Perez-Schindler, J, Summermatter, S, Santos, G, Zorzato, F and Handschin, C (2013) The transcriptional coactivator PGC-1alpha is dispensable for chronic overload-induced skeletal muscle hypertrophy and metabolic remodeling. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. pp. 20314-20319.

Abstract

Skeletal muscle mass loss and dysfunction have been linked to many diseases. Conversely, resistance exercise, mainly by activating mammalian target of rapamycin complex 1 (mTORC1), promotes skeletal muscle hypertrophy and exerts several therapeutic effects. Moreover, mTORC1, along with peroxisome proliferator-activated receptor coactivator 1alpha (PGC-1alpha), regulates skeletal muscle metabolism. However, it is unclear whether PGC-1alpha is required for skeletal muscle adaptations after overload. Here we show that although chronic overload of skeletal muscle via synergist ablation (SA) strongly induces hypertrophy and a switch toward a slow-contractile phenotype, these effects were independent of PGC-1alpha. In fact, SA down-regulated PGC-1alpha expression and led to a repression of energy metabolism. Interestingly, however, PGC-1alpha deletion preserved peak force after SA. Taken together, our data suggest that PGC-1alpha is not involved in skeletal muscle remodeling induced by SA

Item Type:	Article
Additional Information:	pubid: 231 nvp_institute: NIBR contributor_address: (Perez-Schindler, Summermatter, Santos, Handschin) Biozentrum, University of Basel, 4056 Basel, Switzerland (Zorzato) Departments of Anesthesia and Biomedicine, Basel University Hospital, 4031 Basel, Switzerland (Zorzato) Department of Experimental and Diagnostic Medicine, University of Ferrara, 44100 Ferrara, Italy (Summermatter) Novartis Institute for Biomedical Research, 4056 Basel, Switzerland
Date Deposited:	13 Oct 2015 13:12
Last Modified:	13 Oct 2015 13:12
URI:	https://oak.novartis.com/id/eprint/22040