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Title: Fibrogenic cell plasticity blunts tissue regeneration and aggravates muscular dystrophy      
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dateReleased:
04-10-2015
ID:
E-GEOD-67687
description:
Preservation of cell identity is necessary for homeostasis of most adult tissues. This process is challenged every time a tissue undergoes regeneration after stress or injury. In the lethal Duchenne muscular Dystrophy (DMD), skeletal muscle regenerative capacity declines gradually as fibrosis increases. Using genetically engineered-tracing mice, we demonstrate that in dystrophic muscle, specialized cells of muscular, endothelial and hematopoietic origins gain plasticity towards a fibrogenic fate via a TGFβ-mediated pathway. This results in loss of cellular identity and normal function, with deleterious consequences for regeneration. Furthermore, this fibrogenic process involves acquisition of a mesenchymal progenitor multipotent status, illustrating a link between fibrogenesis and gain of progenitor cell functions. As this plasticity was also observed in DMD patients, we propose that mesenchymal transitions impair regeneration and worsen diseases with a fibrotic component. TGFb exposure induced gene expression was measured after 4 days of treatment compared to untreated cells. Three independent experiments were performed both for the treatment and for the control
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accessURL: https://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-67687
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accessURL: www.omicsdi.org/ws/dataset/arrayexpress-repository/E-GEOD-67687.json
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accessURL: http://www.omicsdi.org/ws/dataset/arrayexpress-repository/E-GEOD-67687.xml
ID:
SCR:014747
name:
Omics Discovery Index
abbreviation:
OmicsDI
homePage: http://www.omicsdi.org/