Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Casas 2009 PloS One

From Bioblast
Revision as of 11:37, 16 February 2018 by Beno Marija (talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision β†’ (diff)
Publications in the MiPMap
Casas F, Pessemesse L, Grandemange S, Seyer P, Baris O, Gueguen N, Ramonatxo C, Perrin F, Fouret G, Lepourry L, Cabello G, Wrutniak-Cabello C (2009) Overexpression of the mitochondrial T3 receptor induces skeletal muscle atrophy during aging. PLoS One 4:e5631.

Β» PMID: 19462004 Open Access

Casas F, Pessemesse L, Grandemange S, Seyer P, Baris O, Gueguen N, Ramonatxo C, Perrin F, Fouret G, Lepourry L, Cabello G, Wrutniak-Cabello C (2009) PLoS One

Abstract: In previous studies, we characterized a new hormonal pathway involving a mitochondrial T3 receptor (p43) acting as a mitochondrial transcription factor. In in vitro and in vivo studies, we have shown that p43 increases mitochondrial transcription and mitochondrial biogenesis. In addition, p43 overexpression in skeletal muscle stimulates mitochondrial respiration and induces a shift in metabolic and contractile features of muscle fibers which became more oxidative. Here we have studied the influence of p43 overexpression in skeletal muscle of mice during aging. We report that p43 overexpression initially increased mitochondrial mass. However, after the early rise in mitochondrial DNA occurring at 2 months of age in transgenic mice, we observed a progressive decrease of mitochondrial DNA content which became 2-fold lower at 23 months of age relatively to control animals. Moreover, p43 overexpression induced an oxidative stress characterized by a strong increase of lipid peroxidation and protein oxidation in quadriceps muscle, although antioxidant enzyme activities (catalase and superoxide dismutase) were stimulated. In addition, muscle atrophy became detectable at 6 months of age, probably through a stimulation of the ubiquitin proteasome pathway via two muscle-specific ubiquitin ligases E3, Atrogin-1/MAFbx and MuRF1. Taken together, these results demonstrate that a prolonged stimulation of mitochondrial activity induces muscle atrophy. In addition, these data underline the importance of a tight control of p43 expression and suggest that a deregulation of the direct T3 mitochondrial pathway could be one of the parameters involved in the occurrence of sarcopenia. β€’ Keywords: P43 overexpression, Sarcopenia, Muscle atropy

β€’ O2k-Network Lab: FR Montpellier Wrutniak-Cabello C, FR Angers Gueguen N


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Genetic knockout;overexpression, mt-Medicine  Pathology: Aging;senescence, Myopathy 

Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Regulation: ADP  Coupling state: OXPHOS 

HRR: Oxygraph-2k