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  1. Article ; Online: HMGB1 regulates autophagy of placental trophoblast through ERK signaling pathway.

    Li, Ming-Rui / Chen, En-Xiang / Li, Zhuo-Hang / Song, Hong-Lan / Zhang, Yi / Li, Fang-Fang / Xie, You-Long / Tang, Jing / Ding, Yu-Bin / Fu, Li-Juan

    Biology of reproduction

    2024  

    Abstract: Objective: The purpose of this study is to investigate the role of high mobility group protein B1 (HMGB1) in placental development and fetal growth.: Methods: We employed the Cre-loxP recombination system to establish a placenta-specific HMGB1 ... ...

    Abstract Objective: The purpose of this study is to investigate the role of high mobility group protein B1 (HMGB1) in placental development and fetal growth.
    Methods: We employed the Cre-loxP recombination system to establish a placenta-specific HMGB1 knockout mouse model. Breeding HMGB1flox/flox mice with Elf5-Cre mice facilitated the knockout, leveraging Elf5 expression in extra-embryonic ectoderm, ectoplacental cone, and trophoblast giant cells at 12.5 days of embryonic development. The primary goal of this model was to elucidate the molecular mechanism of HMGB1 in placental development, assessing parameters such as placental weight, fetal weight, and bone development. Additionally, we utilized lentiviral interference and overexpression of HMGB1 in human trophoblast cells to further investigate HMGB1's functional role.
    Results: Our findings indicate that HMGB1flox/floxElf5cre/+ mouse display fetal growth restriction (FGR), characterized by decreased placental and fetal weight and impaired bone development. And the absence of HMGB1 inhibits autophagosome formation, impairs lysosomal degradation, and disrupts autophagic flux. Depletion of HMGB1 in human trophoblast cells also suppresses cell viability, proliferation, migration, and invasion by inhibiting the ERK signaling pathway. Overexpression of HMGB1 observed the opposite phenotypes.
    Conclusions: HMGB1 participates in the regulation of autophagy through the ERK signaling pathway and affects placental development.
    Language English
    Publishing date 2024-04-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1118-6
    ISSN 1529-7268 ; 0006-3363
    ISSN (online) 1529-7268
    ISSN 0006-3363
    DOI 10.1093/biolre/ioae064
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 551: Show issues Location:
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  2. Article ; Online: Palmitic acid impairs human and mouse placental function by inhibiting trophoblast autophagy through induction of acyl-coenzyme A-binding protein (ACBP) upregulation.

    Zhang, Yi / Ruan, Ling-Ling / Li, Ming-Rui / Yao, Lu / Li, Fang-Fang / Xie, You-Long / Tang, Jing / Feng, Qian / Chen, Xiao-Yan / Ding, Yu-Bin / Fu, Li-Juan

    Human reproduction (Oxford, England)

    2024  

    Abstract: Study question: Can exposure to palmitic acid (PA), a common saturated fatty acid, modulate autophagy in both human and mouse trophoblast cells through the regulation of acyl-coenzyme A-binding protein (ACBP)?: Summary answer: PA exposure before and ... ...

