Consequences of Autophagy Deletion on the Age-Related Changes in the Epidermal Lipidome of Mice
Autor: | Yiwen Yang, Christopher Kremslehner, Sophia Derdak, Christina Bauer, Sarah Jelleschitz, Ionela-Mariana Nagelreiter, Heidemarie Rossiter, Marie Sophie Narzt, Florian Gruber, Michaela Sochorová |
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Jazyk: | angličtina |
Rok vydání: | 2022 |
Předmět: |
Mammals
Fatty Acids Organic Chemistry Keratin-14 General Medicine Fatty Acid-Binding Proteins Lipids epidermis autophagy ageing lipidome transcriptome triglyceride cholesterol ester sphingomyelin Catalysis Computer Science Applications Inorganic Chemistry Mice Lipidomics Autophagy Animals Epidermis Physical and Theoretical Chemistry Molecular Biology Spectroscopy |
Zdroj: | International Journal of Molecular Sciences; Volume 23; Issue 19; Pages: 11110 |
ISSN: | 1422-0067 |
DOI: | 10.3390/ijms231911110 |
Popis: | Autophagy is a controlled mechanism of intracellular self-digestion with functions in metabolic adaptation to stress, in development, in proteostasis and in maintaining cellular homeostasis in ageing. Deletion of autophagy in epidermal keratinocytes does not prevent the formation of a functional epidermis and the permeability barrier but causes increased susceptibility to damage stress and metabolic alterations and accelerated ageing phenotypes. We here investigated how epidermal autophagy deficiency using Keratin 14 driven Atg7 deletion would affect the lipid composition of the epidermis of young and old mice. Using mass spectrometric lipidomics we found a reduction of age-related accumulation of storage lipids in the epidermis of autophagy-deficient mice, and specific changes in chain length and saturation of fatty acids in several lipid classes. Transcriptomics and immunostaining suggest that these changes are accompanied by changes in expression and localisation of lipid and fatty acid transporter proteins, most notably fatty acid binding protein 5 (FABP5) in autophagy knockouts. Thus, maintaining autophagic activity at an advanced age may be necessary to maintain epidermal lipid homeostasis in mammals. |
Databáze: | OpenAIRE |
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