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Erythropoietin increases eNOS protein in the mouse heart.
Author(s) -
Melville Sarah,
Rui Tao,
Kvietys Peter
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1153
Subject(s) - enos , erythropoietin , medicine , endocrinology , western blot , agonist , chemistry , receptor , nitric oxide , nitric oxide synthase , biochemistry , gene
It is generally accepted that induction of iNOS, but not eNOS, in the heart renders it less susceptible to the detrimental effects of an ischemia/reperfusion (I/R) challenge. However, there is some evidence to indicate that induction of eNOS in the heart (adenosine receptor agonist) can also provide protection against I/R‐induced myocardial dysfunction and injury. We have recently shown that pretreatment of the heart with erythropoietin (EPO) can ameliorate the inflammation associated with an I/R challenge given 24 hrs later. The aim of the present study was to determine whether EPO can increase myocardial eNOS protein expression. C57BL/6 mice were treated with EPO (5,000 U/kg; intrperitoneally). Twenty four hrs later, the animals were euthanized, the hearts removed and prepared for Western blot analysis. Briefly, 5 μg of protein from heart tissue hydrolysates were resolved on 12.5% SDS‐PAGE and transferred to polyvinylidiene fluoride membranes. After blocking with 5% non‐fat milk, the membranes were blotted with an anti‐EPO eNOS antibody. Our results indicate that EPO can induce eNOS protein expression in the myocardium. The increase in eNOS protein in the myocardium could explain the protective effects of EPO in I/R‐induced myocardial dysfunction and injury. (MOP‐13368; MGC‐12816)