NDLI: Gadd45α as an upstream signaling molecule of p38 MAPK triggers oxidative stress-induced sFlt-1 and sEng upregulation in preeclampsia

Content Provider	Springer Nature Link
Author	Luo, Xin Yao, Zhen wei Qi, Hong bo Liu, Dan dan Chen, Guo qing Huang, Shuai Li, Qing shu
Copyright Year	2011
Abstract	Preeclampsia (PE) is known to be associated with increased circulating levels of anti-angiogenic factors, such as soluble fms-related tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng). However, the way that placental oxidative stress results in the elevation of these two factors remains enigmatic. We have observed the overexpression of growth arrest and DNA damage-inducible 45 alpha (Gadd45α) and excessive activation of p38 mitogen-activated protein kinase (MAPK) in preeclamptic placentas compared with normotensive controls, together with increased levels of sFlt-1 and sEng in maternal sera in patients with PE. Moreover, Gadd45α knockdown or p38 inhibition provides protective effects in hypoxia/reoxygenation (H/R)-exposed human umbilical vein endothelial cells (HUVECs) by suppressing oxidative stress, inhibiting apoptosis, and promoting their potential for in vitro angiogenesis. A regulatory signaling pathway in which H/R intervention causes the induction of Gadd45α leading to p38 activation and ultimately an increase in sFlt-1 and sEng secretion in HUVECs has concurrently been established. Our study opens up a promising new avenue of investigation for increasing the understanding of the origin of sFlt-1 and sEng in PE and provides novel therapeutic targets for pregnancy complications arising from placental endothelial dysfunction.
Starting Page	551
Ending Page	565
Page Count	15
File Format	PDF
ISSN	0302766X
Journal	Cell and Tissue Research
Volume Number	344
Issue Number	3
e-ISSN	14320878
Language	English
Publisher	Springer-Verlag
Publisher Date	2011-04-26
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Preeclampsia Oxidative stress Growth arrest and DNA damage-inducible 45 alpha (Gadd45α) p38 mitogen-activated protein kinase (MAPK) Soluble fms-related tyrosine kinase-1 (sFlt-1) Soluble endoglin (sEng) Human Proteomics Human Genetics Molecular Medicine
Content Type	Text
Resource Type	Article
Subject	Cell Biology Histology Pathology and Forensic Medicine

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Antagonis Soluble Fms-Like Tyrosine Kinase 1 (sFlt-1) dan Soluble Endoglin (sEng) pada Preeklamsia

Soluble endoglin (sEng) joins the soluble fms-like tyrosine kinase (sFlt) receptor as a pre-eclampsia molecule*

Soluble endoglin (sEng) joins the soluble fms-like tyrosine kinase (sFlt) receptor as a pre-eclampsia molecule

Long-term observational study of renal outcome after preeclampsia: Role of soluble fms-like tyrosine kinase-1(sFlt-1)/ placental growth factor (PlGF) and endoglin.

Effects of simvastatin, rosuvastatin and pravastatin on soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sENG) secretion from human umbilical vein endothelial cells, primary trophoblast cells and placenta

Difficulty of predicting early-onset super-imposed preeclampsia in pregnant women with hemodialysis due to diabetic nephropathy by serum levels of sFlt-1, PlGF, and sEng.

Resveratrol inhibits release of soluble fms-like tyrosine kinase (sFlt-1) and soluble endoglin and improves vascular dysfunction – implications as a preeclampsia treatment

Similar Pro- and Antiangiogenic Profiles Close to Delivery in Different Clinical Presentations of Two Pregnancy Syndromes: Preeclampsia and Fetal Growth Restriction.

Paeoniflorin alleviates endothelial dysfunction caused by overexpression of soluble fms-like tyrosine kinase 1 and soluble endoglin in preeclampsia via VEGFA upregulation

Gadd45α as an upstream signaling molecule of p38 MAPK triggers oxidative stress-induced sFlt-1 and sEng upregulation in preeclampsia

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Antagonis Soluble Fms-Like Tyrosine Kinase 1 (sFlt-1) dan Soluble Endoglin (sEng) pada Preeklamsia

Soluble endoglin (sEng) joins the soluble fms-like tyrosine kinase (sFlt) receptor as a pre-eclampsia molecule*

Soluble endoglin (sEng) joins the soluble fms-like tyrosine kinase (sFlt) receptor as a pre-eclampsia molecule

Long-term observational study of renal outcome after preeclampsia: Role of soluble fms-like tyrosine kinase-1(sFlt-1)/ placental growth factor (PlGF) and endoglin.

Effects of simvastatin, rosuvastatin and pravastatin on soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sENG) secretion from human umbilical vein endothelial cells, primary trophoblast cells and placenta

Difficulty of predicting early-onset super-imposed preeclampsia in pregnant women with hemodialysis due to diabetic nephropathy by serum levels of sFlt-1, PlGF, and sEng.

Resveratrol inhibits release of soluble fms-like tyrosine kinase (sFlt-1) and soluble endoglin and improves vascular dysfunction – implications as a preeclampsia treatment

Similar Pro- and Antiangiogenic Profiles Close to Delivery in Different Clinical Presentations of Two Pregnancy Syndromes: Preeclampsia and Fetal Growth Restriction.

Paeoniflorin alleviates endothelial dysfunction caused by overexpression of soluble fms-like tyrosine kinase 1 and soluble endoglin in preeclampsia via VEGFA upregulation

Gadd45α as an upstream signaling molecule of p38 MAPK triggers oxidative stress-induced sFlt-1 and sEng upregulation in preeclampsia