Literature DB >> 33151476

(-)-Epicatechin reduces muscle waste after complete spinal cord transection in a murine model: role of ubiquitin-proteasome system.

Cristian Gonzalez-Ruiz1, Paola Cordero-Anguiano1, Axayacatl Morales-Guadarrama2, Rodrigo Mondragón-Lozano3, Stephanie Sánchez-Torres4, Hermelinda Salgado-Ceballos5, Francisco Villarreal6, Eduardo Meaney1, Guillermo Ceballos7, Nayelli Nájera8.   

Abstract

The skeletal muscle mass reduces 30-60% after spinal cord injury, this is mostly due to protein degradation through ubiquitin-proteasome system. In this work, we propose that the flavanol (-)-epicatechin, due its widespread biological effects on muscle health, can prevent muscle mass decrease after spinal cord injury. Thirty-six female Long Evans rats were randomized into 5 groups: (1) Spinal cord injury 7 days, (2) Spinal cord injury + (-)-epicatechin 7 days, (3) Spinal cord injury 30 days, (4) Spinal cord injury + (-)-epicatechin 30 days and (5) Sham (Only laminectomy). Hind limb perimeter, muscle cross section area, fiber cross section area and ubiquitin-proteasome system protein expression together with total protein ubiquitination were assessed. At 30 days Spinal cord injury group lost 49.52 ± 2.023% of muscle cross section area (-)-epicatechin treated group lost only 24.28 ± 15.45% being a significant difference. Ubiquitin-proteasome markers showed significant changes. FOXO1a increased in spinal cord injury group vs Sham (-)-epicatechin reduced this increase. In spinal cord injury group MAFbx increased significantly vs Sham but decrease in (-)-epicatechin treatment group at 30 days. At 7 and 30 days MuRF1 increased in the spinal cord injury and decreased in the (-)-epicatechin group. The global protein ubiquitination increases after spinal cord injury, epicatechin treatment induce a significant decrease in protein ubiquitination. These results suggest that (-)-epicatechin reduces the muscle waste after spinal cord injury through down regulation of the ubiquitin-proteasome system.

Entities:  

Keywords:  (−)-Epicatechin; FOXO1a; MAFbx; MuRF1; Muscle atrophy; Spinal cord injury

Mesh:

Substances:

Year:  2020        PMID: 33151476     DOI: 10.1007/s11033-020-05954-x

Source DB:  PubMed          Journal:  Mol Biol Rep        ISSN: 0301-4851            Impact factor:   2.316


  46 in total

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4.  The glucocorticoid receptor and FOXO1 synergistically activate the skeletal muscle atrophy-associated MuRF1 gene.

Authors:  David S Waddell; Leslie M Baehr; Jens van den Brandt; Steven A Johnsen; Holger M Reichardt; J David Furlow; Sue C Bodine
Journal:  Am J Physiol Endocrinol Metab       Date:  2008-07-08       Impact factor: 4.310

Review 5.  Spinal cord injury: a review of current therapy, future treatments, and basic science frontiers.

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Journal:  Neurochem Res       Date:  2013-03-06       Impact factor: 3.996

6.  Transcription factor FoxO1, the dominant mediator of muscle wasting in chronic kidney disease, is inhibited by microRNA-486.

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7.  Regulation of autophagy and the ubiquitin-proteasome system by the FoxO transcriptional network during muscle atrophy.

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Review 8.  Electrical stimulation and denervated muscles after spinal cord injury.

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Journal:  Neural Regen Res       Date:  2020-08       Impact factor: 5.135

9.  Inhibition of atrogin-1/MAFbx mediated MyoD proteolysis prevents skeletal muscle atrophy in vivo.

Authors:  Julie Lagirand-Cantaloube; Karen Cornille; Alfredo Csibi; Sabrina Batonnet-Pichon; Marie Pierre Leibovitch; Serge A Leibovitch
Journal:  PLoS One       Date:  2009-03-25       Impact factor: 3.240

Review 10.  Promising neuroprotective strategies for traumatic spinal cord injury with a focus on the differential effects among anatomical levels of injury.

Authors:  Antigona Ulndreaj; Anna Badner; Michael G Fehlings
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Review 1.  Pharmacologic approaches to prevent skeletal muscle atrophy after spinal cord injury.

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