Key result
VEGF121 reverses ~47% of sFlt-1-induced gene changes while easing hypertension in preeclampsia models.
Answers are grounded in this paper and cite their sources.
Inhibitors of angiogenic factors are known to be upregulated, and their levels increase in the maternal circulation before the onset of preeclampsia. We reproduced a previously characterized model of preeclampsia by adenoviral overexpression of the soluble vascular endothelial growth factor (VEGF) receptor sFlt-1 (also referred to as sVEGFR-1) in pregnant and nonpregnant Sprague-Dawley rats. Animals were treated with VEGF121 at 0, 100, 200, or 400 microg/kg once or twice daily (n=8 per group; 64 total) and compared with normal control animals (n=4 per group) by examination of systolic blood pressure, urinary albumin and creatinine, renal histopathology, and glomerular gene expression profiling. sFlt-1 expression induced hypertension with proteinuria and glomerular endotheliosis and significant changes in gene expression. VEGF121 treatment alleviated these symptoms and reversed 125 of 268 sFlt-1-induced changes in gene expression. VEGF121 had beneficial effects in this rat model of preeclampsia without apparent harm to the fetus. Further study of VEGF121 as a potential therapeutic agent for preeclampsia is warranted.
No takes yet. Share an insight, caveat, or question.
Li et al. (2007) studied Preeclampsia (rat model). VEGF121 vs. Normal control animals and 0 microg/kg was evaluated on Systolic blood pressure, urinary albumin and creatinine, renal histopathology, and glomerular gene expression profiling. VEGF121 treatment alleviated hypertension and proteinuria and reversed 125 of 268 sFlt-1-induced changes in gene expression in a rat model of preeclampsia.
Synapse has enriched 10 related papers. Consider them for comparative context: