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Frontiers of Medicine 2022年第6期16卷 919-931页

作者： Han Guo Yuncong Zhang Yaxin Chu Shuo Yang Jie Zhang Rui Qiao Laboratory Medicine Peking University Third HospitalBeijing100191China Department of Clinical Laboratory Peking University International HospitalBeijing102206China

Preeclampsia(PE)is characterized by placenta-mediated pregnancy complication.The only effective treatment for PE is the delivery of the placenta.However,this treatment may cause preterm birth and neonatal death.Therefore,preventing PE is needed.The mechanism of PE involves abnormal placentation,which leads to the release of anti-angiogenic and inflammatory mediators into maternal circulation.These mediators contribute to systemic vascular dysfunction,inflammatory responses,and excessive thrombin generation.Microparticles(MPs)are reportedly involved in PE by promoting the thromboinflammatory response.This study describes a strategy to prevent PE by reducing MP release using the recombinant protein,diannexin.Results showed that the patients with PE had elevated MP number and procoagulant activity and increased NLRP3 inflammasome activation.Additionally,diannexin remarkably reduced the release of MPs from activated cells by binding to phosphatidylserine exposed on the surface of activated cells.Moreover,in vivo results showed that diannexin could prevent PE-like symptoms by decreasing MPs and NLRP3 inflammasome activation in pregnant mice.Furthermore,diannexin effectively inhibited trophoblast cell activation and NLRP3 inflammasome activation in vitro.These findings suggested that diannexin inhibited MP release and might be an effective therapeutic strategy for preventing PE.

关键词： Preeclampsia recombinant protein diannexin microparticle NLRP3 inflammasome phosphatidylserin

Low-molecular-weight heparin and Preeclampsia—does the sword cut both ways?Three case reports and review of literature

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World Journal of Clinical Cases 2024年第9期12卷 1634-1643页

作者： Dan Shan Tao Li Xi Tan Ya-Yi Hu Department of Obstetrics and Gynecology West China Second University HospitalSichuan UniversityChengdu 610000Sichuan ProvinceChina Key Laboratory of Birth Defects and Related Diseases of Women and Children Sichuan UniversityMinistry of EducationChengdu 610000SichuanChina

BACKGROUND Low-molecular-weight heparins(LMWH)are the most commonly used anticoagulants during pregnancy.It is considered to be the drug of choice due to its safety in not crossing placenta.Considering the beneficial effect in the improvement of microcirculation,prophylactic application of LMWH in patients with Preeclampsia became a trend.However,the bleeding risk related with LMWH in Preeclampsia patients has seldomly been evaluated.This current study aimed to identify the potential risks regarding LMWH application in patients with Preeclampsia.CASE SUMMARY Herein we present a case series of three pregnant women diagnosed with Preeclampsia on LMWH therapy during pregnancy.All the cases experienced catastrophic hemorrhagic events.After reviewing the twenty-one meta-analyses,the bleeding risk related with LMWH seems ignorable.Only one study analyzed the bleeding risk of LMWH and found a significantly higher risk of developing PPH in women receiving LMWH.Other studies reported minor bleeding risks,none of these were serious enough to stop LMWH treatment.Possibilities of bleeding either from uterus or from intrabdominal organs in Preeclampsia patients on LMWH therapy should not be ignored.Intensive management of blood pressure even after delivery and homeostasis suture in surgery are crucial.CONCLUSION Consideration should be given to the balance between benefits and risks of LMWH in patients with Preeclampsia.

关键词： Pregnancy Preeclampsia Low-molecular-weight heparin Hemorrhage Case report

Estrogen-Induced Uterine Vasodilation in Pregnancy and Preeclampsia

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Maternal-Fetal Medicine 2022年第1期4卷 52-60页

作者： Yan Li Baoshi Han Alejandra Garcia Salmeron Jin Bai Dong-bao Chen Translational Medical Research Centre The First Flospital Affiliated to Shandong First Medical University and Shandong Provincial Qianfoshan HospitalJinanShandong 250014China Center for Reproductive Medicine Shandong UniversityThe Key Laboratory of Reproductive Endocrinology of Ministry of EducationNational Research Center for Assisted Reproductive Technology and Reproductive GeneticsJinanShandong 250014China Department of Obstetrics and Gynecology University of CaliforniaIrvineCA 92697USA