    Abstract Study question: Can exposure to palmitic acid (PA), a common saturated fatty acid, modulate autophagy in both human and mouse trophoblast cells through the regulation of acyl-coenzyme A-binding protein (ACBP)?
    Summary answer: PA exposure before and during pregnancy impairs placental development through mechanisms involving placental autophagy and ACBP expression.
    What is known already: High-fat diets, including PA, have been implicated in adverse effects on human placental and fetal development. Despite this recognition, the precise molecular mechanisms underlying these effects are not fully understood.
    Study design, size, duration: Extravillous trophoblast (EVT) cell line HTR-8/SVneo and human trophoblast stem cell (hTSC)-derived EVT (hTSCs-EVT) were exposed to PA or vehicle control for 24 h. Female wild-type C57BL/6 mice were divided into PA and control groups (n = 10 per group) and subjected to a 12-week dietary intervention. Afterward, they were mated with male wild-type C57BL/6 mice and euthanized on Day 14 of gestation. Female ACBPflox/flox mice were also randomly assigned to control and PA-exposed groups (each with 10 mice), undergoing the same dietary intervention and mating with ACBPflox/floxELF5-Cre male mice, followed by euthanasia on Day 14 of gestation. The study assessed the effects of PA on mouse embryonic development and placental autophagy. Additionally, the role of ACBP in the pathogenesis of PA-induced placental toxicity was investigated.
    Participants/materials, setting, methods: The findings were validated using real-time PCR, Western blot, immunofluorescence, transmission electron microscopy, and shRNA knockdown approaches.
    Main results and the role of chance: Exposure to PA-upregulated ACBP expression in both human HTR-8/SVneo cells and hTSCs-EVT, as well as in mouse placenta. PA exposure also induced autophagic dysfunction in HTR-8/SVneo cells, hTSCs-EVT, and mouse placenta. Through studies on ACBP placental conditional knockout mice and ACBP knockdown human trophoblast cells, it was revealed that reduced ACBP expression led to trophoblast malfunction and affected the expression of autophagy-related proteins LC3B-II and P62, thereby impacting embryonic development. Conversely, ACBP knockdown partially mitigated PA-induced impairment of placental trophoblast autophagy, observed both in vitro in human trophoblast cells and in vivo in mice.
    Large scale data: N/A.
    Limitations, reasons for caution: Primary EVT cells from early pregnancy are fragile, limiting research use. Maintaining their viability is tough, affecting data reliability. The study lacks depth to explore PA diet cessation effects after 12 weeks. Without follow-up, understanding postdiet impacts on pregnancy stages is incomplete. Placental abnormalities linked to elevated PA diet in embryos lack confirmation due to absence of control groups. Clarifying if issues stem solely from PA exposure is difficult without proper controls.
    Wider implications of the findings: Consuming a high-fat diet before and during pregnancy may result in complications or challenges in successfully carrying the pregnancy to term. It suggests that such dietary habits can have detrimental effects on the health of both the mother and the developing fetus.
    Study funding/competing interest(s): This work was supported in part by the National Natural Science Foundation of China (82171664, 82301909) and the Natural Science Foundation of Chongqing Municipality of China (CSTB2022NS·CQ-LZX0062, cstc2019jcyj-msxmX0749, and cstc2021jcyj-msxmX0236). The authors declare that they have no conflict of interest.
    Trial registration number: N/A.
    Language English
    Publishing date 2024-05-09
    Publishing country England
    Document type Journal Article
    ZDB-ID 632776-x
    ISSN 1460-2350 ; 0268-1161 ; 1477-741X
    ISSN (online) 1460-2350
    ISSN 0268-1161 ; 1477-741X
    DOI 10.1093/humrep/deae091
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.B 2892: Show issues Location:
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  3. Article: [HADHA Inhibits the Migration and Invasion of HTR-8/SVneo Cells by Regulating PI3K/AKT Signaling Pathway].

    Wu, Zhi-Hong / Wang, Yong-Heng / Liu, Tai-Hang / Ruan, Ling-Ling / Xie, You-Long / Li, Fang-Fang / Ding, Yu-Bin

    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition

    2022  Volume 53, Issue 5, Page(s) 805–814

    Abstract: Objective: To explore the effects of hydroxyacyl-CoA dehydrogenase alpha subunit (HADHA) on the migration and invasion of HTR-8/SVneo cells, a human trophoblast cell line, and its potential mechanism of action.: Methods: Immunofluorescence staining ... ...

