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Search results for: Human Uterine Microvascular Endothelial Cells

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#32468067   2020/05/27 To Up

Angiopoietin-2 regulated by progesterone induces uterine vascular remodeling during pregnancy.

During pregnancy, the uterus undergoes intense neovascularization and vascular remodeling to supply oxygen and nutrients to the embryo. During this period, progesterone secreted from the ovary has effects on vascular remodeling in the endometrium and interacts with angiogenic factors. However, the exact mechanism of uterine vascular remodeling during pregnancy is poorly understood. Therefore, the aim of the present study was to investigate the association between angiopoietin-2 (Ang-2), one of the angiopoietins, and intrauterine vessel remodeling during pregnancy, and to determine the effect of progesterone on Ang-2 levels. Changes in Ang-2 expression were observed according to quantitative modification of progesterone using pregnant mice and human uterine microvascular endothelial cells. As a result, Ang-2 was observed mainly in the mesometrial region (MR) of the uterus during the period between implantation and placentation. Furthermore, a substantial amount of Ang-2 also appeared in endothelial cells, particularly of the venous sinus region (VSR). Interestingly, Ang-2 expression was increased by progesterone, whereas estrogen had limited effects. To confirm the association between Ang-2 and progesterone, the function of the progesterone receptor (PR) was inhibited using RU486, a blocker of PR. Ang-2 expression and vascular remodeling of the VSR in the uterus were decreased when the functions of progesterone were inhibited. Overall, the regulation of Ang-2 by progesterone/PR was associated with vascular remodeling in the VSR during pregnancy. The present study proposed a solution to prevent pregnancy failure due to a lack of vascularity in the uterus in advance.
Yang-Gyu Park, Jawun Choi, Jae-Won Seol

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#32253734   2020/04/06 To Up

Galectin-1-Related Modulation of Trophoblast Endothelial Interactions by Integrins α1 and β1.

During normal trophoblast invasion, integrins α6β4 are downregulated, and α1β1 are upregulated in invasive cytotrophoblast cells. In preeclampsia both interstitial and endovascular invasion are shallow and cytotrophoblasts fail to upregulate α1β1 and downregulate α6β4. This study aims to investigate the role of integrins α1β1 and α6β4 on cellular pathways influencing trophoblast integration into endothelial cellular networks in vitro. Red fluorescent-labeled human uterine myometrial microvascular endothelial cells (UtMVECs) were seeded on Matrigel to form endothelial networks. Green fluorescent-labeled trophoblastic HTR-8/SVneo cells pre-incubated with 20 μg/ml of neutralizing antibodies (anti-α1, β1, α6, β4, α1 + β1, or α6 + β4) for 1 h were then co-cultured with endothelial networks with the neutralizing antibodies for 24 h. Fluorescent images were captured, and quantified utilizing Image J. Cells were retrieved to analyze mRNA expression of galectin-1, TIMP-1, and PAI-1 by quantitative PCR. MMP-2, MMP-9, free sFlt-1, and PlGF from conditioned media were measured by ELISA. The integration of trophoblast cells into endothelial cellular networks was inhibited by anti-β1(- 28 ± 3%, p < 0.0001), and increased by anti-α6(+ 19 ± 5%, p < 0.01). Galectin-1 mRNA expression was decreased by anti-α1(- 35 ± 7%, p < 0.001), anti-β1(- 23 ± 5%, p < 0.05), and anti-α1+β1(- 35 ± 5%, p < 0.001). The mRNA expression of TIMP-1 was inhibited by anti-α1(- 59 ± 9%, p < 0.01) and anti-β1(- 63 ± 7%, p < 0.001) while PAI-1 mRNA expression was increased by anti-α1 + β1(+ 285 ± 70%, p < 0.0001). In the conditioned medium, anti-α1 reduced MMP-2(-28 ± 1%, p < 0.001), MMP-9(-27 ± 8%, p < 0.01), and sFlt-1(-27 ± 5%, p < 0.001) production. Anti-β1 reduced MMP-2(- 15 ± 2%, p < 0.05) production. There were no changes in PlGF. Appropriate integrins α1β1 modulate trophoblast cell integration into endothelial cellular networks in vitro through invasive pathways including galectin-1, TIMP-1, PAI-1, MMP-2, and MMP-9 production.
Bei Xu, Renuka Shanmugalingam, Katrina Chau, Angela Makris, Annemarie Hennessy

1304 related Products with: Galectin-1-Related Modulation of Trophoblast Endothelial Interactions by Integrins α1 and β1.

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#32199147   2020/03/04 To Up

Pravastatin as the statin of choice for reducing pre-eclampsia-associated endothelial dysfunction.

