Senescence Induced by UVB in Keratinocytes Impairs Amino Acids Balance

Emilie Bauwens, Tom Parée, Sébastien Meurant, Inès Bouriez, Clotilde Hannart, Anne Catherine Wéra, Alexis Khelfi, Antoine Fattaccioli, Sophie Burteau, Catherine Demazy, Maude Fransolet, Clémentine De Schutter, Nathalie Martin, Julien Théry, Gauthier Decanter, Nicolas Penel, Marina Bury, Olivier Pluquet, Marjan Garmyn, Florence Debacq-Chainiaux

Résultats de recherche: Contribution à un journal/une revueArticleRevue par des pairs


Skin is one of the most exposed organs to external stress. Namely, UV rays are the most harmful stress that could induce important damage leading to skin aging and cancers. At the cellular level, senescence is observed in several skin cell types and contributes to skin aging. However, the origin of skin senescent cells is still unclear but is probably related to exposure to stresses. In this work, we developed an in vitro model of UVB-induced premature senescence in normal human epidermal keratinocytes. UVB-induced senescent keratinocytes display a common senescent phenotype resulting in an irreversible cell cycle arrest, an increase in the proportion of senescence-associated β-galactosidase‒positive cells, unrepaired DNA damage, and a long-term DNA damage response activation. Moreover, UVB-induced senescent keratinocytes secrete senescence-associated secretory phenotype factors that influence cutaneous squamous cell carcinoma cell migration. Finally, a global transcriptomic study highlighted that senescent keratinocytes present a decrease in the expression of several amino acid transporters, which is associated with reduced intracellular levels of glycine, alanine, and leucine. Interestingly, the chemical inhibition of the glycine transporter SLC6A9/Glyt1 triggers senescence features.

langue originaleAnglais
Pages (de - à)554-565.e9
journalJournal of Investigative Dermatology
Numéro de publication4
Les DOIs
Etat de la publicationPublié - avr. 2023

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