    Abstract Objective: To explore the effects of hydroxyacyl-CoA dehydrogenase alpha subunit (HADHA) on the migration and invasion of HTR-8/SVneo cells, a human trophoblast cell line, and its potential mechanism of action.
    Methods: Immunofluorescence staining was done to evaluate the expression levels of HADHA in samples of normal villi and recurrent spontaneous abortion (RSA) villi at 6-8 weeks. Lentiviral infection system was used to construct stable HTR-8/SVneo cell lines with
    Results: HADHA was highly expressed in extravillous trophoblasts (EVT) of RSA villus samples as compared with samples from the normal control group. In HTR-8/SVneo cells overexpressing
    Conclusion: HADHA inhibits the migration and invasion of HTR-8/SVneo cells by inhibiting the PI3K/AKT signaling pathway.
    MeSH term(s) Cell Movement/physiology ; Coenzyme A/metabolism ; Coenzyme A/pharmacology ; Female ; HLA-G Antigens/metabolism ; HLA-G Antigens/pharmacology ; Humans ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 9/metabolism ; Mitochondrial Trifunctional Protein, alpha Subunit/metabolism ; Oxidoreductases/metabolism ; Oxidoreductases/pharmacology ; Phosphatidylinositol 3-Kinases/metabolism ; Pre-Eclampsia ; Pregnancy ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Trophoblasts/metabolism
    Chemical Substances HLA-G Antigens ; Oxidoreductases (EC 1.-) ; HADHA protein, human (EC 1.1.1.211) ; Mitochondrial Trifunctional Protein, alpha Subunit (EC 1.1.1.211) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Coenzyme A (SAA04E81UX)
    Language Chinese
    Publishing date 2022-10-12
    Publishing country China
    Document type Journal Article
    ZDB-ID 2106840-9
    ISSN 1672-173X
    ISSN 1672-173X
    DOI 10.12182/20220960301
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.B 2708: Show issues Location:
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  4. Article ; Online: The roles of ADAMDEC1 in trophoblast differentiation during normal pregnancy and preeclampsia.

    Li, Zhuo-Hang / Li, Xia / Li, Fang-Fang / Wu, Zhi-Hong / Xie, You-Long / Zhang, Shuang / Chen, Xue-Mei / Wang, Ying-Xiong / Ding, Yu-Bin / Liu, Tai-Hang

    Molecular human reproduction

    2022  Volume 28, Issue 5

    Abstract: Human cytotrophoblast (CTB) differentiation into syncytiotrophoblast (STB) is essential for placental formation and function. Understanding the molecular mechanisms involved in trophoblast differentiation is necessary as it would help in the development ... ...

    Abstract Human cytotrophoblast (CTB) differentiation into syncytiotrophoblast (STB) is essential for placental formation and function. Understanding the molecular mechanisms involved in trophoblast differentiation is necessary as it would help in the development of novel therapeutic agents to treat placentation-mediated pregnancy complications. In this study, we found a common upregulated gene, ADAM-like Decysin-1 (ADAMDEC1), from five published microarray and RNA-sequencing datasets. Interference to ADAMDEC1 impaired forskolin-induced BeWo cells differentiation, while ADAMDEC1 overexpression promoted BeWo cells and 3D JEG-3 spheroids differentiation. Interestingly, ADAMDEC1 may inhibit Thrombospondin 1 rather than E-cadherin to trigger the activation of the cAMP signal pathway during CTB differentiation into STB. More importantly, a decreasing in ADAMDEC1 might be involved in the development of preeclampsia. Therefore, ADAMDEC1 is expected to become a new target for prediction of and intervention in placenta-derived pregnancy diseases.
    MeSH term(s) Cell Differentiation/genetics ; Cell Line, Tumor ; Female ; Humans ; Placenta ; Placentation/genetics ; Pre-Eclampsia/genetics ; Pre-Eclampsia/metabolism ; Pregnancy ; Trophoblasts/metabolism
    Language English
    Publishing date 2022-05-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1324348-2
    ISSN 1460-2407 ; 1360-9947
    ISSN (online) 1460-2407
    ISSN 1360-9947
    DOI 10.1093/molehr/gaac014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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