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J Am Soc Nephrol ; 15(8): 2115-24, 2004 Aug.
Article in English | MEDLINE | ID: mdl-15284297

ABSTRACT

Erythropoietin (EPO) is upregulated by hypoxia and causes proliferation and differentiation of erythroid progenitors in the bone marrow through inhibition of apoptosis. EPO receptors are expressed in many tissues, including the kidney. Here it is shown that a single systemic administration of EPO either preischemia or just before reperfusion prevents ischemia-reperfusion injury in the rat kidney. Specifically, EPO (300 U/kg) reduced glomerular dysfunction and tubular injury (biochemical and histologic assessment) and prevented caspase-3, -8, and -9 activation in vivo and reduced apoptotic cell death. In human (HK-2) proximal tubule epithelial cells, EPO attenuated cell death in response to oxidative stress and serum starvation. EPO reduced DNA fragmentation and prevented caspase-3 activation, with upregulation of Bcl-X(L) and XIAP. The antiapoptotic effects of EPO were dependent on JAK2 signaling and the phosphorylation of Akt by phosphatidylinositol 3-kinase. These findings may have major implications in the treatment of acute renal tubular damage.


Subject(s)
Erythropoietin/pharmacology , Kidney Diseases/drug therapy , Reperfusion Injury/drug therapy , Animals , Apoptosis , Blood Proteins/pharmacology , Caspase 3 , Caspase Inhibitors , Caspases/metabolism , Cell Line, Transformed , Creatinine/blood , Disease Models, Animal , Humans , Kidney Diseases/pathology , Kidney Diseases/prevention & control , Kidney Tubules/pathology , Male , Oxidative Stress/drug effects , Phosphorylation , Protein Serine-Threonine Kinases/metabolism , Proto-Oncogene Proteins/metabolism , Proto-Oncogene Proteins c-akt , Rats , Rats, Wistar , Reperfusion Injury/pathology , Reperfusion Injury/prevention & control
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