The expression of serum sEGFR, sFlt-1, sEndoglin and PLGF in preeclampsia

Cui, Lifeng; Shu, Chen; Liu, Zitao; Tong, Wei; Cui, Miao; Wei, Chengguo; Tang, Jianbo; Liu, Xiufen; Hu, Jinghai; Jiang, Jing; He, Junqi; Zhang, David Y.; Ye, Fei; Li, Yulin

doi:10.1016/j.preghy.2018.05.011

Cited by 24 publications

(22 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The evidence has indicated that high circulating levels of sFlt‐1 (anti‐angiogenic protein) combined with low levels of PlGF (proangiogenic protein) may predict subsequent development of PE and can be used as biomedical markers in monitoring the severity of PE (Cui et al, ; Maynard et al, ). Meanwhile, it is reported that excessive placental sFlt1 and low placental PlGF may contribute to hypertension and proteinuria in PE (Vrachnis et al, ).…”

Section: Discussionmentioning

confidence: 99%

Vitexin ameliorates preeclampsia phenotypes by inhibiting TFPI‐2 and HIF‐1α/VEGF in a l‐NAME induced rat model

Zheng

Huang

et al. 2019

Drug Development Research

View full text Add to dashboard Cite

Preeclampsia (PE) is a leading cause of maternal and perinatal morbidity and mortality with few safe, effective, and minimally invasive therapeutics. Inflammation, oxidative stress, and angiogenic imbalance have been reported to contribute to PE pathogenesis. Vitexin (VI) possesses various pharmacological activities including the potent regulation of the above biological processes in different conditions. This study aims to investigate whether VI has therapeutic potential to PE and the underlying mechanisms. Sprague–Dawley pregnant rats pretreated with or without VI were fed with l‐NAME‐containing water to induce experimental PE. Results showed that VI decreased high systolic blood pressure and urinary protein in PE rats time‐ and dose‐dependently. Meanwhile, VI of higher dosage (45, 60 mg/kg) corrected abnormal pregnancy outcomes, including low pup weight and low pups/placenta ratio. In addition, VI of high dosage (60 mg/kg) decreased sFlt‐1, increased PlGF and alleviated oxidative stress both in blood and placental samples compared with nontreated PE group. Furthermore, VI alleviated placental TFPI‐2, HIF 1α, and VEGF in PE rats. In short, the present study suggests that the inhibition of placental TFPI‐2 and HIF‐1α/VEGF might be one of the potential mechanisms underlying the protective effects of VI to experimental PE induced by l‐NAME.

show abstract

Section: Discussionmentioning

confidence: 99%

Vitexin ameliorates preeclampsia phenotypes by inhibiting TFPI‐2 and HIF‐1α/VEGF in a l‐NAME induced rat model

Zheng

Huang

et al. 2019

Drug Development Research

View full text Add to dashboard Cite

show abstract

“…This prompt development of preterm and term PE in association with an increase in the sFlt1/PlGF ratio have been strongly associated with disease severity. 50 In contrast, no clinical characteristics as defined in Table 2 changed over two weeks when sFlt1/PlGF < 38, with 8.2% of encounters resulting in PE diagnosis. These results are consistent with a larger sample of patients suspected to have PE where 7.5% of these patients developed PE within two weeks when sFlt1/PlGF < 38.…”

Section: Resultsmentioning

confidence: 97%

Use of the angiogenic biomarker profile to risk stratify patients with fetal growth restriction

Arenas¹,

Tang

Mueller

et al. 2021

American Journal of Obstetrics & Gynecology MFM

View full text Add to dashboard Cite

This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

show abstract

“…Hence, exploration of the pathways involved in sFlt-1 secretion and other angiogenic factors in first trimester placenta model may be more complex and may involve other pathways, such as Hypoxia-Inducible Factor 1 alpha (HIF-1α) [42]. Other increased biological markers may be regulated during first trimester environmental transition, such as soluble endoglin, which is increased in maternal sera in the case of preeclampsia [43]. The oxygen tension also plays a role in soluble endoglin (sEndo) secretion through TGF-β3 signaling [44] and emphasizes the complex interplay between several actors involved in angiogenic balance and oxygen tension during the first trimester.…”

Section: Discussionmentioning

confidence: 99%

Human Placental NADPH Oxidase Mediates sFlt-1 and PlGF Secretion in Early Pregnancy: Exploration of the TGF-β1/p38 MAPK Pathways

et al. 2021

View full text Add to dashboard Cite

Preeclampsia, a hypertensive disorder occurring during pregnancy, is characterized by excessive oxidative stress and trophoblast dysfunction with dysregulation of soluble Fms-like tyrosine kinase 1 (sFlt-1) and placental growth factor (PlGF) production. Nicotinamide Adenine Dinucleotide Phosphate (NADPH) oxidase (Nox) is the major source of placental superoxide in early pregnancy and its activation with the subsequent formation of superoxide has been demonstrated for various agents including Transforming Growth Factor beta-1 (TGF-β1), a well-known p38 MAPK pathway activator. However, the bridge between Nox and sFlt-1 remains unknown. The purpose of this study was to explore the possible signaling pathway of TGF-β1/Nox/p38 induced sFlt-1 production in human chorionic villi (CV). Methods: Human chorionic villi from first trimester placenta (7–9 Gestational Weeks (GW)) were treated with TGF-β1 or preincubated with p38 inhibitor, SB203580. For NADPH oxidase inhibition, CV were treated with diphenyleneiodonium (DPI). The protein levels of phospho-p38, p38, phospho-Mothers Against Decapentaplegic homolog 2 (SMAD2), and SMAD2 were detected by Western blot. The secretion of sFlt-1 and PlGF by chorionic villi were measured with Electrochemiluminescence Immunologic Assays, and NADPH oxidase activity was monitored by lucigenin method. Results: We demonstrate for the first time that NADPH oxidase is involved in sFlt-1 and PlGF secretion in first trimester chorionic villi. Indeed, the inhibition of Nox by DPI decreases sFlt-1, and increases PlGF secretions. We also demonstrate the involvement of p38 MAPK in sFlt-1 secretion and Nox activation as blocking the p38 MAPK phosphorylation decreases both sFlt-1 secretion and superoxide production. Nevertheless, TGF-β1-mediated p38 activation do not seem to be involved in regulation of the first trimester placental angiogenic balance and no crosstalk was found between SMAD2 and p38 MAPK pathways. Conclusions: Thus, the placental NADPH oxidase play a major role in mediating the signal transduction cascade of sFlt-1 production. Furthermore, we highlight for the first time the involvement of p38 activation in first trimester placental Nox activity.

show abstract

The expression of serum sEGFR, sFlt-1, sEndoglin and PLGF in preeclampsia

Cited by 24 publications

References 29 publications

Vitexin ameliorates preeclampsia phenotypes by inhibiting TFPI‐2 and HIF‐1α/VEGF in a l‐NAME induced rat model

Vitexin ameliorates preeclampsia phenotypes by inhibiting TFPI‐2 and HIF‐1α/VEGF in a l‐NAME induced rat model

Use of the angiogenic biomarker profile to risk stratify patients with fetal growth restriction

Human Placental NADPH Oxidase Mediates sFlt-1 and PlGF Secretion in Early Pregnancy: Exploration of the TGF-β1/p38 MAPK Pathways

Contact Info

Product

Resources

About