There is avid interest in pravastatin as a therapeutic intervention for pre-eclampsia, however little is known on statin action on endothelial dysfunction. This study aimed to evaluate the ability of pravastatin, simvastatin and rosuvastatin to reduce pre-eclampsia-associated markers of endothelial dysfunction in human endothelial cells.
Natasha de Alwis, Sally Beard, Yeukai T Mangwiro, Natalie K Binder, Tu'uhevaha J Kaitu'u-Lino, Fiona C Brownfoot, Stephen Tong, Natalie J Hannan

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#32016802   2020/02/03 To Up

Effect of Placental Growth Factor on Trophoblast-Endothelial Cell Interactions In Vitro.

Placental growth factor (PlGF) is an important angiogenic factor which has an emerging role in the clinical management of suspected preeclampsia. The role of PlGF in normal placental development is not completely understood and it is uncertain whether PlGF influences trophoblast and endothelial cell interactions central to uterine spiral artery remodelling, especially in variable oxygen conditions. A two-cell model of endovascular invasion was used. Tissue culture plates were coated with Matrigel™, on which fluorescent-labelled uterine microvascular endothelial cells (1 × 10/well) and HTR8/SVNeo cells were co-cultured (1 × 10/well) for 20 h. Co-cultures were treated with recombinant human PlGF (rhPlGF) (10 or 100 ng/mL) and incubated at either 21% O or 2% O. Images were captured by fluorescence microscopy and analysed using ImageJ (n = 7). Data was analysed using SPSSv24. Treatment with rhPlGF did not improve integration in co-cultures irrespective of oxygen conditions but increased proliferation in 2% O of both trophoblast and endothelial cells. Expression of angiogenic factors VEGF, sFLT-1, PlGF and CXCL12 in both co-cultures and in isolated trophoblast cells was not altered by rhPlGF treatment. Expression of TLR-3 mRNA in co-cultures was increased by rhPlGF 100 ng/mL at 21% O (p = 0.03). PlGF contributes to trophoblast and endothelial cell proliferation in the setting of physiological hypoxia but does not influence trophoblast and endothelial cell interactions in an in vitro model of spiral artery remodelling. Upregulation of TLR-3 expression in co-cultures may indicate a role for PlGF in the placental inflammatory response.
K Chau, B Xu, A Hennessy, A Makris

2966 related Products with: Effect of Placental Growth Factor on Trophoblast-Endothelial Cell Interactions In Vitro.

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#31982836   2020/01/14 To Up

Calcium deficient placental growth restriction is mediated by an increase in non-invasive integrin α5 and β4 phenotype.

Integrins are cell adhesion receptors that participated in endovascular invasion by cytotrophoblasts in preeclampsia. This study aimed to investigate the effect of calcium on cellular pathways influencing the trophoblast integration into endothelial cellular networks in vitro.
Bei Xu, Angela Makris, Chia-Chi Liu, Annemarie Hennessy

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#31452230   2019/10/07 To Up

Effect of placental growth factor in models of experimental pre-eclampsia and trophoblast invasion.

Placental growth factor (PlGF) is decreased in early gestation of pregnant women who subsequently develop pre-eclampsia. In this study, pre-emptive treatment with PlGF to prevent pre-eclampsia was evaluated in an in vivo rodent model of experimental pre-eclampsia (EPE) induced by TNF-α and in an in vitro model of human first-trimester trophoblast invasion. Pregnant C57/BL6 mice were treated with recombinant mouse placental growth factor-2 (rmPlGF-2) 100 μg/kg/day IP from gestational day (gd) 10. Animals had EPE induced by continuous TNF-α infusion on gd 13 and were subject to either continuous blood pressure monitoring by radiotelemetry throughout pregnancy or live placenta T -weighted magnetic resonance imaging (MRI) to demonstrate placental function on gd 17. There was no difference in BP (P > .99), proteinuria (P = .9) or T values on MRI (P = .9) between control and rmPlGF-2-treated animals. On gd 13, animals treated with rmPlGF-2 demonstrated increased placenta PlGF (P = .01) and Toll-like receptor-3 (P = .03) mRNA expression as compared with controls. Fluorescent-labelled human uterine microvascular endothelial cells and HTR8/SVNeo cells were co-cultured on Matrigel and treated with recombinant human PlGF (rhPlGF) (10 ng/mL) and/or TNF-α (0.5 ng/mL). Trophoblast integration into endothelial networks was reduced by added TNF-α (P = .006), as was rhPlGF concentration in conditioned media (P < .0001). Cell integration was not ameliorated by addition of rhPlGF (P > .9). Although TNF-α-induced EPE was not reversed with pre-emptive rmPlGF-2, a further trial of pre-emptive rhPlGF in vivo is required to determine whether the absence of effect of rhPlGF demonstrated in vitro precludes PlGF as a preventative therapy for pre-eclampsia.
Katrina Chau, Gabriele Bobek, Bei Xu, Timothy Stait-Gardner, William Price, Annemarie Hennessy, Angela Makris

2852 related Products with: Effect of placental growth factor in models of experimental pre-eclampsia and trophoblast invasion.

