%0 Journal Article %T Amphiregulin mediates non-cell-autonomous effect of senescence on reprogramming %+ Plasticité cellulaire et Modélisation des Maladies / Cellular Plasticity and Disease Modelling %+ Plateforme de Protéomique / Proteomics platform %+ Hub Bioinformatique et Biostatistique - Bioinformatics and Biostatistics HUB %A von Joest, Mathieu %A Chen, Cheng %A Douché, Thibaut %A Chantrel, Jeremy %A Chiche, Aurélie %A Gianetto, Quentin Giai %A Matondo, Mariette %A Li, Han %Z Work in the laboratory of H.L. is funded by Institut Pasteur, Centre National pour la Recherche Scientific, and the Agence Nationale de la Recherche, France (Laboratoire d’Excellence Revive, Investissement d’Avenir; ANR-10-LABX-73; ANR-16-CE13-0017; ANR-21-CE13-0006-01). A.C. was funded by the postdoctoral fellowships from the Revive Consortium. %< avec comité de lecture %@ 2211-1247 %J Cell Reports %I Elsevier Inc %V 40 %N 2 %P 111074 %8 2022-07 %D 2022 %R 10.1016/j.celrep.2022.111074 %M 35830812 %K CP: Cell biology %K EGFR %K SASP %K aging %K amphiregulin %K cellular plasticity %K cellular senescence %K in vitro reprogramming %K in vivo reprogramming %K muscle regeneration %K quantitative proteomics. %Z Life Sciences [q-bio]Journal articles %X Cellular senescence is an irreversible growth arrest with a dynamic secretome, termed the senescence-associatedsecretory phenotype (SASP). Senescence is a cell-intrinsic barrier for reprogramming, whereas theSASP facilitates cell fate conversion in non-senescent cells. However, the mechanisms by which reprogramming-induced senescence regulates cell plasticity are not well understood. Here, we investigate how the heterogeneityof paracrine senescence impacts reprogramming. We show that senescence promotes in vitro reprogrammingin a stress-dependent manner. Unbiased proteomics identifies a catalog of SASP factorsinvolved in the cell fate conversion. Amphiregulin (AREG), frequently secreted by senescent cells, promotesin vitro reprogramming by accelerating proliferation and the mesenchymal-epithelial transition via EGFRsignaling. AREG treatment diminishes the negative effect of donor age on reprogramming. Finally, AREG enhances in vivo reprogramming in skeletal muscle. Hence, various SASP factors can facilitate cellular plasticityto promote reprogramming and tissue repair. %G English %Z We are indebted to Jun Zhang for his excellent technical support in image analysis. We are grateful to the Central Animal Facility, the Proteomic Platform, the Cytometry Platform, and the Bioinformatics and Biostatistics Hub of the Institut Pasteur. %2 https://pasteur.hal.science/pasteur-04093575/document %2 https://pasteur.hal.science/pasteur-04093575/file/1-s2.0-S2211124722008725-main.pdf %L pasteur-04093575 %U https://pasteur.hal.science/pasteur-04093575 %~ PASTEUR %~ CNRS %~ INC-CNRS %~ UNIV-PARIS %~ UNIVERSITE-PARIS %~ ANR %~ TEST2-HALCNRS %~ UMR3738 %~ CELLULAR-PLASTICITY-AGE-RELATED-PATHOLOGY %~ FRANCE-GENOMIQUE %~ BIOINFO_BIOSTAT_HUB