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Mechanisms linking stress and ageing in two avian species exhibiting contrasted natural resistance to stress (NAtural REsistance to Stress-Induced Cellular Ageing)

Descripción del proyecto

El papel del estrés sobre el envejecimiento celular

El envejecimiento celular es un proceso enigmático del que todavía se desconocen muchos aspectos. El objetivo principal del proyecto NARESICA, financiado con fondos europeos, es investigar el papel del estrés en el proceso de envejecimiento. Empleando la longitud de los telómeros como biomarcador del envejecimiento, los investigadores del proyecto estudiarán cómo el estrés crónico y, en particular, las hormonas glucocorticoides del estrés aceleran el envejecimiento en dos especies aviares. Se hará hincapié en varios factores potenciales de envejecimiento como la función mitocondrial, el estrés oxidativo, los daños en el ADN y la vía de señalización celular de mTOR. En conjunto, los hallazgos del proyecto revelarán información importante sobre un proceso biológico fundamental con implicaciones clínicas.

Objetivo

Previous research has identified stress exposure as a key factor influencing health state and ageing rate. The overall aim of the proposed project is to investigate the precise mechanisms linking stress exposure to accelerated cellular ageing (using telomere length as a biomarker of ageing), and to identify potential mechanisms allowing some species to better prevent stress-induced ageing than others. To this aim I will use two avian species (Japanese quail and king penguin) to investigate (1) if chronic stress affects telomere shortening differently between species exhibiting contrasted stress resistance, (2) if glucocorticoid ‘stress’ hormones are directly responsible of the stress-induced alterations in telomere dynamics, (3) by which mechanisms (i.e. alterations of mitochondrial function, oxidative stress and DNA damage, impaired mTOR cellular signalling or telomere maintenance) stress exposure is accelerating telomere shortening, and if king penguin have specific mechanisms preventing/limiting stress-induced telomere shortening, and (4) if chronic stress / glucocorticoid hormones modify the acute oxidative stress responses of individuals. To this end, I will employ experimental approaches manipulating stress exposure and glucocorticoid hormones in captive Japanese quail and wild king penguins, and measure the resulting impact on telomere shortening and its potential cellular drivers (mitochondrial function, oxidative stress, mTOR cellular signalling). This project will enable a two-way transfer of skills and competences between the applicant and the host, by providing training to the applicant regarding mitochondrial biology, cellular signalling and gene expression, and by providing the host with the opportunity to integrate an ageing component through the use of telomeres in his current and future projects.

Coordinador

UNIVERSITE LYON 1 CLAUDE BERNARD
Aportación neta de la UEn
€ 184 707,84
Dirección
BOULEVARD DU 11 NOVEMBRE 1918 NUM43
69622 Villeurbanne Cedex
Francia

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Región
Auvergne-Rhône-Alpes Rhône-Alpes Rhône
Tipo de actividad
Higher or Secondary Education Establishments
Enlaces
Coste total
€ 184 707,84