Key result
Monocrotaline-induced heart failure increased MMP9 mRNA expression and activity in soleus, extensor digitorum longus, and diaphragm muscles, and MMP2 mRNA expression in the diaphragm of rats.
Why the study?
Does heart failure alter matrix metalloproteinase gene expression and activity in rat skeletal muscle?
Does heart failure alter matrix metalloproteinase gene expression and activity in rat skeletal muscle?
Heart failure increases MMP9 and MMP2 expression and activity in skeletal muscles of rats, suggesting a role in HF-associated myopathy.
Answers are grounded in this paper and cite their sources.
May implicate MMPs in experimental HF myopathy; leaves open translation to human skeletal muscle dysfunction.
Heart failure is associated with a skeletal muscle myopathy with cellular and extracellular alterations. The hypothesis of this investigation is that extracellular changes may be associated with enhanced mRNA expression and activity of matrix metalloproteinases (MMP). We examined MMP mRNA expression and MMP activity in Soleus (SOL), extensor digitorum longus (EDL), and diaphragm (DIA) muscles of young Wistar rat with monocrotaline-induced heart failure. Rats injected with saline served as age-matched controls. MMP2 and MMP9 mRNA contents were determined by RT-PCR and MMP activity by electrophoresis in gelatin-containing polyacrylamide gels in the presence of SDS under non-reducing conditions. Heart failure increased MMP9 mRNA expression and activity in SOL, EDL and DIA and MMP2 mRNA expression in DIA. These results suggest that MMP changes may contribute to the skeletal muscle myopathy during heart failure.
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Carvalho et al. (2006) studied Heart failure. Monocrotaline-induced heart failure vs. Saline injection was evaluated on MMP2 and MMP9 mRNA expression and MMP activity in skeletal muscles. Monocrotaline-induced heart failure increased MMP9 mRNA expression and activity in soleus, extensor digitorum longus, and diaphragm muscles, and MMP2 mRNA expression in the diaphragm of rats.
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