Cardioprotective effects of recombinant human erythropoietin in rats with experimental autoimmune myocarditis

Erythropoietin (EPO) has been known to have cytoprotective effects on several types of tissues, presumably through modulation of apoptosis and inflammation. The effect of EPO on myocardial inflammation, however, has not yet been clarified. We investigated the cardioprotective effects of EPO in rats...

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Published in:Biochemical and biophysical research communications 2006-06, Vol.344 (3), p.987-994
Main Authors: Mitsuma, Wataru, Ito, Masahiro, Kodama, Makoto, Fuse, Koichi, Okamura, Kazuki, Minagawa, Shiro, Kato, Kiminori, Hanawa, Haruo, Toba, Ken, Nakazawa, Mikio, Aizawa, Yoshifusa
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - drug effects
Autoimmune Diseases - drug therapy
Autoimmune Diseases - metabolism
Cardiotonic Agents - administration & dosage
Cytokines - metabolism
Erythropoietin
Erythropoietin - administration & dosage
Erythropoietin - genetics
Erythropoietin receptor
Experimental autoimmune myocarditis
Humans
Male
Myocarditis - drug therapy
Myocarditis - metabolism
Myocarditis - pathology
Rats
Rats, Inbred Lew
Recombinant Proteins - administration & dosage
Treatment Outcome
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Summary:Erythropoietin (EPO) has been known to have cytoprotective effects on several types of tissues, presumably through modulation of apoptosis and inflammation. The effect of EPO on myocardial inflammation, however, has not yet been clarified. We investigated the cardioprotective effects of EPO in rats with experimental autoimmune myocarditis (EAM). Seven-week-old Lewis rats immunized with cardiac myosin were treated either with EPO or vehicle and were examined on day 22. EPO attenuated the functional and histological severity of EAM along with suppression of mRNAs of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in the hearts as well as a reduction of apoptotic cardiomyocytes. The EPO receptor (EPO-R) was upregulated in the myocardium of EAM compared with that of healthy rats. These results may suggest that EPO ameliorated the progression of EAM by modulating myocardial inflammation and apoptosis.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2006.03.230