Document Detail

Intracellular Inactivation of Thyroid Hormone Is a Survival Mechanism for Muscle Stem Cell Proliferation and Lineage Progression.
MedLine Citation:
PMID:  25456740     Owner:  NLM     Status:  Publisher    
Precise control of the thyroid hormone (T3)-dependent transcriptional program is required by multiple cell systems, including muscle stem cells. Deciphering how this is achieved and how the T3 signal is controlled in stem cell niches is essentially unknown. We report that in response to proliferative stimuli such as acute skeletal muscle injury, type 3 deiodinase (D3), the thyroid hormone-inactivating enzyme, is induced in satellite cells where it reduces intracellular thyroid signaling. Satellite cell-specific genetic ablation of dio3 severely impairs skeletal muscle regeneration. This impairment is due to massive satellite cell apoptosis caused by exposure of activated satellite cells to the circulating TH. The execution of this proapoptotic program requires an intact FoxO3/MyoD axis, both genes positively regulated by intracellular TH. Thus, D3 is dynamically exploited in vivo to chronically attenuate TH signaling under basal conditions while also being available to acutely increase gene programs required for satellite cell lineage progression.
Monica Dentice; Raffaele Ambrosio; Valentina Damiano; Annarita Sibilio; Cristina Luongo; Ombretta Guardiola; Siham Yennek; Paola Zordan; Gabriella Minchiotti; Annamaria Colao; Alessandro Marsili; Silvia Brunelli; Luigi Del Vecchio; P Reed Larsen; Shahragim Tajbakhsh; Domenico Salvatore
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-11-13
Journal Detail:
Title:  Cell metabolism     Volume:  20     ISSN:  1932-7420     ISO Abbreviation:  Cell Metab.     Publication Date:  2014 Dec 
Date Detail:
Created Date:  2014-12-3     Completed Date:  -     Revised Date:  2014-12-3    
Medline Journal Info:
Nlm Unique ID:  101233170     Medline TA:  Cell Metab     Country:  -    
Other Details:
Languages:  ENG     Pagination:  1038-1048     Citation Subset:  -    
Copyright Information:
Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.
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