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#30993566   2019/04/15 To Up

Cancer-derived exosomal miR-221-3p promotes angiogenesis by targeting THBS2 in cervical squamous cell carcinoma.

Recently, cancer-derived exosomes were shown to have pro-metastasis function in cancer, but the mechanism remains unclear. Angiogenesis is essential for tumor progression and is a great promising therapeutic target for advanced cervical cancer. Here, we investigated the role of cervical cancer cell-secreted exosomal miR-221-3p in tumor angiogenesis.
Xiang-Guang Wu, Chen-Fei Zhou, Yan-Mei Zhang, Rui-Ming Yan, Wen-Fei Wei, Xiao-Jing Chen, Hong-Yan Yi, Luo-Jiao Liang, Liang-Sheng Fan, Li Liang, Sha Wu, Wei Wang

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#30935090   2019/03/31 To Up

Transcriptomics and Immunological Analyses Reveal a Pro-Angiogenic and Anti-Inflammatory Phenotype for Decidual Endothelial Cells.

In pregnancy, excessive inflammation and break down of immunologic tolerance can contribute to miscarriage. Endothelial cells (ECs) are able to orchestrate the inflammatory processes by secreting pro-inflammatory mediators and bactericidal factors by modulating leakiness and leukocyte trafficking, via the expression of adhesion molecules and chemokines. The aim of this study was to analyse the differences in the phenotype between microvascular ECs isolated from decidua (DECs) and ECs isolated from human skin (ADMECs).
Chiara Agostinis, Elisa Masat, Fleur Bossi, Giuseppe Ricci, Renzo Menegazzi, Letizia Lombardelli, Gabriella Zito, Alessandro Mangogna, Massimo Degan, Valter Gattei, Marie-Pierre Piccinni, Uday Kishore, Roberta Bulla

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#30789661   // To Up

Hemodynamic forces enhance decidualization via endothelial-derived prostaglandin E2 and prostacyclin in a microfluidic model of the human endometrium.

Does the uterine vasculature play a localized role in promoting stromal cell decidualization in the human endometrium?
Juan S Gnecco, Tianbing Ding, Caroline Smith, Jacky Lu, Kaylon L Bruner-Tran, Kevin G Osteen

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#30084973   // To Up

Electroacupuncture facilitates implantation by enhancing endometrial angiogenesis in a rat model of ovarian hyperstimulation.

Controlled ovarian hyperstimulation (COH) impairs the synchronized development of endometrium and embryo, resulting in the failure of embryo implantation. Here, we investigated what effects electroacupuncture had on embryo implantation in COH rats. Female rats were randomly assigned to four groups: normal (N), model (M), electroacupuncture (EA), and electroacupuncture pretreatment (PEA). Rats in groups M, EA, PEA were injected with pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin to establish the COH model. Rats in group EA received electroacupuncture treatment from the PMSG injection day to the 3rd day of pregnancy (D3), while those in group PEA received electroacupuncture treatment for 3 days before the PMSG day and continuing to D3. Furthermore, another 30 female rats who received the same treatment as the rats in group PEA were injected with siVEGFR2 into uterine lumen. The endometrial microvascular density (MVD) and the expression levels of vascular endothelial growth factor-A, angiopoietin-1, and fibroblast growth factor-2 were significantly lower in groups M than in groups N and PEA. The percentage of dolichos biflorus agglutinin positive uterine natural killer cells in groups N, EA and PEA was higher than that in group M. After the siVEGFR2 injection, the protein expression levels of vascular endothelial growth factor receptor 2 (VEGFR2), PI3K, p-AKT and p-ERK, the embryo number and the MVD were significantly reduced. In conclusion, electroacupuncture can facilitate embryo implantation in COH rats by activating the VEGFR2/PI3K/AKT and VEGFR2/ERK signaling pathways which have a positive relationship with endometrial angiogenesis.
Wei Chen, Jie Chen, Menghao Xu, Zhiyan Zhong, Qing Zhang, Wei Yang, Guangying Huang

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