: Cell Death Differ
Pays: England
ID NLM: 9437445

Informations de publication

Date de publication:
22 Apr 2024
Historique:
received: 16 12 2023
accepted: 11 04 2024
revised: 09 04 2024
medline: 23 4 2024
pubmed: 23 4 2024
entrez: 22 4 2024
Statut: aheadofprint

Résumé

Our skin provides a physical and immunological barrier against dehydration and environmental insults ranging from microbial attacks, toxins and UV irradiation to wounding. Proper functioning of the skin barrier largely depends on the interplay between keratinocytes- the epithelial cells of the skin- and immune cells. Two spatially distinct populations of keratinocyte stem cells (SCs) maintain the epidermal barrier function and the hair follicle. These SCs are inherently long-lived, but cell death can occur within their niches and impacts their functionality. The default cell death programme in skin is apoptosis, an orderly and non-inflammatory suicide programme. However, recent findings are shedding light on the significance of various modes of regulated necrotic cell death, which are lytic and can provoke inflammation within the local skin environment. While the presence of dying cells was generally regarded as a mere consequence of inflammation, findings in various human dermatological conditions and experimental mouse models of aberrant cell death control demonstrated that cell death programmes in keratinocytes (KCs) can drive skin inflammation and even tumour initiation. When cells die, they need to be removed by phagocytosis and KCs can function as non-professional phagocytes of apoptotic cells with important implications for their SC capacities. It is becoming apparent that in conditions of heightened SC activity, distinct cell death modalities differentially impact the different skin SC populations in their local niches. Here, we describe how regulated cell death modalities functionally affect epidermal SC niches along with their relevance to injury repair, inflammatory skin disorders and cancer.

Identifiants

pubmed: 38649745
doi: 10.1038/s41418-024-01297-3
pii: 10.1038/s41418-024-01297-3
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Fonds Wetenschappelijk Onderzoek (Research Foundation Flanders)
ID : 3G032320
Organisme : Fonds Wetenschappelijk Onderzoek (Research Foundation Flanders)
ID : 3G032320
Organisme : Stichting Tegen Kanker (Belgian Foundation Against Cancer)
ID : 365L04523
Organisme : Stichting Tegen Kanker (Belgian Foundation Against Cancer)
ID : 365L04523
Organisme : Universiteit Gent (UGent)
ID : BOF24J/2023/138

Informations de copyright

© 2024. The Author(s).

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Auteurs

Kim Lecomte (K)

VIB Center for Inflammation Research, 9052, Ghent, Belgium.
Department of Biomedical Molecular Biology, Ghent University, 9052, Ghent, Belgium.

Annagiada Toniolo (A)

VIB Center for Inflammation Research, 9052, Ghent, Belgium.
Department of Biomedical Molecular Biology, Ghent University, 9052, Ghent, Belgium.

Esther Hoste (E)

VIB Center for Inflammation Research, 9052, Ghent, Belgium. esther.hoste@irc.vib-ugent.be.
Department of Biomedical Molecular Biology, Ghent University, 9052, Ghent, Belgium. esther.hoste@irc.vib-ugent.be.

Classifications MeSH