Normal pregnancy is associated with dramatically increased estrogen biosynthesis whose role is believed to raise uterine blood flow to facilitate the bi-directional maternal-fetal exchanges of gases(O_(2) and CO_(2)),to deliver nutrients,and exhaust wastes to support fetal development and survival.Constrained uterine blood flow in pregnancy is a leading cause of Preeclampsia with fetal growth restriction,rendering investigations of uterine hemodynamics to hold a high promise to inform pathways as targets for therapeutic interventions for Preeclampsia.The mechanisms of estrogen-induced uterine vasodilation in pregnancy have long been attributed to enhanced endothelium production of nitric oxide,but clinical trials targeting this pathway that dominates uterine hemodynamics have achieved no to little success.Emerging evidence has recently shown a novel proangiogenic vasodilatory role of hydrogen sulfide in regulating uterine hemodynamics in pregnancy and Preeclampsia,provoking a new field of perinatal research in searching for alternative pathways for pregnancy disorders especially Preeclampsia and intrauterine growth restriction.This minireview is intended to summarize the nitric oxide pathway and to discuss the emerging hydrogen sulfide pathway in modulating estrogen-induced uterine vasodilation in pregnancy and Preeclampsia.

关键词： Estrogens Uterine vasodilation Nitric oxide Hydrogen sulfide Pregnancy Preeclampsia

First Trimester Preeclampsia Screening and Prevention:Perspective in Chinese Mainland

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Maternal-Fetal Medicine 2024年第2期6卷 84-91页

作者： Jiao Liu Yunyu Chen Sin Ting Tai Long Nguyen-Hoang Kunping Li Jing Lin Xiaohong Lu Liona C.Poon Department of Obstetrics and Gynecology The Chinese University of Hong KongShatinHong Kong 999077China.

Preeclampsia(PE),a multisystem disorder in pregnancy,is one of the leading causes of perinatal morbidity and mortality that poses financial and physical burdens worldwide.Preterm PE with delivery at<37 weeks of gestation is associated with a higher risk of adverse maternal and perinatal outcomes than term PE with delivery at≥37 weeks of gestation.A myriad of first trimester screening models have been developed to identifying women at risk of preterm PE.In fact,the Fetal Medicine Foundation(FMF)first trimester prediction model has undergone successful internal and external validation.The FMF triple test enables the estimation of patient-specific risks,using Bayes theorem to combine maternal characteristics and medical history together with measurements of mean arterial pressure,uterine artery pulsatility index,and serum placental growth factor.Establishing a quality control process for regular monitoring and to ensure data standardization,reliability,and accuracy is key to maintaining optimal screening performance.The rate of preterm PE can be reduced by 62%by using the FMF prediction model,followed by the administration of low-dose aspirin.Recent evidence has also demonstrated that metformin has the potential for preventing PE in patients at high-risk of the disorder.In this article,we will summarize the existing literature on the different screening methods,different components of risk assessment,therapeutic interventions,and clinical implementation of the first trimester screening and prevention program for PE with specific considerations for Chinese mainland.

关键词： Preeclampsia Chinese population First trimester Screening Prevention

Placenta-derived IL-32β activates neutrophils to promote Preeclampsia development

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Cellular & Molecular Immunology 2021年第4期18卷 979-991页

作者： Dan Liu Qiang Li Hailin Ding Guangfeng Zhao Zhiyin Wang Chenrui Cao Yimin Dai Mingming Zheng Xiangyu Zhu Qianwen Wu Ya Wang Honglei Duan Huirong Tang Xianyan Lu Yayi Hou Yali Hu Department of Obstetrics and Gynecology The Affiliated Drum Tower Hospital of Nanjing University Medical SchoolNanjingChina Department of Obstetrics and Gynecology Drum Tower Clinic Medical College of Nanjing Medical UniversityNanjingJiangsuChina The State Key Laboratory of Pharmaceutical Biotechnology Division of ImmunologyMedical SchoolNanjing UniversityNanjingChina

