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Oral supplementation with sulodexide inhibits neo-angiogenesis in a rat model of peritoneal perfusion

Anneleen Pletinck UGent, MARIA VAN LANDSCHOOT UGent, Sonja Steppan, Debby Laukens UGent, Jutta Passlick-Deetjen, Raymond Vanholder UGent and Wim Van Biesen UGent (2012) NEPHROLOGY DIALYSIS TRANSPLANTATION. 27(2). p.548-556
abstract
Background. Peritoneal dialysis (PD) is associated with functional and morphological alterations of the peritoneal membrane (PM). It is hypothesized that vascular endothelial growth factor (VEGF) plays a role in this process. Sulodexide is a glycosaminoglycan with effects on vascular biology. Therefore, the impact of oral sulodexide on PM function and morphology in a rat model of peritoneal perfusion was evaluated. Methods. Rats received 10 mL peritoneal dialysate fluid (PDF) twice daily via a tunnelled PD catheter. The test-PD group (Sul) received 15 mg/kg/day oral sulodexide versus none in the control–PD group (Con). A third group received no PDF (Sham). After 12 weeks, a peritoneal equilibration test was performed and the PM was sampled. Neo-angiogenesis was evaluated using immunostaining with von Willebrand, and epithelial-to-mesenchymal transition (EMT) using co-localization of cytokeratin and α-smooth muscle actin. VEGF was determined in the dialysate by enzyme-linked immunosorbent assay. Results. PD induced loss of ultrafiltration, also in the sulodexide group. Creatinine and glucose transport were better preserved, and sodium dip was more pronounced in the sulodexide group versus control. Submesothelial thickness, neo-angiogenesis and EMT were more pronounced in the Con versus Sul versus Sham group. VEGF in the dialysate, corrected for diffusion was higher in Con and Sul versus Sham. Conclusion. Oral sulodexide administration diminishes neo-vascularization, submesothelial thickening and EMT induced by exposure to PDF in a rat model. As there was no difference in VEGF at the protein level in the dialysate, we hypothesize that oral sulodexide inhibits VEGF locally by binding.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
journal title
NEPHROLOGY DIALYSIS TRANSPLANTATION
Nephrol. Dial. Transplant.
volume
27
issue
2
pages
548 - 556
Web of Science type
Article
Web of Science id
000300421300015
JCR category
UROLOGY & NEPHROLOGY
JCR impact factor
3.371 (2012)
JCR rank
14/73 (2012)
JCR quartile
1 (2012)
ISSN
0931-0509
DOI
10.1093/ndt/gfr370
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1998755
handle
http://hdl.handle.net/1854/LU-1998755
date created
2012-01-20 15:22:42
date last changed
2012-09-12 14:58:41
@article{1998755,
  abstract     = {Background. Peritoneal dialysis (PD) is associated with functional and morphological alterations of the peritoneal membrane (PM). It is hypothesized that vascular endothelial growth factor (VEGF) plays a role in this process. Sulodexide is a glycosaminoglycan with effects on vascular biology. Therefore, the impact of oral sulodexide on PM function and morphology in a rat model of peritoneal perfusion was evaluated. 
Methods. Rats received 10 mL peritoneal dialysate fluid (PDF) twice daily via a tunnelled PD catheter. The test-PD group (Sul) received 15 mg/kg/day oral sulodexide versus none in the control--PD group (Con). A third group received no PDF (Sham). After 12 weeks, a peritoneal equilibration test was performed and the PM was sampled. Neo-angiogenesis was evaluated using immunostaining with von Willebrand, and epithelial-to-mesenchymal transition (EMT) using co-localization of cytokeratin and \ensuremath{\alpha}-smooth muscle actin. VEGF was determined in the dialysate by enzyme-linked immunosorbent assay. 
Results. PD induced loss of ultrafiltration, also in the sulodexide group. Creatinine and glucose transport were better preserved, and sodium dip was more pronounced in the sulodexide group versus control. Submesothelial thickness, neo-angiogenesis and EMT were more pronounced in the Con versus Sul versus Sham group. VEGF in the dialysate, corrected for diffusion was higher in Con and Sul versus Sham. 
Conclusion. Oral sulodexide administration diminishes neo-vascularization, submesothelial thickening and EMT induced by exposure to PDF in a rat model. As there was no difference in VEGF at the protein level in the dialysate, we hypothesize that oral sulodexide inhibits VEGF locally by binding.},
  author       = {Pletinck, Anneleen and VAN LANDSCHOOT, MARIA and Steppan, Sonja and Laukens, Debby and Passlick-Deetjen, Jutta and Vanholder, Raymond and Van Biesen, Wim},
  issn         = {0931-0509},
  journal      = {NEPHROLOGY DIALYSIS TRANSPLANTATION},
  language     = {eng},
  number       = {2},
  pages        = {548--556},
  title        = {Oral supplementation with sulodexide inhibits neo-angiogenesis in a rat model of peritoneal perfusion},
  url          = {http://dx.doi.org/10.1093/ndt/gfr370},
  volume       = {27},
  year         = {2012},
}

Chicago
Pletinck, Anneleen, Maria Van Landschoot, Sonja Steppan, Debby Laukens, Jutta Passlick-Deetjen, Raymond Vanholder, and Wim Van Biesen. 2012. “Oral Supplementation with Sulodexide Inhibits Neo-angiogenesis in a Rat Model of Peritoneal Perfusion.” Nephrology Dialysis Transplantation 27 (2): 548–556.
APA
Pletinck, A., Van Landschoot, M., Steppan, S., Laukens, D., Passlick-Deetjen, J., Vanholder, R., & Van Biesen, W. (2012). Oral supplementation with sulodexide inhibits neo-angiogenesis in a rat model of peritoneal perfusion. NEPHROLOGY DIALYSIS TRANSPLANTATION, 27(2), 548–556.
Vancouver
1.
Pletinck A, Van Landschoot M, Steppan S, Laukens D, Passlick-Deetjen J, Vanholder R, et al. Oral supplementation with sulodexide inhibits neo-angiogenesis in a rat model of peritoneal perfusion. NEPHROLOGY DIALYSIS TRANSPLANTATION. 2012;27(2):548–56.
MLA
Pletinck, Anneleen, Maria Van Landschoot, Sonja Steppan, et al. “Oral Supplementation with Sulodexide Inhibits Neo-angiogenesis in a Rat Model of Peritoneal Perfusion.” NEPHROLOGY DIALYSIS TRANSPLANTATION 27.2 (2012): 548–556. Print.