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Epoetin delta reduces oxidative stress in primary human renal tubular cells.

De Beuf A, Hou XH, D'Haese PC, Verhulst A - J. Biomed. Biotechnol. (2010)

Bottom Line: Erythropoietin (EPO) exerts (renal) tissue protective effects.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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Pathophysiology, Faculties of Medicine and Biomedical, Pharmaceutical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, 2610 Antwerp, Belgium.

ABSTRACT
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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Related in: MedlinePlus

Induction of oxidative stress in confluent hTECs by incubation with GO (0 to 100 IU/mL) during 0 to 240 minutes. By measuring DCF fluorescence, a concentration-dependent accumulation of ROS was observed during the time.
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Related In: Results  -  Collection


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fig1: Induction of oxidative stress in confluent hTECs by incubation with GO (0 to 100 IU/mL) during 0 to 240 minutes. By measuring DCF fluorescence, a concentration-dependent accumulation of ROS was observed during the time.

Mentions: Quantification of oxidative stress resulting from the addition of GO to hTECs at different concentrations (0 to 100 IU/mL) and time points (10 to 240 minutes) shows that incubation of hTECs with GO resulted in a concentration-dependent accumulation of ROS during time (Figure 1).


Epoetin delta reduces oxidative stress in primary human renal tubular cells.

De Beuf A, Hou XH, D'Haese PC, Verhulst A - J. Biomed. Biotechnol. (2010)

Induction of oxidative stress in confluent hTECs by incubation with GO (0 to 100 IU/mL) during 0 to 240 minutes. By measuring DCF fluorescence, a concentration-dependent accumulation of ROS was observed during the time.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2864893&req=5

fig1: Induction of oxidative stress in confluent hTECs by incubation with GO (0 to 100 IU/mL) during 0 to 240 minutes. By measuring DCF fluorescence, a concentration-dependent accumulation of ROS was observed during the time.
Mentions: Quantification of oxidative stress resulting from the addition of GO to hTECs at different concentrations (0 to 100 IU/mL) and time points (10 to 240 minutes) shows that incubation of hTECs with GO resulted in a concentration-dependent accumulation of ROS during time (Figure 1).

Bottom Line: Erythropoietin (EPO) exerts (renal) tissue protective effects.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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Pathophysiology, Faculties of Medicine and Biomedical, Pharmaceutical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, 2610 Antwerp, Belgium.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus