Erythropoietin reduces the expression of myostatin in mdx dystrophic mice

D Feder; M Rugollini; A Santomauro; L P Oliveira; V P Lioi; R dos Santos; L G Ferreira; M T Nunes; M H Carvalho; P O Delgado; A A S Carvalho; F L A Fonseca

doi:10.1590/1414-431X20143858

Erythropoietin reduces the expression of myostatin in mdx dystrophic mice

D Feder, M Rugollini, A Santomauro, L P Oliveira, V P Lioi, R dos Santos, L G Ferreira, M T Nunes, M H Carvalho, P O Delgado, A A S Carvalho, F L A Fonseca

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

7 Downloads (Pure)

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.

Original language	English
Pages (from-to)	966-971
Number of pages	6
Journal	Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
Volume	47
Issue number	11
Early online date	5 Sept 2014
DOIs	https://doi.org/10.1590/1414-431X20143858
Publication status	Published - Nov 2014
Externally published	Yes

Bibliographical note

This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Keywords

Animals
Disease Models, Animal
Down-Regulation/drug effects
Dystrophin/deficiency
Erythropoietin/therapeutic use
Gene Expression/drug effects
Male
Mice, Inbred mdx
Muscle Strength/drug effects
Muscle, Skeletal/metabolism
Muscular Dystrophy, Duchenne/drug therapy
Myostatin/genetics
Phenotype
Real-Time Polymerase Chain Reaction
Recombinant Proteins/therapeutic use
Transforming Growth Factor beta1/genetics
Tumor Necrosis Factor-alpha/genetics

Access to Document

10.1590/1414-431X20143858Licence: CC BY

PublishedFinal published version, 572 KBLicence: CC BY

Cite this

Feder, D., Rugollini, M., Santomauro, A., Oliveira, L. P., Lioi, V. P., Santos, R. D., Ferreira, L. G., Nunes, M. T., Carvalho, M. H., Delgado, P. O., Carvalho, A. A. S., & Fonseca, F. L. A. (2014). Erythropoietin reduces the expression of myostatin in mdx dystrophic mice. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas, 47(11), 966-971. Advance online publication. https://doi.org/10.1590/1414-431X20143858

Feder, D, Rugollini, M, Santomauro, A, Oliveira, LP, Lioi, VP, Santos, RD, Ferreira, LG, Nunes, MT, Carvalho, MH, Delgado, PO, Carvalho, AAS & Fonseca, FLA 2014, 'Erythropoietin reduces the expression of myostatin in mdx dystrophic mice', Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas, vol. 47, no. 11, pp. 966-971. https://doi.org/10.1590/1414-431X20143858

@article{c85052d3d55a46b6988c531b7f7b2db4,

title = "Erythropoietin reduces the expression of myostatin in mdx dystrophic mice",

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.",

keywords = "Animals, Disease Models, Animal, Down-Regulation/drug effects, Dystrophin/deficiency, Erythropoietin/therapeutic use, Gene Expression/drug effects, Male, Mice, Inbred mdx, Muscle Strength/drug effects, Muscle, Skeletal/metabolism, Muscular Dystrophy, Duchenne/drug therapy, Myostatin/genetics, Phenotype, Real-Time Polymerase Chain Reaction, Recombinant Proteins/therapeutic use, Transforming Growth Factor beta1/genetics, Tumor Necrosis Factor-alpha/genetics",

author = "D Feder and M Rugollini and A Santomauro and Oliveira, {L P} and Lioi, {V P} and Santos, {R dos} and Ferreira, {L G} and Nunes, {M T} and Carvalho, {M H} and Delgado, {P O} and Carvalho, {A A S} and Fonseca, {F L A}",

note = "This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.",

year = "2014",

month = nov,

doi = "10.1590/1414-431X20143858",

language = "English",

volume = "47",

pages = "966--971",

journal = "Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas",

issn = "0100-879X",

publisher = "Associacao Brasileira de Divulgacao Cientifica",

number = "11",

}

TY - JOUR

T1 - Erythropoietin reduces the expression of myostatin in mdx dystrophic mice

AU - Feder, D

AU - Rugollini, M

AU - Santomauro, A

AU - Oliveira, L P

AU - Lioi, V P

AU - Santos, R dos

AU - Ferreira, L G

AU - Nunes, M T

AU - Carvalho, M H

AU - Delgado, P O

AU - Carvalho, A A S

AU - Fonseca, F L A

N1 - This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

PY - 2014/11

Y1 - 2014/11

N2 - 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.

AB - 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.

KW - Animals

KW - Disease Models, Animal

KW - Down-Regulation/drug effects

KW - Dystrophin/deficiency

KW - Erythropoietin/therapeutic use

KW - Gene Expression/drug effects

KW - Male

KW - Mice, Inbred mdx

KW - Muscle Strength/drug effects

KW - Muscle, Skeletal/metabolism

KW - Muscular Dystrophy, Duchenne/drug therapy

KW - Myostatin/genetics

KW - Phenotype

KW - Real-Time Polymerase Chain Reaction

KW - Recombinant Proteins/therapeutic use

KW - Transforming Growth Factor beta1/genetics

KW - Tumor Necrosis Factor-alpha/genetics

U2 - 10.1590/1414-431X20143858

DO - 10.1590/1414-431X20143858

M3 - Article

C2 - 25296358

SN - 0100-879X

VL - 47

SP - 966

EP - 971

JO - Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas

JF - Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas

IS - 11

ER -

Erythropoietin reduces the expression of myostatin in mdx dystrophic mice

Abstract

Bibliographical note

Keywords

Access to Document

Fingerprint

Cite this