Article
Subtotal nephrectomy impairs ischemia-induced angiogenesis and hindlimb re-perfusion in rats.
Department of Nephrology and Hypertension, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Kidney International (impact factor:
6.61).
07/2006;
69(11):2013-21.
DOI:10.1038/sj.ki.5000448
pp.2013-21
Source: PubMed
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Citations (0)
- Cited In (3)
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ABSTRACT: Endothelial dysfunction contributes to the increased cardiovascular risk that accompanies CKD. We hypothesized that the soluble VEGF receptor 1 (sFlt-1), a VEGF antagonist, plays a role in endothelial dysfunction and decreased angiogenesis in CKD. We enrolled 130 patients with CKD stages 3 to 5 and 56 age- and gender-matched control patients. Plasma sFlt-1 levels were higher in patients with CKD and, after multivariate regression analyses, exclusively associated with renal function and levels of vWF, a marker of endothelial dysfunction. Compared with serum from control patients, both recombinant sFlt-1 and serum from patients with CKD had antiangiogenic activity in the chick chorioallantoic membrane (CAM) assay, induced endothelial cell apoptosis in vitro, and decreased nitric oxide generation in two different endothelial cell lines. Pretreating the sera with an antibody against sFlt-1 abrogated all of these effects. Furthermore, we observed increased sFlt1 levels in 5/6-nephrectomized rats compared with sham-operated animals. Finally, using real-time PCR and ELISA, we identified monocytes as a possible source of increased sFlt-1 in patients with CKD. Our findings show that excess sFlt-1 associates with endothelial dysfunction in CKD and suggest that increased sFlt-1 may predict cardiovascular risk in CKD.Journal of the American Society of Nephrology 08/2009; 20(10):2235-45. · 9.66 Impact Factor -
Article: High phosphate directly affects endothelial function by downregulating annexin II.
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ABSTRACT: Hyperphosphatemia is associated with increased cardiovascular risk in patients with renal disease and in healthy individuals. Here we tested whether high phosphate has a role in the pathophysiology of cardiovascular events by interfering with endothelial function, thereby impairing microvascular function and angiogenesis. Protein expression analysis found downregulation of annexin II in human coronary artery endothelial cells, an effect associated with exacerbated shedding of annexin II-positive microparticles by the cells exposed to high phosphate media. EAhy926 endothelial cells exposed to sera from hyperphosphatemic patients also display decreased annexin II, suggesting a negative correlation between serum phosphate and annexin II expression. By using endothelial cell-based assays in vitro and the chicken chorioallantoic membrane assay in vivo, we found that angiogenesis, vessel wall morphology, endothelial cell migration, capillary tube formation, and endothelial survival were impaired in a hyperphosphatemic milieu. Blockade of membrane-bound extracellular annexin II with a specific antibody mimicked the effects of high phosphate. In addition, high phosphate stiffened endothelial cells in vitro and in rats in vivo. Thus, our results link phosphate and adverse clinical outcomes involving the endothelium in both healthy individuals and patients with renal disease.Kidney International advance online publication, 22 August 2012; doi:10.1038/ki.2012.300.Kidney International 08/2012; · 6.61 Impact Factor -
Article: Capillary rarefaction, hypoxia, VEGF and angiogenesis in chronic renal disease.
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ABSTRACT: Tubulointerstitial hypoxia and peritubular capillary rarefaction are typical features of chronic progressive renal disease. In response to low oxygen supply, hypoxia-inducible factors (HIFs) are activated but until now, it is unclear if this increased expression leads to a stabilization of the disease process and thus is nephroprotective or contributes to interstitial fibrosis and/or tubular atrophy. This duality has also been described as far as vascular endothelial growth factor (VEGF), one of the major target genes of HIFs, is concerned. On the one hand, neoangiogenesis driven by VEGF, if intact, ameliorates hypoxia, on the other, VEGF is a potent pro-inflammatory mediator and neoangiogenesis, if defective because interference by other pathologies exaggerates injury. In summary, experimental data support the idea that dependent on timing and predominant pathology, hypoxia counter-regulatory factors exert beneficial or undesirable effects. Thus, before their therapeutic potential can be fully explored, a better way to characterize the clinical and pathophysiological situation in an individual patient is mandatory.Nephrology Dialysis Transplantation 02/2011; 26(4):1132-7. · 3.40 Impact Factor
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Keywords
endothelial nitric oxide
Hindlimb perfusion
Impaired hindlimb re-perfusion
ischemic hindlimbs
Kidney disease
Laser Doppler hindpaw perfusion
laser Doppler perfusion imaging
limb perfusion
male Sprague-Dawley rats
non-ischemic limb
peripheral arterial disease
poor prognosis
rat hindlimb ischemia model
rat model
real-time reverse transcription-polymerase chain reaction
relative perfusion
sham surgery
sham-operated animals
unilateral hindlimb ischemia
VEGFR-1/2 mRNA expression
