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1 Departamento Fisiologia, Universidad Complutense, Madrid, Madrid, Spain
2 Departamento Ciencias Morfologicas y Fisiologia, Universidad Europea, Madrid, Madrid, Spain
* To whom correspondence should be addressed. E-mail: ALC{at}med.ucm.es.
ABSTRACT Chronic arthritis is a catabolic state associated with an inhibition of the IGF system and a decrease in body weight. Caquexia and muscular wasting is secondary to protein degradation by the ubiquitin-proteasome pathway. The aim of this work was to analyze the effect of adjuvant-induced arthritis on the muscle-specific ubiquitin ligases MuRF1 and MAFbx as well as on IGF-I and IGF binding protein-5 (IGFBP-5) gene expression in the skeletal muscle. We also studied whether the synthetic ghrelin receptor agonist, GHRP-2, was able to prevent arthritis-induced changes in the skeletal muscle. Arthritis induced an increase in MuRF1, MAFbx (P<0.01) and TNF-
mRNA (P<0.05) in the skeletal muscle. Arthritis decreased the serum IGF-I and its gene expression in the liver (P<0.01), whereas it increased IGF-I and IGFBP-5 gene expression in the skeletal muscle (P<0.01). Administration of GHRP-2 for 8 days prevented arthritis-induced increase in muscular MuRF1, MAFbx and TNF- gene expression. GHRP-2 treatment increased the serum concentrations of IGF-I and the IGF-I mRNA in the liver and in the cardiac muscle, and decreased muscular IGFBP-5 mRNA both in control and in arthritic rats (P<0.05). GHRP-2 treatment increased muscular IGF-I mRNA in control rats (P<0.01), but it did not modify the muscular IGF-I gene expression in arthritic rats. These data indicate that arthritis induces an increase in the activity of the ubiquitin-proteasome proteolytic pathway which is prevented by GHRP-2 administration. The parallel changes in muscular IGFBP-5 and TNFá gene expression with the ubiquitin ligases suggest that they can participate in skeletal muscle alterations during chronic arthritis.
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