Epoetin Delta Reduces Oxidative Stress in Primary Human Renal Tubular Cells

被引：22
作者：
De Beuf, Annelies [1 ]
Hou, Xiang-hua [1 ,2 ]
D'Haese, Patrick C. [1 ]
Verhulst, Anja [1 ]
机构：
[1] Univ Antwerp, Fac Med & Biomed Pharmaceut & Vet Sc, Lab Pathophysiol, B-2610 Antwerp, Belgium
[2] Shandong Univ, Hosp 2, Dept Nephrol, Jinan 250033, Peoples R China
来源：
JOURNAL OF BIOMEDICINE AND BIOTECHNOLOGY | 2010年
关键词：
CARBOXYPEPTIDASE-M; ERYTHROPOIETIN PROTECTS; RAT-KIDNEY; ISCHEMIA/REPERFUSION INJURY; OVEREXPRESSION PROTECTS; ISCHEMIA-REPERFUSION; PEPTIDASE-IV; DNA-DAMAGE; DPP-IV; EXPRESSION;
D O I：
10.1155/2010/395785
中图分类号：
Q81 [生物工程学（生物技术）]; Q93 [微生物学];
学科分类号：
071005 ; 0836 ; 090102 ; 100705 ;
摘要：
Erythropoietin (EPO) exerts (renal) tissue protective effects. Since it is unclear whether this is a direct effect of EPO on the kidney or not, we investigated whether EPO is able to protect human renal tubular epithelial cells (hTECs) from oxidative stress and if so which pathways are involved. EPO (epoetin delta) could protect hTECs against oxidative stress by a dose-dependent inhibition of reactive oxygen species formation. This protective effect is possibly related to the membranous expression of the EPO receptor (EPOR) since our data point to the membranous EPOR expression as a prerequisite for this protective effect. Oxidative stress reduction went along with the upregulation of renoprotective genes. Whilst three of these, heme oxygenase-1 (HO-1), aquaporin-1 (AQP-1), and B-cell CLL/lymphoma 2 (Bcl-2) have already been associated with EPO-induced renoprotection, this study for the first time suggests carboxypeptidase M (CPM), dipeptidyl peptidase IV (DPPIV), and cytoglobin (Cygb) to play a role in this process.
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页数：9
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