Immune activation at the maternal-fetal interface is a main pathogenic factor of Preeclampsia(PE).Neutrophils(PMNs)are activated in PE patients,but the mechanism and consequences of PMN activation need to be further explored.Here,we demonstrated that interleukin-32(IL-32)expression was significantly upregulated in syncytiotrophoblasts(STBs)and that IL-32β was the major isoform with increased expression in the placenta of severe PE(sPE)patients.Furthermore,the level of IL-32 expression in the placenta was correlated with its level in the serum of sPE patients,indicating that IL-32 in the serum is derived mainly from the placenta.Then,in vitro experiments showed that IL-32β could highly activate PMNs and that these IL-32β-activated PMNs were better able to adhere to endothelial cells(HUVECs)and enhance the expression of vascular cell adhesion molecule-1(VCAM-1)and intercellular cell adhesion molecule-1(ICAM-1)in HUVECs,which could be reversed by preincubation with the NADPH oxidase inhibitor VAS 2870.In addition,we showed that IL-32β mainly activated PMNs by binding to proteinase 3.Finally,IL-32β administration induced a PE-like phenotype in a pregnant mouse model.This study provides evidence of the involvement of IL-32β in the pathogenesis of PE.

关键词： IL-32 Neutrophil Preeclampsia ROS HUVEC

THBS1 regulates trophoblast fusion through a CD36-dependent inhibition of cAMP,and its upregulation participates in Preeclampsia

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Genes & Diseases 2021年第3期8卷 353-363页

作者： Fu-Mei Duan Li-Juan Fu Yong-Heng Wang Enoch Appiah Adu-Gyamfi Ling-Ling Ruan Zeng-Wei Xu Shi-Quan Xiao Xue-Mei Chen Ying-Xiong Wang Tai-Hang Liu Yu-Bin Ding School of Public Health and Management Chongqing Medical UniversityChongqing400016PR China Department of Bioinformatics The School of Basic MedicineChongqing Medical UniversityChongqing400016PR China The Joint International Research Laboratory of Reproduction and Development Ministry of EducationChongqing400016PR China Department of Herbal Medicine School of Traditional Chinese MedicineChongqing Medical UniversityChongqing400016PR China Department of Reproductive Medicine The Third Affiliated HospitalChongqing Medical UniversityChongqing401120PR China

Preeclampsia is a pregnancy complication which threatens the survival of mothers and fetuses.It originates from abnormal placentation,especially insufficient fusion of the cytotrophoblast cells to form the syncytiotrophoblast.In this study,we found that THBS1,a matricellular protein that mediates cell-to-cell and cell-to-matrix interactions,is downregulated during the fusion of primary cytotrophoblast and BeWo cells,but upregulated in the placenta of pregnancies complicated by Preeclampsia.Also,THBS1 was observed to interact with CD36,a membrane signal receptor and activator of the cAMP signaling pathway,to regulate the fusion of cytotrophoblast cells.Overexpression of THBS1 inhibited the cAMP signaling pathway and reduced the BeWo cells fusion ratio,while the effects of THBS1 were abolished by a CD36-blocking antibody.Our results suggest that THBS1 signals through a CD36-mediated cAMP pathway to regulate syncytialization of the cytotrophoblast cells,and that its upregulation impairs placental formation to cause Preeclampsia.Thus,THBS1 can serve as a therapeutic target regarding the mitigation of abnormal syncytialization and Preeclampsia.

关键词： cAMP Cell fusion Preeclampsia THBS1 Trophoblast

An alternative splicing variant of mineralocorticoid receptor discovered in Preeclampsia tissues and its effect on endothelial dysfunction

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Science China(Life Sciences) 2020年第3期63卷 388-400页

作者： Mengxi Guo Chengliang Zhou Gufeng Xu Lin Tang Yechun Ruan Ying Yu Xianhua Lin Dandan Wu Hao Chen Priscilla Yu Luyang Jin Yinyu Wang Yimei Wu Kamran Ullah Tanzil Ur Rahman Xinmei Liu Jianzhong Sheng Hsiao-Chang Chan Hefeng Huang Women’s Hospital Zhejiang University School of MedicineHangzhou 310058China International Peace Maternal and Child Health Hospital Shanghai Jiao Tong University School of MedicineShanghai 200030China Epithelial Cell Biology Research Center Faculty of MedicineSchool of Biomedical SciencesThe Chinese University of Hong KongHong KongChina Key Laboratory of Reproductive Genetics Ministry of Education(Zhejiang University)Hangzhou 310058China Department of Pathology and Pathophysiology Zhejiang University School of MedicineHangzhou 310058China Shanghai Key Laboratory of Embryo Original Disease Shanghai 20030China

