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UCK2 promotes the proliferation,migration,and invasion of trophoblast cells in preeclampsia by activating the STAT3 pathway

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BIOCELL 2023年第4期47卷 837-847页

作者： WEI XIA NING YANG XIAOYAN FENG TING XIN YONGLE JING YUMING LI CHENGZHI LU Department of Cardiology Tianjin First Central HospitalTianjin300192China Department of Hypertension TEDA International Cardiovascular HospitalTianjin300457China Department of Dermatology Tianjin Children’s HospitalTianjin300134China TEDA International Cardiovascular Hospital Tianjin300457China School of Medicine Nankai UniversityTianjin300071China

Background:Preeclampsia(PE),characterized by hypertension and proteinuria,leads to serious maternal and infant complications.Uridine-cytidine kinase 2(UCK2)belongs to the UCK family,a class of enzymes that catalyzes the conversion of uridine and cytidine to monophosphate form.However,the role of UCK2 in PE has not been reported.Methods:The expression of UCK2 was detected in the placenta of PE patients and N(ω)-nitro-L-arginine methyl esterinduced PE mouse model.Through forced up-regulation or down-regulation of UCK2 in vitro,we examined the effects of UCK2 on the proliferation,apoptosis,migration,and invasion of trophoblast cells.Stattic,the inhibitor of STAT3 pathway,was used to investigate whether the STAT3 pathway mediates the biological function of UCK2 in trophoblast cells.Results:The present study found that UCK2 showed low expression in the placenta of PE patients and PE mouse model.MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide)and flow cytometry assays verified that up-regulation of UCK2 promoted the proliferation of trophoblast cells,while the silence of UCK2 suppressed cell proliferation.Besides,flow cytometry and TdT-mediated dUTP Nick-End Labeling assays demonstrated that knockdown of UCK2 resulted in apoptosis of trophoblast cells.The wound healing and transwell assays showed that the migration and invasion activities of the trophoblast cells were facilitated by the overexpression of UCK2 and were blocked by the silence of UCK2.Furthermore,the expression of phosphorylated STAT3 was increased with the upregulation of UCK2 and decreased with the inhibition of UCK2.When the STAT3 pathway was blocked by its inhibitor stattic,the promotion effects of UCK2 on trophoblast cells were suppressed.Conclusion:UCK2 promotes the proliferation,migration,and invasion of trophoblast cells,and these effects may be partly mediated by the activation of the STAT3 pathway.

关键词： UCK2 Preeclampsia STAT3 trophoblast Invasion

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Esrrb plays important roles in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs

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Journal of Molecular Cell Biology 2019年第6期11卷 463-473页

作者： Haibo Gao Rui Gao Linfeng Zhang Wenchao Xiu Ruge Zang Hong Wang Yong Zhang Jiayu Chen Yawei Gao Shaorong Gao Clinical and Translational Research Center of Shanghai First Maternity and Infant Hospital Shanghai Key Laboratory of Signaling and Disease Research School of Life Sciences and Technology Tongji University Shanghai 200092 China Peking University-Tsinghua University-National Institute of Biological Sciences Joint Graduate Program School of Life Sciences Tsinghua University Beijing 100084 China

trophoblast stem cells (TSCs), which can be derived from the trophoectoderm of a blastocyst, have the ability to sustain self-renewal and differentiate into various placental trophoblast cell types. Meanwhile, essential insights into the molecular mechanisms controlling the placental development can be gained by using TSCs as the cell model. Esrrb is a transcription factor that has been shown to play pivotal roles in both embryonic stem cell (ESC) and TSC, but the precise mechanism whereby Esrrb regulates TSC-specific transcriptome during differentiation and reprogramming is still largely unknown. In the present study, we elucidate the function of Esrrb in self-renewal and differentiation of TSCs, as well as during the induced TSC (iTSC) reprogramming. We demonstrate that the precise level of Esrrb is critical for stem state maintenance and further trophoblast differentiation of TSCs, as ectopically expressed Esrrb can partially block the rapid differentiation of TSCs in the absence of fibroblast growth factor 4. However, Esrrb depletion results in downregulation of certain key TSC-specific transcription factors, consequently causing a rapid differentiation of TSCs and these Esrrb-deficient TSCs lose the ability of hemorrhagic lesion formation in vivo. This function of Esrrb is exerted by directly binding and activating a core set of TSC-specific target genes including Cdx2, Eomes, Sox2, Fgfr4, and Bmp4. Furthermore, we show that Esrrb overexpression can facilitate the MEF-to-iTSC conversion. Moreover, Esrrb can substitute for Eomes to generate GEsTM-iTSCs. Thus, our findings provide a better understanding of the molecular mechanism of Esrrb in maintaining TSC self-renewal and during iTSC reprogramming.

