The Effect of Immune Factors, Tumor Necrosis Factor- , and Agonistic Autoantibodies to the Angiotensin II Type I Receptor on Soluble fms-Like Tyrosine-1 and Soluble Endoglin Production in Response to Hypertension During Pregnancy
| Autor: | Kedra Wallace, Sarah Rutland, Babbette LaMarca, Gerd Wallukat, Sharon D. Keiser, Lillian Fournier Ray, Marc Parrish, Sydney R. Murphy, James N. Martin, Katrin Wenzel, Ralf Dechend, Joey P. Granger |
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| Rok vydání: | 2010 |
| Předmět: |
Placental growth factor
medicine.medical_specialty Angiotensin receptor Pregnancy Complications Cardiovascular Ischemia Article Receptor Angiotensin Type 1 Preeclampsia Rats Sprague-Dawley chemistry.chemical_compound Pregnancy Internal medicine Internal Medicine medicine Animals Autoantibodies Vascular Endothelial Growth Factor Receptor-1 Tumor Necrosis Factor-alpha business.industry Endoglin Intracellular Signaling Peptides and Proteins medicine.disease Angiotensin II Rats Vascular endothelial growth factor Endocrinology chemistry Hypertension embryonic structures Female business Soluble fms-like tyrosine kinase-1 |
| Zdroj: | American Journal of Hypertension. 23:911-916 |
| ISSN: | 1941-7225 0895-7061 |
| DOI: | 10.1038/ajh.2010.70 |
| Popis: | Preeclampsia is a complex disease that affects 5–7% of pregnancies in the United States. Although preeclampsia is one of the leading causes of maternal and perinatal mortality and morbidity, the pathophysiologic mechanism(s) underlying this disease has yet to be fully elucidated. However, reductions in blood flow to the uteroplacental unit are thought to be an important initiating factor in the etiology of preeclampsia. Thus, the physiologic mechanisms linking placental ischemia with abnormalities in the maternal circulation remain to be an important area of investigation.1,2 Recent clinical evidence has demonstrated an imbalance between proangiogenic (e.g., vascular endothelial growth factor and placental growth factor) and antiangiogenic factors (e.g., soluble fms-like tyrosine kinase (sFlt-1) and sEndoglin (sEng)) in the maternal circulation.3–9 Subsequent research indicates that plasma, placental mRNA and amniotic fluid concentrations of sFlt-1 are increased in preeclamptic patients.3–9 Elevated sFlt-1 and sEng levels in preeclamptic women are associated with increased levels of tumor necrosis factor-α (TNF-α) and autoantibodies to the angiotensin II receptor (AT1-AA).10–16 Whereas an abnormality in sFlt-1 and sEng production is thought to be a trigger in the pathogenesis of preeclampsia, the mechanisms that regulate sFlt-1 and sEng production remain unclear. We have recently reported that the hypertension in response to placental ischemia is associated with increases in plasma levels of sFlt-1, sEng, TNF-α, and AT1-AA.17,18 We also demonstrated that chronic infusion of TNF-α or AT1-AA, at rates to mimic the increase of these factors observed in placental ischemic pregnant rats, significantly contributes to elevated blood pressures.17–21 Moreover, we found that chronic infusion of TNF-α in pregnant rats stimulated the production of AT1-AA and the blood pressure response to TNF-α or AT1-AA were attenuated by treatment with an angiotensin type 1 receptor antagonist.18,21 Although these findings suggest an important interaction between TNF-α and AT1-AA in the blood pressure response to placental ischemia, it is unknown whether these factors interact in regulating sFlt-1 and sEng production. Therefore, we repeated previous studies in order to determine whether chronic infusion of TNF-α or AT1-AA, at a rate to mimic levels previously observed in placental ischemic pregnant rats,18,19 effects placental and plasma levels of sFlt-1 and sEng. |
| Databáze: | OpenAIRE |
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