The pathophysiology of Preeclampsia(PE)remains unclear.PE spiral artery remodeling dysfunction and PE offspring cardiovascular future development has been a worldwide concern.We collected placental and umbilical artery samples from normotensive and PE pregnancies.Mineralocorticoid receptor(MR)and its alternative splicing variant(ASV)expression and their biological effects on PE were examined.An MR ASV was found to be highly expressed in all PE samples and slightly expressed in about half of the normotensive samples(umbilical artery,~57.58%;placenta,~36.84%).The MR ASV expression was positively associated with blood pressure in both groups.The MR ASV protein changed the aldosterone-induced expression pattern of MR target genes related to ion exchanges and cell signaling pathways.The MR ASV can also impair the proliferation,migration,and tube formation ability of endothelial cells.These findings indicate that MR ASV in PE placenta plays a pathogenic role in PE pathophysiology,especially in endothelial dysfunction,and the existence of the MR ASV in PE umbilical artery provides a new direction in the study of PE offspring with increased risk of cardiovascular diseases.

关键词： Preeclampsia mineralocorticoid receptor alternative splicing variant offspring endothelial dysfunction

Investigation of FOXP3 (rs3761548) polymorphism with the risk of Preeclampsia and recurrent spontaneous abortion: A systemic review and meta-analysis

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Asian pacific Journal of Reproduction 2022年第3期11卷 117-124页

作者： Govinda Sri Varshini Sivakumar Harshini Muhammed Ali Siham Govindaraj Krishnamurthy Tejaswini Yasam Santhosh Kumar Langeswaran Kulanthaivel Gowtham Kumar Subbaraj Faculty of Allied Health Sciences Chettinad Hospital and Research InstituteChettinad Academy of Research and Education(Deemed to be University)KelambakkamTamil Nadu 603103India Department of Bioinformatics Alagappa UniversityKaraikudi-630003Tamil NaduIndia

Objective:To investigate the association between forkhead box P3(FOXP3)(rs3761548)polymorphism and the risk of Preeclampsia and recurrent spontaneous abortion.Methods:Literature on the association of FOXP3 gene polymorphisms and susceptibility to Preeclampsia and unexplained recurrent spontaneous abortion was retrieved by searching databases such as PubMed,Science Direct,Google Scholar and Embase from 2000 to 2021.The association measure was analyzed using an odds ratio(OR)and 95%confidence interval(CI).All the statistical analyses were executed using RevMan 5.4 software.Results:In the present meta-analysis,11 articles were analyzed.The pooled results showed no association between FOXP3 gene polymorphism(rs3761548)and Preeclampsia risk in allelic,recessive,dominant and over dominant contrast models.FOXP3 gene polymorphism(rs3761548)showed an association with recurrent abortion in allelic,recessive and dominant models(OR 1.85,CI 1.59-2.14;OR 2.02,95%CI 1.56-2.62;OR 2.69,95%CI 1.50-4.83,respectively),while no association in the over dominant contrast model(OR 1.35,CI 0.87-2.10).Conclusions:In the present study,FOXP3 gene(rs3761548)polymorphism is associated with risk of recurrent spontaneous abortion but not Preeclampsia.However,larger sample size and multiracial studies are needed in the future to confirm the findings.

关键词： Preeclampsia FOXP3 gene Single nucleotide polymorphism rs3761548 Unexplained recurrent spontaneous abortion

Role of mammalian target of rapamycin signaling pathway in regulation of fatty acid oxidation in a Preeclampsia-like mouse model treated with pravastatin

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Chinese Medical Journal 2019年第6期132卷 671-679页

作者： Jing Huai Zi Yang Yan-Hong Yi Guang-Jiao Wang Department of Obstetrics and Gynecology. Peking University Third Hospital Beijing 100191 China

