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Chronic heart failure-induced skeletal muscle atrophy, necrosis, and changes in myogenic regulatory factors.
- Source :
-
Medical science monitor : international medical journal of experimental and clinical research [Med Sci Monit] 2010 Dec; Vol. 16 (12), pp. BR374-83. - Publication Year :
- 2010
-
Abstract
- Background: Although intrinsic skeletal muscle abnormalities can influence exercise intolerance during heart failure (HF), the factors responsible for muscle changes have not been elucidated. In this study we evaluated the expression of myogenic regulatory factors (MRF), myosin heavy chain (MyHC) isoforms, and fiber trophism in the soleus muscle of rats with myocardial infarction-induced heart failure.<br />Method/results: Six months after surgery, 2 groups of rats were studied: sham, and infarcted rats with HF (MI/HF+, MI size: 41.1±6.3% of total left ventricular area). In the infarcted group, microscopic evaluation revealed scattered foci of fiber necrosis in combination with inflammatory cells, phagocytosis, and increased fibrous tissue. The frequency of necrotic fibers was significantly higher in the MI/HF+ group than in the sham. The MI/HF+ group had atrophy of type I, IC/IIC, and IIA fibers compared to the sham group (P<0.05). MyoD gene expression was higher in the MI/HF+ group (sham: 1.00±0.49; MI/HF+: 2.53±0.71 arbitrary units; P<0.001). Myogenin and MRF4 gene expression was similar in both groups. Myogenin protein levels were reduced in the MI/HF+ group (sham: 1.00±0.21; MI/HF+: 0.74±0.21 arbitrary units; P=0.026). MyoD and MRF4 protein levels, as well as the MyHC distribution, were not different between groups. The MI/HF+ group had higher TNF-α and IL-6 serum concentrations than the sham group.<br />Conclusions: Heart failure-induced skeletal muscle atrophy is combined with fiber necrosis, increased MyoD gene expression and decreased myogenin protein levels.
- Subjects :
- Animals
Blotting, Western
Electrocardiography
Heart Failure etiology
Interleukin-6 blood
Male
Muscular Atrophy metabolism
Muscular Atrophy pathology
Necrosis pathology
Protein Isoforms metabolism
Rats
Rats, Wistar
Reverse Transcriptase Polymerase Chain Reaction
Tumor Necrosis Factor-alpha blood
Heart Failure complications
Muscle, Skeletal pathology
Muscular Atrophy etiology
Myocardial Infarction complications
Myogenic Regulatory Factors metabolism
Myosin Heavy Chains metabolism
Necrosis etiology
Subjects
Details
- Language :
- English
- ISSN :
- 1643-3750
- Volume :
- 16
- Issue :
- 12
- Database :
- MEDLINE
- Journal :
- Medical science monitor : international medical journal of experimental and clinical research
- Publication Type :
- Academic Journal
- Accession number :
- 21119570