Expression of placenta growth factor, soluble fms‐like tyrosine kinase‐1, metal‐responsive transcription factor‐1, heme oxygenase 1 and hypoxia inducible factor‐1α <scp>mRNAs</scp> in pre‐eclampsia placenta and the effect of pre‐eclampsia sera on their expression of choriocarcinoma cells

Maebayashi, Aki; Yamamoto, Tatsuo; Azuma, Hiromitsu; Kato, Eisuke; Yamamoto, Norio; Murase, Takayuki; Chishima, Fumihisa; Suzuki, Manami

doi:10.1111/jog.12462

Cited by 12 publications

(8 citation statements)

References 42 publications

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“…It should be noted that in pre-eclamptic (PE) pregnancies, the role of Nrf2 is somewhat more controversial. Studies have documented that placental Nrf2 levels are reduced in PE [106] and that Nrf2 target gene HO-1 is downregulated in placental trophoblast derived JEG-3 cells following exposure to PE serum [107]. Nrf2-dependent HO-1 expression can negatively regulate soluble fms-like tyrosine kinase-1 (sFlt-1) levels [107][108][109], with enhanced sFlt-1 strongly implicated in the pathogenesis of PE and the development of maternal hypertensive symptoms during pregnancy.…”

Section: Role Of Nrf2 In Pregnancymentioning

confidence: 98%

“…Studies have documented that placental Nrf2 levels are reduced in PE [106] and that Nrf2 target gene HO-1 is downregulated in placental trophoblast derived JEG-3 cells following exposure to PE serum [107]. Nrf2-dependent HO-1 expression can negatively regulate soluble fms-like tyrosine kinase-1 (sFlt-1) levels [107][108][109], with enhanced sFlt-1 strongly implicated in the pathogenesis of PE and the development of maternal hypertensive symptoms during pregnancy. Conversely, upregulation of Nrf2-dependent antioxidant defences specifically in cytotrophoblasts [110] or syncytiotrophoblasts [104] has been postulated to actively contribute to the increased shedding of syncytial knots (fused cytotrophoblasts and syncytiotrophoblasts) found to be raised in PE and implicated in maternal hypertension [110].…”

Section: Role Of Nrf2 In Pregnancymentioning

confidence: 98%

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Keap1–Nrf2 regulated redox signaling in utero: Priming of disease susceptibility in offspring

Chapple

Puszyk

Mann

2015

Free Radical Biology and Medicine

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Section: Role Of Nrf2 In Pregnancymentioning

confidence: 98%

Section: Role Of Nrf2 In Pregnancymentioning

confidence: 98%

Keap1–Nrf2 regulated redox signaling in utero: Priming of disease susceptibility in offspring

Chapple

Puszyk

Mann

2015

Free Radical Biology and Medicine

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“…In preeclampsia pregnancies, the role of Nrf2 has been reported to be somehow controversial, whereas reduced expression of Nrf2 was noted in placental oxidative stress-induced preeclampsia [ 110 ]. Inappropriate regulation of Nrf2-based HO-1 expression mediates soluble fms-like typrsine kinase-1 (sFlt-1) [ 111 ]. Increased level of sFtl-1 has been recorded in the pathogenesis of PE and development of maternal hypertensive condition during pregnancy.…”

Section: Significant Impact Of Nrf2 Pathway On Pregnancymentioning

confidence: 99%

Modulatory Mechanism of Polyphenols and Nrf2 Signaling Pathway in LPS Challenged Pregnancy Disorders

Hussain

Tan

Liu

et al. 2017

Oxidative Medicine and Cellular Longevity

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Early embryonic loss and adverse birth outcomes are the major reproductive disorders that affect both human and animals. The LPS induces inflammation by interacting with robust cellular mechanism which was considered as a plethora of numerous reproductive disorders such as fetal resorption, preterm birth, teratogenicity, intrauterine growth restriction, abortion, neural tube defects, fetal demise, and skeletal development retardation. LPS-triggered overproduction of free radicals leads to oxidative stress which mediates inflammation via stimulation of NF-κB and PPARγ transcription factors. Flavonoids, which exist in copious amounts in nature, possess a wide array of functions; their supplementation during pregnancy activates Nrf2 signaling pathway which encounters pregnancy disorders. It was further presumed that the development of strong antioxidant uterine environment during gestation can alleviate diseases which appear at adult stages. The purpose of this review is to focus on modulatory properties of flavonoids on oxidative stress-mediated pregnancy insult and abnormal outcomes and role of Nrf2 activation in pregnancy disorders. These findings would be helpful for providing new insights in ameliorating oxidative stress-induced pregnancy disorders.