Background: Fatty acid oxidation (FAO) disorder is involved in the pathogenesis of some cases of Preeclampsia (PE). Several show that mammalian target of rapamycin (mTOR) signaling pathway is related to FAO. Pravastatin (Pra) can promote FAO in Nio-nitro-L-arginine methyl ester (L-NAME) PE-like mouse model in our previous study. This study aimed to investigate the effect of mTOR signaling pathway in PE-like model treated with Pra. Methods: Pregnant mice were randomly injected with L-NAME as PE-like model group or saline as control group respectively, from gestational 7th to 18th day. Giving Pra (L-NAME + Pra, Control + Pra, n= 8) or normal saline (NS;L-NAME + NS, Control + NS, n = 8) from gestational 8th to 18th day, the mice were sacrificed on day 18 and their liver and placental tissues were collected. Then the activation of mTOR and its substrates in the liver and placenta were detected. And the association between mTOR activation and mice were randomly injected with L-NAME as PE-like model group or saline as control group respectively, from serum free fatty acid (FFA) levels and the expression of long-chain 3-hydroxyacyl-coenzyme A dehydrogenase (LCHAD) were evaluated using Pearson correlation test. Differences between groups were analyzed using independent t-test or one-way analysis of variance (ANOVA). Results: Both in the maternal liver and placenta, the activation of mTOR protein and its effect on substrates increased significantly in the L-NAME + NS group and decreased significantly in the L-NAME + Pra group. The p-mTOR/mTOR protein ratio decreased in the L-NAME + Pra group significantly than that in the L-NAME + NS group both in liver and placenta (liver: 0.74±0.08 vs. 0.85± 0.06, t=2.95, P<0.05;placenta: 0.63±0.06 vs.0.77±0.06, t=4.64, P<0.05). The activation of mTOR protein in the liver and placenta negatively correlated with the expression of LCHAD in the L-NAME + NS group (liver: r=—0.745, P<0.05;placenta: r=-0.833, P< 0.05) and that in the maternal liver negatively correlated with the expression of

关键词： Preeclampsia mTOR signaling pathway Pravastatin Fatty acid oxidation

miRNA-141-5p Affects the Levels of Neutrophil Elastase in Preeclampsia by Regulating MAPK1

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Maternal-Fetal Medicine 2022年第4期4卷 238-244页

作者： Keyan Cheng Jialei Cui Wenli Zhou Huiqiang Liu Taotao Yang Yonghong Wang Department of Gynecology and Obstetrics The Second Hospital of Shanxi Medical UniversityTaiyuan 030001China.

Objective:The objective of this study was to investigate the expression levels of microRNA-141-5p(miRNA-141-5p),MAPK1 and neutrophil elastase in patients with and without Preeclampsia(PE),and the relationship between miRNA-141-5p and MAPK1 with respect to the secretion of elastase by neutrophils in patients with PE.Methods:Thirty patients with PE and 30 healthy pregnant(HP)women were recruited from The Second Hospital of Shanxi Medical University,Taiyuan,China,between February 2017 and July 2018.Neutrophils were isolated from 8 mL peripheral blood samples and cultured.We recorded neutrophil count and morphology during culture.Apoptosis was detected by flow cytometry in different groups at 0,24,and 48 h.The expression levels of elastase were detected in neutrophils by enzyme-linked immunosorbent assay,whereas the expression levels of miRNA-141-5p in peripheral blood neutrophils were detected by real-time polymerase chain reaction.We used TargetScanHuman Release 7.2 to analyze the target genes of miRNA-141-5p.The expression of MAPK1 in peripheral blood neutrophils was detected by western blotting.Data were analyzed by SPSS version 21.0 software,and comparisons between groups were carried out with the Studentt test.Results:There was no significant difference between the PE and HP groups(P>0.050)with regard to age or body mass index.The weight of newborns in the PE group(2846.00±600.00 g)was significantly lower than that in the HP group(3055.00±230.68 g).The number of neutrophilic granulocytes(NGs)in blood samples from the PE group was significantly higher than that in the HP group(P=0.003).There was no significant difference between the groups with regard to morphology.Apoptosis in the PE group was delayed when compared with the HP group at different time points.TheP value of apoptosis in the PE and HP groups were respectively 0.790,<0.001 and 0.030 at 0 h,24 h and 48 h.The expression levels of miRNA-141-5p in the PE group were significantly lower than those in the HP group(P<0.050).The expression levels of MAPK1 in

关键词： Preeclampsia Neutrophil miRNA-141-5p MAPK1 Neutrophil elastase