Angiotensin II Induces Soluble fms-Like Tyrosine Kinase-1 Release via Calcineurin Signaling Pathway in Pregnancy

Zhou, Cissy Chenyi; Ahmad, Shakil; Mi, Tiejuan; Xia, Lingwei; Abbasi, Shahrzad; Hewett, Peter W.; Sun, Chenxing; Ahmed, Asif; Kellems, Rodney E.; Xia, Yang

doi:10.1161/01.res.0000254703.11154.18

Cited by 144 publications

(117 citation statements)

References 46 publications

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“…Evidence of a relationship between AT1-AA and angiogenic factors also exists. In mice, the presence of AT1-AA seems to induce sFlt-1 release via activation of the calcineurin/nuclear factor of activated t cells pathway (58). Furthermore, AT1-AA stimulates sFlt-1 and sEng by inducing TNF-a and overcoming its negative regulator, HO (59).…”

Section: Angiotensin Receptor 1 Autoantibodiesmentioning

confidence: 99%

Preeclampsia: Updates in Pathogenesis, Definitions, and Guidelines

Phipps

Prasanna

Brima

et al. 2016

CJASN

455

302

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Preeclampsia is becoming an increasingly common diagnosis in the developed world and remains a high cause of maternal and fetal morbidity and mortality in the developing world. Delay in childbearing in the developed world feeds into the risk factors associated with preeclampsia, which include older maternal age, obesity, and/or vascular diseases. Inadequate prenatal care partially explains the persistent high prevalence in the developing world. In this review, we begin by presenting the most recent concepts in the pathogenesis of preeclampsia. Upstream triggers of the well described angiogenic pathways, such as the heme oxygenase and hydrogen sulfide pathways, as well as the roles of autoantibodies, misfolded proteins, nitric oxide, and oxidative stress will be described. We also detail updated definitions, classification schema, and treatment targets of hypertensive disorders of pregnancy put forth by obstetric and hypertensive societies throughout the world. The shift has been made to view preeclampsia as a systemic disease with widespread endothelial damage and the potential to affect future cardiovascular diseases rather than a selflimited occurrence. At the very least, we now know that preeclampsia does not end with delivery of the placenta. We conclude by summarizing the latest strategies for prevention and treatment of preeclampsia. A better understanding of this entity will help in the care of at-risk women before delivery and for decades after.

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Section: Angiotensin Receptor 1 Autoantibodiesmentioning

confidence: 99%

Preeclampsia: Updates in Pathogenesis, Definitions, and Guidelines

Phipps

Prasanna

Brima

et al. 2016

CJASN

455

302

View full text Add to dashboard Cite

show abstract

“…Kumasawa et al (36) demonstrated that lentiviral vector-mediated placenta-specific expression of sFlt-1 caused maternal hypertension, proteinuria and IUGR in mice. It has also been reported that Ang II significantly elevated circulating levels of sFlt-1 in pregnant mice (37). The plasma levels of sFlt-1 in mice with PAH were significantly increased at E19 (20).…”

Section: Discussionmentioning

confidence: 65%

Short-term suppression of the renin-angiotensin system in mice associated with hypertension during pregnancy

et al. 2012

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Abstract. Pregnancy-induced hypertension or pre-eclampsia is a major disorder that may result in serious complications for the mother and fetus. It is characterized from maternal hypertension in late pregnancy and peripheral tissue damage, including kidney, heart and placenta, and the fetus suffers from intrauterine growth retardation (IUGR) and high perinatal mortality. Recently, it has been postulated that angiotensin II (Ang II), a potent vasoconstrictor in the renin-angiotensin system (RAS), plays a pivotal role in the pathogenesis of pre-eclampsia; however, the beneficial effect of the suppression of RAS has not yet been fully elucidated. Previously, we generated a transgenic mouse model that developed pregnancyassociated hypertension (PAH) by the overproduction of Ang II in maternal circulation during late pregnancy. In addition, mice with PAH exhibited maternal and fetal abnormalities, such as proteinuria, cardiac hypertrophy, placental morphological changes and IUGR. In this study, in order to attenuate the activity of redundant RAS during the advanced stages of PAH, we administered olmesartan (Olm), an angiotensin receptor blocker, and captopril (Cp), an angiotensin converting enzyme inhibitor, from E17 to E19 days of gestation, and evaluated its effect on cardiac and placental abnormalities and fetal growth. Olm and Cp administration significantly lowered the blood pressure of mice with PAH, and placental histological change and severe IUGR were markedly ameliorated in both groups. On the contrary, Olm or Cp treatment had little effect on cardiac remodeling during the advanced stages of PAH. These findings highlight a variety of therapeutic actions of RAS repression on the progressive pathology of PAH in mice.

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“…It has been speculated that the formation of the ProMBP-PAPPA complex and formation of ProMBP-angio tensinogen complex may be competing reactions [32,33]. Research indicates that sFlt-1 is produced with RAAS activation, as pregnant mouse models have shown that infused Angiotensin II (Ang II) regulates sFlt-1 production via activation of the Ang II receptor Type 1 (AT1 receptor) [34]. As a result, it seems similar patterns in PAPP-A and sFlt-1 levels in pregnancy may reflect their common connections to maternal or placental vascular dysfunction or the placental RAAS.…”

Section: Discussionmentioning

confidence: 99%