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<dc:title xml:lang="fr">Protéomique des adaptations métaboliques et de la préservation musculaire chez l'ours brun hibernant</dc:title>
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<dc:subject xml:lang="fr">Ours brun</dc:subject>
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<dcterms:abstract xml:lang="fr">Les muscles s’atrophient chez l’homme en cas de sédentarité ou de malnutrition, mais pas chez l’ours brun inactif et à jeun en hibernation. Cette préservation implique des composés sériques encore non identifiés et une réduction du catabolisme protéique. Après enrichissement des protéines sériques peu abondantes sur billes magnétiques fonctionnalisées, une analyse protéomique quantitative a identifié la protéine WFIKKN2 comme candidate pour inhiber la voie TGFβ et le catabolisme protéique. Des immunoprécipitations et isolements d’organites combinés à des analyses protéomiques ont montré que i) le protéasome musculaire reste fonctionnel mais sélectif en hiver, ii) l’activité mitochondriale, bien que réduite, est préservée via le maintien de l’activité SDH, et iii) les interactions cellules-cellules sont renforcées et les signaux mécaniques restent transmis vers le noyau. Ces travaux suggèrent de nouveaux leviers potentiels de lutte contre l’atrophie musculaire humaine.</dcterms:abstract>
<dcterms:abstract xml:lang="en">Muscles atrophy in humans due to sedentary lifestyle, but not in the brown bear, which remains inactive and fasting during hibernation. This preservation involves yet unidentified serum compounds and a reduction in protein catabolism. After enrichment of low-abundance serum proteins on functionalized magnetic beads, quantitative proteomic analysis identified the protein WFIKKN2 as a candidate for inhibiting the muscle TGFβ pathway and protein catabolism. Immunoprecipitations and organelle isolation combined with proteomic analyses showed that (i) the muscle proteasome remains functional but becomes selective in winter, (ii) mitochondrial activity, although reduced, is preserved through maintenance of SDH activity, and (iii) cell–cell interactions are strengthened and mechanical signals continue to be transmitted to the nucleus. These findings suggest new potential strategies to combat human muscle atrophy.</dcterms:abstract>
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