关键词： Esrrb trophoblast stem cell self-renwwal differentiation iTSC reprogramming

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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

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Tissue factor expression and methylation regulation in differentiation of embryonic stem cells into trophoblast

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Asian Pacific Journal of Tropical Medicine 2014年第7期7卷 557-561页

作者： Lin-Xin Liu Hui Zeng En-Yi Liu Fang-Ping Chen Department of Hematology Xiangya Hospital of Central South University

Objective:To explore tissue factor(TF)expression and methylation regulation in differentiation of human embryonic stem cells(hESCs)into trophoblast.Methods:Differentiation of hESCs into trophoblast was induced by bone morphogenetic protein 4(BMP4).Expression of gene,protein of TF and DNA methylation at different time points during induction process was detected by RTPCT,Western blot,flow cytometry and MSP-PCR method.Results:The expression of mRNA,protein level of TF could be detected during directional differentiation of hESCs to trophoblast cells,semi methylation-semi non methylation expression appeared at TF DNA promoter region,and it showed decreased methylation level and increased non methylation level with formation of trophoblast cell and increased expression of TF.Conclusions:It shows that during differentiation of hESCs into trophoblast,the differential expression of TF is related with DNA methylation level,and it is changed with the methylation or non methylated degree.It provids new platform to furtherly explore the regulation mechanisms of specific expression of tissue factor in the process of the embryonic stem cell development.

关键词： Embryonic stem cells trophoblast cell Tissue factor Methylation

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Effect of hypoxia on expression of placental trophoblast cells SATB1 and β-catenin and its correlation with the pathogenesis of preeclampsia

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Asian Pacific Journal of Tropical Medicine 2016年第6期9卷 548-552页

作者： Qiang Wu Gang Wu Jing-Xiang Li Department of Clinical Laboratory Linyi People's Hospital Department of Obstetrics General Hospital of Laiwu Iron and Steel Company Department of Proctology Dongzhimen Hospital Beijing University of Chinese Medicine

Objective: To study the effect of hypoxia on the expression of placental trophoblast cells SATB1 and β-catenin and its correlation with the pathogenesis of preeclampsia. Methods: trophoblastic cell lines HRT8/SVneo were cultured, SATB1 and β-catenin expression and cell biological behavior were determined after hypoxia reoxygenation treatment; cell biological behavior and the expression of related genes were determined after the transfection of SATB1 and β-catenin siR NA; preeclampsia placenta and normal placenta tissues were collected and the expression of SATB1 and β-catenin were determined. Results: OD value, cell migration rate, m RNA contents of SATB1 and β-catenin of H/R group were significantly lower than those of Nor group, cell apoptosis rate was higher than that of Nor group and the number of invasive cells was less than that of Nor group; OD value and bcl-2 mRNA content of SATB1-siRNA group were lower than those of NC group; cell apoptosis rate as well as Bax, Caspase-3, caspase-6 and caspase-9 mRNA contents were higher than those of NC group; cell migration rate as well as CTSB, CTSD, MMP2 and MMP9 mRNA contents of β-catenin-siRNA group were lower than those of NC group; the number of invasive cells was less than that of NC group; the expression levels of SATB1 and β-catenin in preeclampsia placenta tissue were significantly lower than those in normal placenta tissue. Conclusions: Hypoxia can inhibit the expression of SATB1 and β-catenin in the pathogenesis of preeclampsia, which can affect the proliferation, apoptosis, migration and invasion of cells.

