Progress toward identifying potential markers for preeclampsia: role of agonistic autoantibody to the angiotensin II type I receptor.
Progress toward identifying potential markers for preeclampsia: role of agonistic autoantibody to the angiotensin II type I receptor.
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识别先兆子痫潜在标志物的进展：血管紧张素 II I 型受体激动性自身抗体的作用。
DOI：
10.1161/hypertensionaha.109.141465
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
LaMarca,Babbette
中科院分区：
文献类型：
--
作者：
LaMarca,Babbette
As early as 20 weeks of gestation, preeclamptic women develop new-onset hypertension with proteinuria and display increased circulating factors, ranging from metabolic and proinflammatory to antiangiogenic in nature. These factors have been shown in various experimental models to possibly contribute to the development of hypertension in response to placental ischemia. 1–4 A major focus of preeclamptic research has been the identification a molecular marker that could be used to predict early in gestation the development of this disease. Two potential factors associated with the development of preeclampsia are the imbalance of angiogenic factors (vascular endothelial growth factor/placental growth factor) and the antiangiogenic factor (soluble fms-like tyrosine kinase 1 [sFlt-1]), as well as agonistic autoantibody to the angiotensin II type I receptor (AT1-AA). 1–5 The AT1-AA has been purified, and specificity for the second extracellular loop of the angiotensin II type I receptor (AT1R) has been demonstrated by Western blotting, colocalization, and coimmunoprecipitation experiments. 5 The AT1-AA induces signaling in vascular cells, including activating protein 1, calcineurin, reactive oxygen species, and nuclear factor κB activation, which are blocked by an AT1R antagonist. 5–8 In addition, the AT1-AAs appear to be responsible for other effects among different tissues, including stimulation of interleukin 6 production from mesangial cells, and most recently our laboratory has demonstrated AT1-AA activation of the endothelin pathway in human endothelial cells and in pregnant rats. 9, 10 Clinical studies indicate that both plasma and amniotic fluid concentrations, as well as placental sFlt-1 mRNA, are increased in preeclamptic patients. 2 Moreover, increases in plasma levels of sFlt-1 in pregnant rodent models lead to pathophysiological alterations that mimic many of the characteristics observed in women with preeclampsia. 2, 3 Thus, these studies suggest that sFlt-1 may contribute to the pathophysiology observed in preeclampsia. However, the exact mechanism responsible for sFlt-1 overexpression has yet to be clearly elucidated (Figure).Previous studies by Zhou et al11, 12 demonstrated that AT1-AA from preeclamptic women induces sFlt-1 production via AT1R and calcineurin/nuclear factor of activated T-cell signaling. The authors demonstrated by injecting the IgG or affinity-purified AT1-AAs from women into pregnant mice caused hypertension, proteinuria, glomerular endotheliosis, placental abnormalities, intrauterine growth restriction, and elevated sFlt-1. 12 The onset of these symptoms was prevented by an AT1R antagonist or an AT1-AA–neutralizing 7-amino acid epitope-binding peptide. 12 Most recently, in agreement with the Xia laboratory, we have confirmed that AT1-AA infusion increased blood pressure and plasma sFlt-1 in pregnant rats. 13
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