ABSTRACT
Erythropoietin (EPO) has been well characterized as a renal glycoprotein hormone regulating red blood cell production by inhibiting apoptosis of erythrocyte progenitors in hematopoietic tissues. EPO exerts regulatory effects in cardiac and skeletal muscles. Duchenne muscular dystrophy is a lethal degenerative disorder of skeletal and cardiac muscle. In this study, we tested the possible therapeutic beneficial effect of recombinant EPO (rhEPO) in dystrophic muscles in mdx mice. Total strength was measured using a force transducer coupled to a computer. Gene expression for myostatin, transforming growth factor-β1 (TGF-β1), and tumor necrosis factor-α (TNF-α) was determined by quantitative real time polymerase chain reaction. Myostatin expression was significantly decreased in quadriceps from mdx mice treated with rhEPO (rhEPO=0.60±0.11, control=1.07±0.11). On the other hand, rhEPO had no significant effect on the expression of TGF-β1 (rhEPO=0.95±0.14, control=1.05±0.16) and TNF-α (rhEPO=0.73±0.20, control=1.01±0.09). These results may help to clarify some of the direct actions of EPO on skeletal muscle.
Subject(s)
Animals , Male , Down-Regulation/drug effects , Erythropoietin/therapeutic use , Gene Expression/drug effects , Muscular Dystrophy, Duchenne/drug therapy , Myostatin/metabolism , Recombinant Proteins/therapeutic use , Disease Models, Animal , Dystrophin/deficiency , Mice, Inbred mdx , Muscle Strength/drug effects , Muscle, Skeletal/metabolism , Muscular Dystrophy, Duchenne/metabolism , Myostatin/genetics , Phenotype , Real-Time Polymerase Chain Reaction , Transforming Growth Factor beta1/genetics , Transforming Growth Factor beta1/metabolism , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Erythropoietin (EPO) has been well characterized as a renal glycoprotein hormone regulating red blood cell production by inhibiting apoptosis of erythrocyte progenitors in hematopoietic tissues. EPO exerts regulatory effects in cardiac and skeletal muscles. Duchenne muscular dystrophy is a lethal degenerative disorder of skeletal and cardiac muscle. In this study, we tested the possible therapeutic beneficial effect of recombinant EPO (rhEPO) in dystrophic muscles in mdx mice. Total strength was measured using a force transducer coupled to a computer. Gene expression for myostatin, transforming growth factor-ß1 (TGF-ß1), and tumor necrosis factor-α (TNF-α) was determined by quantitative real time polymerase chain reaction. Myostatin expression was significantly decreased in quadriceps from mdx mice treated with rhEPO (rhEPO = 0.60 ± 0.11, control = 1.07 ± 0.11). On the other hand, rhEPO had no significant effect on the expression of TGF-ß1 (rhEPO = 0.95 ± 0.14, control = 1.05 ± 0.16) and TNF-α (rhEPO = 0.73 ± 0.20, control = 1.01 ± 0.09). These results may help to clarify some of the direct actions of EPO on skeletal muscle.
Subject(s)
Down-Regulation/drug effects , Erythropoietin/therapeutic use , Gene Expression/drug effects , Muscular Dystrophy, Duchenne/drug therapy , Myostatin/metabolism , Recombinant Proteins/therapeutic use , Animals , Disease Models, Animal , Dystrophin/deficiency , Male , Mice, Inbred mdx , Muscle Strength/drug effects , Muscle, Skeletal/metabolism , Muscular Dystrophy, Duchenne/metabolism , Myostatin/genetics , Phenotype , Real-Time Polymerase Chain Reaction , Transforming Growth Factor beta1/genetics , Transforming Growth Factor beta1/metabolism , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Leprosy is an infectious disease of prevalence still high in endemic areas in Brazil. The neurological presentation depends on the involved nerve and is usually associated with skin lesions and the formation of multiple abscesses. We present a case of isolated tuberculoid leprosy, discuss the occurrence, the differential diagnosis and the treatment of this rare presentation and reaffirm the importance of considering leprosy in the differential diagnosis of patients with polyneuropathy or nerve enlargement with no skin lesions.