关键词： Preeclampsia Placental trophoblast SATB1 Beta-catenin

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Molecular Mechanisms Underlying Cell-Fate Specification and Cellular Diversity of the trophoblast Lineage during Placental Morphogenesis in Mice

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Reproductive and Developmental Medicine 2021年第4期5卷 220-236页

作者： Jian-Qi Wang Change Mu Yang Sun Jin-Hua Lu Hai-Bin Wang Department of Obstetrics and Gynecology The First Affiliated Hospital of Xiamen UniversitySchool of MedicineXiamen UniversityXiamenFujian 361003China Fujian Provincial Key Laboratory of Reproductive Health Research School of MedicineXiamen UniversityXiamenFujian 361102China

Placental morphogenesis is a highly dynamic process involving mutual recognition and interlacing between the trophoblast-uterus and ultimately the initiation of the maternal-fetal circulatory system.During placental morphogenesis in mice,the trophoblast lineage,which integrates maternal and fetal signaling,undergoes stage-specific changes in gene regulatory programs directing cellular proliferation and fate specification,generating diverse trophoblast subtypes.While accumulating evidence from studies on genetically engineered and mutant mice has revealed the involvement of cell-specific core transcription factors in certain key events during placental morphogenesis,the precise molecular mechanisms by which multipotent trophoblasts gradually differentiate into different subtypes are still largely unknown.In this review,we primarily focus on mutant mouse models with placental phenotypes to provide a comprehensive understanding of the molecular mechanisms underlying cell-fate specification and cellular diversity of the trophoblast lineage during the placental morphogenesis.

关键词： Differentiation Morphogenesis Multipotency Placenta trophoblast

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Regulation of activin A in cell proliferation and hormone secretion by human normal trophoblast cells

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Chinese Science Bulletin 1999年第7期44卷 609-612页

作者： Yanling Wang J. P. Mathe T. Woodroff Shuyi Luo Linzhi Zhuang Chinese Acad Sci Inst Zool State Key Lab Reprod Biol Beijing 100080 Peoples R China Genentech Inc S San Francisco CA 94080 USA

Regulation of activin A in cell proliferation as well as hCG and progesterone secretion was investigated using primary cultured cytotrophoblast cells and normal placenta origin cytotrophoblast cell line-NPC cells in serum-free system. It was shown that activin A promoted hCG and progesterone secretion in primary cultured cytotrophoblast cells as well as progesterone secretion in NPC cells, while it had no effect on cell proliferation and hCG secretion in NPC cells. lmportant evidence is provided for the autocrine regulatory mechanism of activin A on hormone secretion in placental trophoblast cells at early pregnancy.

关键词： human placental trophoblast cells at early pregnancy activin A cell proliferation hCG progesterone.

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Human HAND1 inhibits the conversion of cholesterol to steroids in trophoblasts

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Journal of Genetics and Genomics 2022年第4期49卷 350-363页

作者： Haibin Zhu Qianlei Ren Ziyi Yan Shouying Xu Jiahao Luo Ximei Wu Chao Tang National Clinical Research Center for Child Health of the Children’s Hospital Zhejiang University School of MedicineHangzhouZhejiang 310052China Department of Obstetrics and Gynaecology The First Affiliated Hospital of Zhejiang University School of MedicineHangzhouZhejiang 310003China Department of Pharmacology School of MedicineZhejiang UniversityHangzhouZhejiang 310058China

Steroidogenesis from cholesterol in placental trophoblasts is fundamentally involved in the establishment and maintenance of pregnancy.The transcription factor gene heart and neural crest derivatives expressed1(Hand1)promotes differentiation of mouse trophoblast giant cells.However,the role of HAND1 in human trophoblasts remains unknown.Here,we report that HAND1 inhibits human trophoblastic progesterone(P4)and estradiol(E2)from cholesterol through downregulation of the expression of steroidogenic enzymes,including aromatase,P450 cholesterol side-chain cleavage enzyme(P450 scc),and 3β-hydroxysteroid dehydrogenase type 1(3β-HSD1).Mechanically,although HAND1 inhibits transcription of aromatase by directly binding to aromatase gene promoter,it restrains transcription of P450 scc by upregulation of the methylation status of P450 scc gene promoter through its binding to ALKBH1,a demethylase.Unlike aromatase and P450 scc,HAND1 decreases 3β-HSD1 m RNA levels by the reduction of its RNA stability through binding to and subsequent destabilizing protein Hu R.Finally,HAND1 suppresses circulating P4 and E2 levels derived from JEG-3 xenograft and attenuates uterine response to P4 and E2.Thus,our results uncover a hitherto uncharacterized role of HAND1 in the regulation of cholesterol metabolism in human trophoblasts,which may help pinpoint the underlying mechanisms involved in supporting the development and physiological function of the human placenta.

