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10.1038/s41598-017-06178-z http://scihub22266oqcxt.onion/10.1038/s41598-017-06178-z C5517616!5517616!28725005     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28725005&cmd=llinks): Failed to open stream: HTTP request failed! 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Endothelial Dysfunction in Severe Preeclampsia is Mediated by Soluble Factors, Rather than Extracellular Vesicles |pdf=|usr=}}{{28725005}} gab.com Text Endothelial Dysfunction in Severe Preeclampsia is Mediated by Soluble Factors, Rather than Extracellular Vesicles JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28725005 #FOAvip In severe early-onset preeclampsia (sPE) the placenta releases soluble angiogenesis-regulating proteins, trophoblast-derived fragments, and extracellular vesicles (EVs). Their relative importance in disease pathogenesis is not presently understood. We explanted placental villi from healthy and sPE women then separated the media into: total-conditioned, EV-depleted and EV-enriched media. Three fractions were compared for; angiogenic protein secretion by ELISA, angiogenic and inflammation gene mRNA expression and leukocyte adhesion assay. sPE placental villi secreted significantly less PlGF (70?±?18?pg/mL) than preterm controls (338?±?203; p?=?0.03). sFlt-1:PlGF ratios in total-conditioned (115?±?29) and EV-depleted media (136?±?40) from sPE placental villi were significantly higher than in EV-enriched media (42?±?12; p?<?0.01) or any preterm or term media. Fluorescent-labeled EVs derived across normal gestation, but not from sPE, actively entered HUVECs. From sPE placental villi, the soluble fraction, but not EV-enriched fraction, significantly repressed angiogenesis (0.83?±?0.05 fold, p?=?0.02), induced HO-1 mRNA (15.3?±?5.1 fold, p?<?0.05) and induced leukocyte adhesion (2.2?±?0.4 fold, p?=?0.04). Soluble media (total-conditioned and EV-depleted media) from sPE placental villi induced endothelial dysfunction in HUVEC, while the corresponding EV-enriched fraction showed no such effects. Our data suggest that soluble factors including angiogenesis-regulating proteins, dominate the vascular pathology of this disease. Twit Text FOAVip Endothelial Dysfunction in Severe Preeclampsia is Mediated by Soluble Factors, Rather than Extracellular Vesicles ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28725005 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28725005 #FOAvip English Wikipedia <ref>{{Cite pmid|28725005}}</ref> Endothelial Dysfunction in Severe Preeclampsia is Mediated by Soluble Factors, Rather than Extracellular Vesicles #MMPMID28725005 O?Brien M; Baczyk D; Kingdom JC Sci Rep 2017[]; 7 (ä): ä PMID28725005show ga In severe early-onset preeclampsia (sPE) the placenta releases soluble angiogenesis-regulating proteins, trophoblast-derived fragments, and extracellular vesicles (EVs). Their relative importance in disease pathogenesis is not presently understood. We explanted placental villi from healthy and sPE women then separated the media into: total-conditioned, EV-depleted and EV-enriched media. Three fractions were compared for; angiogenic protein secretion by ELISA, angiogenic and inflammation gene mRNA expression and leukocyte adhesion assay. sPE placental villi secreted significantly less PlGF (70?±?18?pg/mL) than preterm controls (338?±?203; p?=?0.03). sFlt-1:PlGF ratios in total-conditioned (115?±?29) and EV-depleted media (136?±?40) from sPE placental villi were significantly higher than in EV-enriched media (42?±?12; p? äEndothelial Dysfunction in Severe Preeclampsia is Mediated by Soluble (epmc).pdf DeepDyve Pubget Overpricing