Differential morphofunctional characteristics and gene expression in fast and slow muscle of rats with monocrotaline-induced heart failure

Heart failure (HF) is characterized by limited exercise tolerance, skeletal muscle atrophy, a shift toward fast muscle fiber, and myogenic regulatory factor (MRF) changes. Reactive oxygen species (ROS) also contribute to target organ damage in this syndrome. In this study, we investigated and compar...

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Bibliographic Details
Published in:	Journal of molecular histology Vol. 42; no. 3; pp. 205 - 215
Main Authors:	Bertaglia, Raquel Santilone, Reissler, Joyce, Lopes, Francis Silva, Cavalcante, Walter Luiz Garrido, Carani, Fernanda Regina, Padovani, Carlos Roberto, Rodrigues, Sergio Augusto, Cigogna, Antônio Carlos, Carvalho, Robson Francisco, Fernandes, Ana Angélica Henrique, Gallacci, Marcia, Silva, Maeli Dal Pai
Format:	Journal Article
Language:	English
Published:	Dordrecht Springer Netherlands 01-06-2011 Springer Nature B.V
Subjects:	Animals Biomedical and Life Sciences Biomedicine Cell Biology Developmental Biology Gene Expression Regulation Heart Failure - chemically induced Heart Failure - physiopathology Life Sciences Male Monocrotaline Muscle Contraction - physiology Muscle Fibers, Fast-Twitch - metabolism Muscle Fibers, Fast-Twitch - pathology Muscle Fibers, Slow-Twitch - metabolism Muscle Fibers, Slow-Twitch - pathology Muscular Atrophy - metabolism Muscular Atrophy - pathology MyoD Protein - genetics Myogenin - genetics Original Paper Rats Rats, Wistar RNA, Messenger - genetics Oxidative stress Fiber types Monocrotaline Skeletal muscle Myogenic regulatory factors
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Summary:	Heart failure (HF) is characterized by limited exercise tolerance, skeletal muscle atrophy, a shift toward fast muscle fiber, and myogenic regulatory factor (MRF) changes. Reactive oxygen species (ROS) also contribute to target organ damage in this syndrome. In this study, we investigated and compared morphofunctional characteristics and gene expression in Soleus (SOL—oxidative and slow twitching muscle) and in Extensor Digitorum Longus (EDL—glycolytic and fast twitching muscle) during HF. Two groups of rats were used: control (CT) and heart failure (HF), induced by a single injection of monocrotaline. MyoD and myogenin gene expression were determined by RT-qPCR, and MHC isoforms by SDS–PAGE; muscle fiber type frequency and cross sectional area (CSA) were analyzed by mATPase. A biochemical study was performed to determine lipid hydroperoxide (LH), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD); myography was used to determine amplitude, rise time, fall time, and fatigue resistance in both muscles. HF showed SOL and EDL muscle atrophy in all muscle fiber types; fiber frequency decreased in type IIC and muscle contraction fall time increased only in SOL muscle. Myogenin mRNA expression was lower in SOL and myoD decreased in HF EDL muscle. LH increased, and SOD and GSH-Px activity decreased only in HF SOL muscle. HF EDL muscle did not present changes in MHC distribution, contractile properties, HL concentration, and antioxidant enzyme activity. In conclusion, our results indicate that monocrotaline induced HF promoted more prominent biochemical, morphological and functional changes in SOL (oxidative and slow twitching muscle). Although further experiments are required to better determine the mechanisms involved in HF pathophysiology, our results contribute to understanding the muscle-specific changes that occur in this syndrome.
ISSN:	1567-2379 1567-2387
DOI:	10.1007/s10735-011-9325-7