Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis

Inflammatory activity in rheumatoid arthritis may alter the regulation of muscle mass leading to a secondary sarcopenia, commonly termed rheumatoid cachexia (RC). We characterized alterations to muscle structure and various pro-inflammatory, catabolic and regenerative markers in an animal model of R...

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Authors: Little, Robert D.; Prieto-Potin, Iván; Pérez-Baos, Sandra; Villalvilla, Amanda; Gratal, Paula; Cicuttini, Flavia; Largo, Raquel; Herrero-Beaumont Cuenca, Gabriel
Format: Article
Publication date:2017
Country:España
Institution:Universidad Autónoma de Madrid
Repository:Biblos-e Archivo. Repositorio Institucional de la UAM
Language:English
OAI Identifier:oai:repositorio.uam.es:10486/680224
Online Access:http://hdl.handle.net/10486/680224
https://dx.doi.org/10.1038/s41598-017-06581-6
Access Level:Open access
Keyword:Arthritis
Sarcopenia
Chronic arthritis
Compensatory anabolic
Medicina
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author Little, Robert D.
author2 Prieto-Potin, Iván
Pérez-Baos, Sandra
Villalvilla, Amanda
Gratal, Paula
Cicuttini, Flavia
Largo, Raquel
Herrero-Beaumont Cuenca, Gabriel
author2_role author
author
author
author
author
author
author
author_browse Cicuttini, Flavia
Gratal, Paula
Herrero-Beaumont Cuenca, Gabriel
Largo, Raquel
Little, Robert D.
Prieto-Potin, Iván
Pérez-Baos, Sandra
Villalvilla, Amanda
author_facet Little, Robert D.
Prieto-Potin, Iván
Pérez-Baos, Sandra
Villalvilla, Amanda
Gratal, Paula
Cicuttini, Flavia
Largo, Raquel
Herrero-Beaumont Cuenca, Gabriel
author_role author
collection Biblos-e Archivo. Repositorio Institucional de la UAM
description Inflammatory activity in rheumatoid arthritis may alter the regulation of muscle mass leading to a secondary sarcopenia, commonly termed rheumatoid cachexia (RC). We characterized alterations to muscle structure and various pro-inflammatory, catabolic and regenerative markers in an animal model of RC. Antigen induced arthritis (AiA) was performed in 20 male adult rabbits. AiA animals exhibited significantly less weight gain, a markedly elevated serum C-reactive protein (CRP), lighter muscles with shorter cross-sectional diameter and increased myonuclei when compared to controls. Atrogin-1 and MuRF-1 were up-regulated alongside an increase in IL-1β, active NF-κB and a higher ratio of phosphorylated to inactive p38 MAPK. CCL-2 and TNF levels were reduced and IL-6 was unchanged between groups. We observed decreased pSTAT3, unchanged pSTAT1 and Myf5, but increased Pax7, MyoD and myogenin. AiA rabbits had a reduction in myostatin from gastrocnemii and synovium with a congruent decrease in serum myostatin compared to controls. Chronic arthritis induced an RC-like secondary sarcopenia with increased muscle protein breakdown. Elevated IL-1β may trigger proteolysis via elevated NF-κB and p38 MAPK signaling with a compensatory anabolic response suggested by myonuclear expansion, increased Pax7, MyoD and myogenin, reduced pSTAT3 as well as reduced serum, synovial and muscular myostatin
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publishDate 2017
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reponame_str Biblos-e Archivo. Repositorio Institucional de la UAM
spelling Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis Little, Robert D. Prieto-Potin, Iván Pérez-Baos, Sandra Villalvilla, Amanda Gratal, Paula Cicuttini, Flavia Largo, Raquel Herrero-Beaumont Cuenca, Gabriel Arthritis Sarcopenia Chronic arthritis Compensatory anabolic Medicina Inflammatory activity in rheumatoid arthritis may alter the regulation of muscle mass leading to a secondary sarcopenia, commonly termed rheumatoid cachexia (RC). We characterized alterations to muscle structure and various pro-inflammatory, catabolic and regenerative markers in an animal model of RC. Antigen induced arthritis (AiA) was performed in 20 male adult rabbits. AiA animals exhibited significantly less weight gain, a markedly elevated serum C-reactive protein (CRP), lighter muscles with shorter cross-sectional diameter and increased myonuclei when compared to controls. Atrogin-1 and MuRF-1 were up-regulated alongside an increase in IL-1β, active NF-κB and a higher ratio of phosphorylated to inactive p38 MAPK. CCL-2 and TNF levels were reduced and IL-6 was unchanged between groups. We observed decreased pSTAT3, unchanged pSTAT1 and Myf5, but increased Pax7, MyoD and myogenin. AiA rabbits had a reduction in myostatin from gastrocnemii and synovium with a congruent decrease in serum myostatin compared to controls. Chronic arthritis induced an RC-like secondary sarcopenia with increased muscle protein breakdown. Elevated IL-1β may trigger proteolysis via elevated NF-κB and p38 MAPK signaling with a compensatory anabolic response suggested by myonuclear expansion, increased Pax7, MyoD and myogenin, reduced pSTAT3 as well as reduced serum, synovial and muscular myostatin This work was partially supported by research grants from the Instituto de Salud Carlos III (PI13/00570, PI15/00340, PI16/00065 and RETICEF RD12/0043/0008), co-funded by Fondo Europeo de Desarrollo Regional (FEDER) and ASPIRE IIR grant from Pfizer. Nature Publishing Group http://hdl.handle.net/10486/680224 https://dx.doi.org/10.1038/s41598-017-06581-6
spellingShingle Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
Little, Robert D.
Arthritis
Sarcopenia
Chronic arthritis
Compensatory anabolic
Medicina
title Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
title_full Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
title_fullStr Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
title_full_unstemmed Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
title_short Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
title_sort Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
topic Arthritis
Sarcopenia
Chronic arthritis
Compensatory anabolic
Medicina
topic_facet Arthritis
Sarcopenia
Chronic arthritis
Compensatory anabolic
Medicina
url http://hdl.handle.net/10486/680224
https://dx.doi.org/10.1038/s41598-017-06581-6