A novel bridge between oxidative stress and immunity: the interaction between hydrogen peroxide and human leukocyte antigen G in placental trophoblasts during preeclampsia

Zhou, Xue; Zhang, Guoying; Wang, Jue; Lu, Sha; Cao, Jun; Sun, Lichao

doi:10.1016/j.ajog.2012.03.013

Cited by 36 publications

(33 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies of PE have shown interactions between inflammation and endothelial dysfunction [6] and between inflammation and oxidative stress [7]. We also previously found a relationship between oxidative stress and immunity in placental trophoblasts in PE [8]. Karumanchi and Bdolah proposed that the relationship between endothelial dysfunction and oxidative stress might be a ''chicken-and-egg'' question [9].…”

Section: Introductionmentioning

confidence: 83%

A Role of sFlt-1 in Oxidative Stress and Apoptosis in Human and Mouse Pre-Eclamptic Trophoblasts1

Jiang

Zou

et al. 2015

Biology of Reproduction

View full text Add to dashboard Cite

Pre-eclampsia (PE) is a hypertensive disorder that occurs during pregnancy, and is a multifactorial disease. The antiangiogenic factor, soluble fms-like tyrosine kinase 1 (sFlt-1), has been reported to be important in the pathogenesis of PE, but the mechanism of its involvement remains unknown. To test the effects of sFlt-1 on pregnancy, we injected pregnant mice with exogenous mouse sFlt-1. After 18 days of gestation, higher blood pressure, proteinuria, and histological differences were observed compared with controls. Mitochondrial swelling inside the trophoblast cells in the placenta of sFlt-1-treated pregnant mice was observed by electron microscopy, which suggested a role of sFlt-1 in oxidative stress in trophoblasts in PE. Furthermore, apoptosis markers were upregulated in sFlt-1-treated mice. In conclusion, sFlt-1 appears to play a role in oxidative stress, which promotes apoptosis of trophoblasts. This may be an important mechanism in the development of PE.

show abstract

Section: Introductionmentioning

confidence: 83%

A Role of sFlt-1 in Oxidative Stress and Apoptosis in Human and Mouse Pre-Eclamptic Trophoblasts1

Jiang

Zou

et al. 2015

Biology of Reproduction

View full text Add to dashboard Cite

show abstract

“…Previous studies have revealed that ROS concentrations are higher in PE placentas than in normotensive placentas [6]. Excessive oxidative stress leads to higher cell apoptosis, inhibition of proliferation, and increased invasion of trophoblasts [34].…”

Section: Discussionmentioning

confidence: 99%

“…Reports from Graham et al strongly support the invasion-promoting function of low oxygen tension via elevating expression of cell surface uPAR in HTR8/SVneo cells [5]. Increasing evidence suggests that hypoxiaereoxygenation (H/R) within the placenta leads to reactive oxygen species (ROS) production, and these H/R-induced ROS (such as hydrogen peroxide) can cause apoptosis and resulting cellular invasion [6].…”

Section: Introductionmentioning

confidence: 97%

Laminin α4 (LAMA4) expression promotes trophoblast cell invasion, migration, and angiogenesis, and is lowered in preeclamptic placentas

Shan¹,

Zhang²,

Xiao³

et al. 2015

Placenta

View full text Add to dashboard Cite

“…Besides structural birth defects, oxidative stress is also involved in the etiology of other pregnancy complications 118 . Studies using human maternal blood samples have revealed several important oxidative stress markers for early diagnosis of adverse pregnancy outcomes 119-121 .…”

Section: Clinical Significance and Future Prospectivementioning

confidence: 99%

Advances in revealing the molecular targets downstream of oxidative stress–induced proapoptotic kinase signaling in diabetic embryopathy

Wang

Reece

Yang

2015

American Journal of Obstetrics and Gynecology

View full text Add to dashboard Cite

Pre-existing maternal diabetes is a high risk factor of diabetic embryopathy, such as neural tube defects (NTDs) and congenital heart defects (CHD). Maternal diabetes significantly increases the production of reactive oxygen species (ROS) resulting in oxidative stress and diabetic embryopathy. Multiple cellular and metabolic factors contribute to these processes. FoxO3a has been demonstrated as a key transcription factor in the signaling transduction pathways responsible for maternal diabetes-induced birth defects. ASK1 activated by oxidative stress stimulates nuclear translocation of FoxO3a, resulting in over-expression of TRADD, which, in turn, leads to caspase 8 activation and apoptosis. Maternal diabetes-activated JNK1/2, downstream effectors of ASK1, can be blocked by SOD1 overexpression, suggesting that oxidative stress is responsible for JNK1/2 signaling activation. Deletion of JNK1/2 significantly suppressed the activity of FoxO3a. These obersvations indicate that maternal diabetes-induced oxidative stress stimulates the activation of ASK1, JNK1/2, FoxO3a, TRADD, caspase 8 cleavage, finally, apoptosis and diabetic embryopathy.

show abstract

A novel bridge between oxidative stress and immunity: the interaction between hydrogen peroxide and human leukocyte antigen G in placental trophoblasts during preeclampsia

Cited by 36 publications

References 31 publications

A Role of sFlt-1 in Oxidative Stress and Apoptosis in Human and Mouse Pre-Eclamptic Trophoblasts1

A Role of sFlt-1 in Oxidative Stress and Apoptosis in Human and Mouse Pre-Eclamptic Trophoblasts1

Laminin α4 (LAMA4) expression promotes trophoblast cell invasion, migration, and angiogenesis, and is lowered in preeclamptic placentas

Advances in revealing the molecular targets downstream of oxidative stress–induced proapoptotic kinase signaling in diabetic embryopathy

Contact Info

Product

Resources

About