Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis

Abstract 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 m...

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Autores principales:	Robert D. Little, Iván Prieto-Potin, Sandra Pérez-Baos, Amanda Villalvilla, Paula Gratal, Flavia Cicuttini, Raquel Largo, Gabriel Herrero-Beaumont
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a7caba8f206c4e95a39746ba05d766d8
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spelling	oai:doaj.org-article:a7caba8f206c4e95a39746ba05d766d82021-12-02T16:06:36ZCompensatory anabolic signaling in the sarcopenia of experimental chronic arthritis10.1038/s41598-017-06581-62045-2322https://doaj.org/article/a7caba8f206c4e95a39746ba05d766d82017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06581-6https://doaj.org/toc/2045-2322Abstract 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.Robert D. LittleIván Prieto-PotinSandra Pérez-BaosAmanda VillalvillaPaula GratalFlavia CicuttiniRaquel LargoGabriel Herrero-BeaumontNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Robert D. Little Iván Prieto-Potin Sandra Pérez-Baos Amanda Villalvilla Paula Gratal Flavia Cicuttini Raquel Largo Gabriel Herrero-Beaumont Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
description	Abstract 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.
format	article
author	Robert D. Little Iván Prieto-Potin Sandra Pérez-Baos Amanda Villalvilla Paula Gratal Flavia Cicuttini Raquel Largo Gabriel Herrero-Beaumont
author_facet	Robert D. Little Iván Prieto-Potin Sandra Pérez-Baos Amanda Villalvilla Paula Gratal Flavia Cicuttini Raquel Largo Gabriel Herrero-Beaumont
author_sort	Robert D. Little
title	Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
title_short	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_sort	compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/a7caba8f206c4e95a39746ba05d766d8
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Compensatory anabolic signaling in the sarcopenia of experimental chronic arthritis

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