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10.1016/j.ajog.2014.01.024

http://scihub22266oqcxt.onion/10.1016/j.ajog.2014.01.024
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C4041388!4041388!24440566
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suck abstract from ncbi


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pmid24440566      Am+J+Obstet+Gynecol 2014 ; 210 (6): 547.e1-7
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  • Synthesis of sFlt-1 by platelet-monocyte aggregates contributes to the pathogenesis of preeclampsia #MMPMID24440566
  • Major HD; Cambell RA; Silver RM; Branch DW; Weyrich AS
  • Am J Obstet Gynecol 2014[Jun]; 210 (6): 547.e1-7 PMID24440566show ga
  • Objective: Soluble fms-like tyrosine kinase (sFlt-1) is an important mediator in the pathogenesis of preeclampsia. We sought to determine if platelet-monocyte aggregates (PMAs) produced sFlt-1 and if PMAs contributed to sFlt-1 production in preeclampsia. Study Design: Case-control study of sFlt-1 release from PMAs using blood samples from women with preeclampsia matched by gestational age to pregnant controls. A third group of nonpregnant, reproductive-age women comprised an additional control group. Experiments were also performed using blood from non-pregnant women to elucidate if inducing PMAs could stimulate sFlt-1 production, and if so, to determine the necessary receptors and pathways. Results: Women with preeclampsia had increased total Flt-1 concentrations in platelets and monocytes at baseline compared to pregnant controls (25 vs. 10 pg/ml, p=0.0003). sFlt-1 production was elicited from monocytes incubated with thrombin-activated platelets from non-pregnant women. sFlt-1 production was regulated at the transcriptional level by p38 and NF-?B dependent pathways. Conclusion: Activated platelets in preeclampsia bind monocytes to generate sFlt-1. PMAs are a previously unrecognized source of sFlt-1 that may contribute to endothelial dysfunction and systemic inflammation commonly observed in preeclampsia.
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