Eliane R. Popa
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Eliane R. Popa has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Casper F. M. Franssen
Division of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
1 shared publication Femke Waanders
Stem Cell and Tissue Engineering Research Group, Department of Pathology and Medical Biology, 2Division of Nephrology, Department of Internal Medicine, and 3Dialysis Center Groningen, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
1 shared publication- Guido Krenning
Department of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713GZ Groningen, the Netherlands; Sulfateq B.V., Admiraal de Ruyterlaan 5, 9726GN, Groningen, the Netherlands
1 shared publication Johannes W. Drouven
Stem Cell and Tissue Engineering Research Group, Department of Pathology and Medical Biology, 2Division of Nephrology, Department of Internal Medicine, and 3Dialysis Center Groningen, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
1 shared publicationMarja J. A. van Luyn
Stem Cell and Tissue Engineering Research Group, Department of Pathology and Medical Biology, 2Division of Nephrology, Department of Internal Medicine, and 3Dialysis Center Groningen, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
1 shared publication- Martin Conrad Harmsen
Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, 9713 GZ Groningen, The Netherlands
1 shared publication
Latest Publications
- 1 June 2009
- Published by American Physiological Society in American Journal of Physiology-Renal Physiology
- Vol. 296 (6) , F1314-F1322
Endothelial progenitor cell dysfunction in patients with progressive chronic kidney disease
Endothelial progenitor cells (EPC) contribute to repair and maintenance of the vascular system, but in patients with chronic kidney disease (CKD), the number and function of EPC may be affected by kidney dysfunction. We assessed numbers and the angiogenic function of EPC from patients with CKD in relation to disease progression. In a cross-sectional, prospective study, 50 patients with varying degrees of CKD, including 20 patients undergoing dialysis and 10 healthy controls, were included. Mononuclear cells were isolated, and circulating EPC were quantified by flow cytometry based on expression of CD14 and CD34. EPC were cultured on fibronectin-coated supramolecular films of oligocaprolactone under angiogenic conditions to determine their angiogenic capacity and future use in regenerative medicine. CKD patients had normal numbers of circulating CD14+ EPC but reduced numbers of circulating CD34+ EPC. Furthermore, EPC from patients with CKD displayed functional impairments, i.e., hampered adherence, reduced endothelial outgrowth potential, and reduced antithrombogenic function. These impairments were already observed at stage 1 CKD and became more apparent when CKD progressed. Dialysis treatment only partially ameliorated EPC impairments in patients with CKD. In conclusion, EPC number and function decrease with advancing CKD, which may hamper physiological vascular repair and can add to the increased risk for cardiovascular diseases observed in CKD patients.
- 1 June 2009
- Published by American Physiological Society in American Journal of Physiology-Renal Physiology
- Vol. 296 (6) , F1314-F1322
Endothelial progenitor cell dysfunction in patients with progressive chronic kidney disease
Endothelial progenitor cells (EPC) contribute to repair and maintenance of the vascular system, but in patients with chronic kidney disease (CKD), the number and function of EPC may be affected by kidney dysfunction. We assessed numbers and the angiogenic function of EPC from patients with CKD in relation to disease progression. In a cross-sectional, prospective study, 50 patients with varying degrees of CKD, including 20 patients undergoing dialysis and 10 healthy controls, were included. Mononuclear cells were isolated, and circulating EPC were quantified by flow cytometry based on expression of CD14 and CD34. EPC were cultured on fibronectin-coated supramolecular films of oligocaprolactone under angiogenic conditions to determine their angiogenic capacity and future use in regenerative medicine. CKD patients had normal numbers of circulating CD14+ EPC but reduced numbers of circulating CD34+ EPC. Furthermore, EPC from patients with CKD displayed functional impairments, i.e., hampered adherence, reduced endothelial outgrowth potential, and reduced antithrombogenic function. These impairments were already observed at stage 1 CKD and became more apparent when CKD progressed. Dialysis treatment only partially ameliorated EPC impairments in patients with CKD. In conclusion, EPC number and function decrease with advancing CKD, which may hamper physiological vascular repair and can add to the increased risk for cardiovascular diseases observed in CKD patients.