| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1Facultad de Medicina, Departamento Fisiología, Universidad Complutense y 2Departamento Ciencias Morfológicas y Fisiología, Universidad Europea, Madrid, Spain
Submitted 11 March 2005 ; accepted in final form 14 July 2005
Chronic arthritis is a catabolic state associated with an inhibition of the IGF system and a decrease in body weight. Cachexia 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 muscle ring finger 1 (MuRF1) and muscle atrophy F-box (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, growth hormone releasing peptide-2 (GHRP-2), was able to prevent arthritis-induced changes in the skeletal muscle. Arthritis induced an increase in MuRF1, MAFbx (P < 0.01), and tumor necrosis factor (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 the 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 that is prevented by GHRP-2 administration. The parallel changes in muscular IGFBP-5 and TNF- gene expression with the ubiquitin ligases suggest that they can participate in skeletal muscle alterations during chronic arthritis.
growth hormone-releasing peptide-2; atrogenes; insulin-like growth factor I; insulin-like growth factor-binding protein-5; tumor necrosis factor; arthritic rats
This article has been cited by other articles:
|
|
 |
|
  A I Martin, E Castillero, M Granado, M Lopez-Menduina, M A Villanua, and A Lopez-Calderon Adipose tissue loss in adjuvant arthritis is associated with a decrease in lipogenesis, but not with an increase in lipolysis J. Endocrinol., April 1, 2008; 197(1): 111 - 119. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Granado, A. I. Martin, M. Lopez-Menduina, A. Lopez-Calderon, and M. A. Villanua GH-releasing peptide-2 administration prevents liver inflammatory response in endotoxemia Am J Physiol Endocrinol Metab, January 1, 2008; 294(1): E131 - E141. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Granado, A. I Martin, M{a} A. Villanua, and A. Lopez-Calderon Experimental arthritis inhibits the insulin-like growth factor-I axis and induces muscle wasting through cyclooxygenase-2 activation Am J Physiol Endocrinol Metab, June 1, 2007; 292(6): E1656 - E1665. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Filigheddu, V. F. Gnocchi, M. Coscia, M. Cappelli, P. E. Porporato, R. Taulli, S. Traini, G. Baldanzi, F. Chianale, S. Cutrupi, et al. Ghrelin and Des-Acyl Ghrelin Promote Differentiation and Fusion of C2C12 Skeletal Muscle Cells Mol. Biol. Cell, March 1, 2007; 18(3): 986 - 994. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