关键词： HAND1 trophoblast Cholesterol Steroids

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Reduced cell invasion may be a characteristic of placental defects in pregnant women of advanced maternal age at single-cell level

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2022年第9期23卷 747-759页

作者： Bin ZHANG Feng ZHANG Fengying LU Jing WANG Wenbai ZHOU Huihui WANG Bin YU Department of Medical Genetics Changzhou Maternal and Child Health Care HospialChangzhou Medical CenterNanjing Medical UniversityChangzhou 213000China

The mechanisms underlying pregnancy complications caused by advanced maternal age(AMA)remain unclear.We analyzed the cellular signature and transcriptomes of human placentas in AMA women to elucidate these mechanisms.Placental tissues from two AMA women and two controls were used for single-cell RNA-sequencing(scRNA-seq).Controls consisted of AMA women who did not experience any pregnancy complications and pregnant women below the age of 35 years without pregnancy complications.trophoblast cells were obtained from the placentas of another six pregnant women(three AMA women and three controls),and in-vitro transwell assays were conducted to observe the cell invasion ability.Thirty additional samples(from 15 AMA women and 15 controls)were analyzed to verify the specific expression of serine protease inhibitor clade E member 1(SERPINE1).Preliminary study of the role of SERPINE1 in cell invasion was carried out with HTR8-S/Vneo cells.High-quality transcriptomes of 27607 cells were detected.Three types of trophoblast cells were detected,which were further classified into eight subtypes according to differences in gene expression and Gene Ontology(GO)function.We identified 110 differentially expressed genes(DEGs)in trophoblast cells between the AMA and control groups,and the DEGs were enriched in multiple pathways related to cell invasion.In-vitro transwell assays suggested that the invading trophoblast cells in AMA women were reduced.SERPINE1 was specifically expressed in the trophoblast,and its expression was higher in AMA women(Ptrophoblast cells showed fewer invading cells in the hSERPINE1 group.Impaired cell invasion may underlie the increased risk of adverse pregnancy outcomes in AMA women.Abnormal expression of SERPINE1 in extravillous trophoblast(EVT)cells appears to play an important role.

关键词： Advanced maternal age(AMA) Pregnancy complications Placenta trophoblast Cell invasion Serine protease inhibitor clade E member 1(SERPINE1)

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Focal adhesion kinase signaling is necessary for the hydrogen sulfide-enhanced proliferation,migration,and invasion of HTR8/SVneo human trophoblasts

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Reproductive and Developmental Medicine 2023年第2期7卷 75-82页

作者： Xian-Li Wang Jing Tang Department of Pharmacy Obstetrics and Gynecology HospitalFudan UniversityShanghai 200011China

Objective:Hydrogen sulfide(H_(2)S)has been elucidated that it promotes migration and invasion in human placenta trophoblasts.However,the signaling pathway underlying H_(2)S-based regulation of trophoblasts remains unknown.Hence,we investigated the potential effect of sodium hydrosulfide(NaHS),an exogenous H_(2)S donor,on extravillous trophoblasts.Methods:The Cell Counting Kit-8 was used to detect the proliferative activity of trophoblasts and to screen the optimal concentration of NaHS.The migration and invasion of HTR8/SVneo cells were measured by Transwell assays.Gene expression was determined by quantitative real-time PCR analysis.Protein expression was determined by western blot.Results:We found that NaHS could promote the proliferation,migration,and invasion of HTR8/SVneo cells.The phosphorylation of focal adhesion kinase(FAK),Src,and extracellular signal-regulated kinase(ERK)were activated by NaHS.Moreover,NaHS also upregulated the expression of matrix metalloproteinase-2(MMP-2)and MMP-9,downregulated the expression of E-cadherin in HTR8/SVneo cells.The application of NaHS could increase the expression of cystathionine-β-synthase.Conclusion:Both FAK-Src signaling and the upstream signaling cascade of ERK activation play a significant important role in NaHS-induced proliferation,migration,and invasion via upregulating activity of MMP-2,MMP-9,and downregulating E-cadherin in HTR8/SVneo cells.These novel findings may provide a strong foundation for the clinical application of H_(2)S donor drugs.

关键词： Hydrogen sulfide trophoblast Proliferation Migration Invasion Focal adhesion kinase signaling

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