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GROWTH HORMONE ADMINISTRATION ALTERS PROTEIN EXPRESSION IN SKELETAL MUSCLE OF RATS WITH AORTIC STENOSIS‐INDUCED HEART FAILURE
Author(s) -
Lima Aline Regina Ruiz,
Damatto Ricardo Luiz,
Pagan Luana Urbano,
Bonomo Camila,
Cezar Marcelo Diarcádia Mariano,
Guizoni Daniele Mendes,
Martinez Paula Felippe,
Gomes Mariana Janini,
Okoshi Katashi,
Okoshi Marina Politi
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.386.3
Subject(s) - medicine , myostatin , endocrinology , follistatin , myod , myogenin , heart failure , skeletal muscle , cardiology , myogenesis
In this study we evaluated the effects of growth hormone (GH) administration on protein expression of myostatin, follistatin, and the myogenic regulatory factors in skeletal muscle of rats with ascending aortic stenosis‐induced heart failure. Methods Male Wistar rats were subjected to thoracotomy to induce aortic stenosis (AS). After developing tachypnea/labored respiration, rats were subjected to echocardiogram and assigned to three groups (n=8): Sham, AS, and AS treated with GH (AS‐GH, 2 mg/kg/day) for 14 days. After treatment, rats were subjected to echocardiogram and euthanatized. Protein expression was evaluated by Western‐blot. Statistical analysis Anova and Tukey. Results Before GH treatment, cardiac parameters did not differ between AS and AS‐GH groups. GH preserved body weight. Right ventricular weight/BW ratio and left ventricular posterior wall thickness were higher in both AS groups than Sham. MyoD was higher in AS than Sham and similar between AS‐GH and Sham (Sham 1.0±1.3; AS 1.7±1.4; AS‐GH 1.2±1.2 arbitrary units). MRF4 expression was higher in AS‐GH than Sham (Sham 1.0±0.7; AS 1.6±0.4; AS‐GH 3.1±1.6 arbitrary units). Myostatin, follistatin, and myogenin expression did not differ between groups. Conclusion Growth hormone increases MRF4 and normalizes MyoD expression in skeletal muscle of heart failure rats. Myostatin/follistatin pathway is not changed in this experimental model.