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“…The cascade of events linking placental ischemia to maternal hypertension has been a subject of intense focus in our laboratory and others. While both placental and circulating levels of VEGF and PlGF are reduced in preeclamptic women, the levels of the VEGF/PlGF receptor sFlt-1 are elevated (27,102,143,161,193). By using the RUPP model, we have shown that placental ischemia/hypoxia elicits the release of sFlt-1 (58).…”

Section: Effects Of Obesity On the Release Of Soluble Placental Factorsmentioning

confidence: 99%

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Spradley

Palei

Granger

2015

American Journal of Physiology-Regulatory, Integrative and Comp

113

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) is a pregnancy-specific disorder typically presenting as new-onset hypertension and proteinuria. While numerous epidemiological studies have demonstrated that obesity increases the risk of PE, the mechanisms have yet to be fully elucidated. Growing evidence from animal and human studies implicate placental ischemia in the etiology of this maternal syndrome. It is thought that placental ischemia is brought about by dysfunctional cytotrophoblast migration and invasion into the uterus and subsequent lack of spiral arteriole widening and placental perfusion. Placental ischemia/ hypoxia stimulates the release of soluble placental factors into the maternal circulation where they cause endothelial dysfunction, particularly in the kidney, to elicit the clinical manifestations of PE. The most recognized of these factors are the anti-angiogenic sFlt-1 and pro-inflammatory TNF-␣ and AT1-AA, which promote endothelial dysfunction by reducing levels of the provasodilator nitric oxide and stimulating production of the potent vasoconstrictor endothelin-1 and reactive oxygen species. We hypothesize that obesity-related metabolic factors increase the risk for developing PE by impacting various stages in the pathogenesis of PE, namely, 1) cytotrophoblast migration and placental ischemia; 2) release of soluble placental factors into the maternal circulation; and 3) maternal endothelial and vascular dysfunction. This review will summarize the current experimental evidence supporting the concept that obesity and metabolic factors like lipids, insulin, glucose, and leptin affect placental function and increase the risk for developing hypertension in pregnancy by reducing placental perfusion; enhancing placental release of soluble factors; and by increasing the sensitivity of the maternal vasculature to placental ischemia-induced soluble factors. body mass index; inflammation; placental ischemia; pregnancy; RUPP; sFlt-1 PE IS A PREGNANCY-SPECIFIC DISORDER typically identified by new-onset hypertension in the second half of pregnancy. Although often accompanied by new-onset proteinuria, PE can be associated with many other signs and symptoms including headaches, visual disturbances, epigastric pain, and the development of edema (4,192). Globally, this disease affects over 8 million pregnancies per year and is estimated to account for 40 -60% of maternal deaths in developing countries (125). In the United States, there was a 25% increase in the rate of PE between the years 1987-2004 (189). This significant increase highlights the importance of understanding how risk factors like obesity play a role in the pathogenesis of this maternal syndrome. Obesity is defined as a body mass index (BMI) of greater than or equal to 30 kg/m 2 . Greater than one-half of pregnant women are overweight or obese (48), and more than two-thirds of reproductive-aged women in the United States are overweight or obese (49). Although mounting epidemiological evidence supports obesity as a major risk factor for PE, the mechanisms linking these two morbidities are...

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Expression of placenta growth factor, soluble fms‐like tyrosine kinase‐1, metal‐responsive transcription factor‐1, heme oxygenase 1 and hypoxia inducible factor‐1α mRNAs in pre‐eclampsia placenta and the effect of pre‐eclampsia sera on their expression of choriocarcinoma cells

Cited by 12 publications

References 42 publications

Keap1–Nrf2 regulated redox signaling in utero: Priming of disease susceptibility in offspring

Keap1–Nrf2 regulated redox signaling in utero: Priming of disease susceptibility in offspring

Modulatory Mechanism of Polyphenols and Nrf2 Signaling Pathway in LPS Challenged Pregnancy Disorders

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

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