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Increased glucocorticoid concentrations in early life cause mitochondrial inefficiency and short telomeres

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Increased glucocorticoid concentrations in early life cause mitochondrial inefficiency and short telomeres

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CASAGRANDE, Stefania, Antoine STIER, Pat MONAGHAN, Jasmine L. LOVELAND, Winifred BONER, Sara LUPI, Rachele TREVISI, Michaela HAU, 2020. Increased glucocorticoid concentrations in early life cause mitochondrial inefficiency and short telomeres. In: The Journal of experimental biology. Company of Biologists. 223(15), jeb222513. ISSN 0022-0949. eISSN 1477-9145. Available under: doi: 10.1242/jeb.222513

@article{Casagrande2020-08-04Incre-51152, title={Increased glucocorticoid concentrations in early life cause mitochondrial inefficiency and short telomeres}, year={2020}, doi={10.1242/jeb.222513}, number={15}, volume={223}, issn={0022-0949}, journal={The Journal of experimental biology}, author={Casagrande, Stefania and Stier, Antoine and Monaghan, Pat and Loveland, Jasmine L. and Boner, Winifred and Lupi, Sara and Trevisi, Rachele and Hau, Michaela}, note={Article Number: jeb222513} }

<rdf:RDF xmlns:dcterms="http://purl.org/dc/terms/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bibo="http://purl.org/ontology/bibo/" xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#" xmlns:foaf="http://xmlns.com/foaf/0.1/" xmlns:void="http://rdfs.org/ns/void#" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > <rdf:Description rdf:about="https://kops.uni-konstanz.de/rdf/resource/123456789/51152"> <dcterms:issued>2020-08-04</dcterms:issued> <dc:contributor>Trevisi, Rachele</dc:contributor> <dc:contributor>Monaghan, Pat</dc:contributor> <dc:creator>Loveland, Jasmine L.</dc:creator> <bibo:uri rdf:resource="https://kops.uni-konstanz.de/handle/123456789/51152"/> <dc:contributor>Hau, Michaela</dc:contributor> <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/> <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> <dc:contributor>Casagrande, Stefania</dc:contributor> <dc:creator>Monaghan, Pat</dc:creator> <dc:creator>Lupi, Sara</dc:creator> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-10-01T09:24:22Z</dc:date> <dc:contributor>Boner, Winifred</dc:contributor> <dc:language>eng</dc:language> <dc:creator>Boner, Winifred</dc:creator> <foaf:homepage rdf:resource="http://localhost:8080/jspui"/> <dcterms:abstract xml:lang="eng">Telomeres are DNA structures that protect chromosome ends. However, telomeres shorten during cell replication and at critically low lengths can reduce cell replicative potential, induce cell senescence and decrease fitness. Stress exposure, which elevates glucocorticoid hormone concentrations, can exacerbate telomere attrition. This phenomenon has been attributed to increased oxidative stress generated by glucocorticoids ('oxidative stress hypothesis'). We recently suggested that glucocorticoids could increase telomere attrition during stressful periods by reducing the resources available for telomere maintenance through changes in the metabolic machinery ('metabolic telomere attrition hypothesis'). Here, we tested whether experimental increases in glucocorticoid levels affected telomere length and mitochondrial function in wild great tit (Parus major) nestlings during the energy-demanding early growth period. We monitored resulting corticosterone (Cort) concentrations in plasma and red blood cells, telomere lengths and mitochondrial metabolism (metabolic rate, proton leak, oxidative phosphorylation, maximal mitochondrial capacity and mitochondrial inefficiency). We assessed oxidative damage caused by reactive oxygen species (ROS) metabolites as well as the total non-enzymatic antioxidant protection in plasma. Compared with control nestlings, Cort-nestlings had higher baseline corticosterone, shorter telomeres and higher mitochondrial metabolic rate. Importantly, Cort-nestlings showed increased mitochondrial proton leak, leading to a decreased ATP production efficiency. Treatment groups did not differ in oxidative damage or antioxidants. Hence, glucocorticoid-induced telomere attrition is associated with changes in mitochondrial metabolism, but not with ROS production. These findings support the hypothesis that shortening of telomere length during stressful periods is mediated by glucocorticoids through metabolic rearrangements.</dcterms:abstract> <dc:creator>Casagrande, Stefania</dc:creator> <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> <dcterms:title>Increased glucocorticoid concentrations in early life cause mitochondrial inefficiency and short telomeres</dcterms:title> <dc:contributor>Stier, Antoine</dc:contributor> <dc:rights>terms-of-use</dc:rights> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-10-01T09:24:22Z</dcterms:available> <dc:creator>Hau, Michaela</dc:creator> <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/> <dc:creator>Stier, Antoine</dc:creator> <dc:contributor>Lupi, Sara</dc:contributor> <dc:creator>Trevisi, Rachele</dc:creator> <dc:contributor>Loveland, Jasmine L.</dc:contributor> </rdf:Description> </rdf:RDF>

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