Only in Titles

           Search results for: Human Uterine Microvascular Endothelial Cells   

paperclip

#31452230   // Save this 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.

2979 related Products with: Effect of placental growth factor in models of experimental pre-eclampsia and trophoblast invasion.

Rat monoclonal anti mouse Mouse Anti-Insulin-Like G Rat monoclonal anti mouse Human Insulin-like Growth Mouse Insulin-like Growth Human Insulin-like Growth Growth Factor (Human) Ant Rat monoclonal anti mouse IGF1, Insulin-like growth Rat monoclonal anti mouse Hamster anti mouse Insuli Goat Anti-Human Fibroblas

Related Pathways

paperclip

#30935090   // Save this 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).

2392 related Products with: Transcriptomics and Immunological Analyses Reveal a Pro-Angiogenic and Anti-Inflammatory Phenotype for Decidual Endothelial Cells.

Rabbit Anti-Human Androge Anti Androgen Receptor pr Rabbit Anti-Human Androge Mouse Anti-Human Endothel Rabbit Anti-Rat Androgen Goat Anti-Human Androgen Mouse Anti-Pig Endothelia Anti-Androgen Receptor pr Rat Anti-Human Endothelia Rabbit anti Androgen Rece Rabbit Anti-Human Androge Mouse Anti-Human Endothel

Related Pathways

paperclip

#30789661   // Save this 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?

1552 related Products with: Hemodynamic forces enhance decidualization via endothelial-derived prostaglandin E2 and prostacyclin in a microfluidic model of the human endometrium.

GFP Expressing Human Inte Goat Anti-Human EP4 prost Goat Anti-Human Endotheli Human Internal Mammary Ar Goat Anti-Human E2F7, (in Goat Anti-Human GCDFP15 P Goat Anti-Human TCL1A, (i Goat Anti-Human VPS41, (i Goat Anti-Human CACNB4 (i Mouse Anti-Human CD103 (I Beta Amyloid (1 40) ELISA Angiogenesis (Human) Anti

Related Pathways

paperclip

#30084973   // Save this 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.

2412 related Products with: Electroacupuncture facilitates implantation by enhancing endometrial angiogenesis in a rat model of ovarian hyperstimulation.

Angiogenesis (Human) Anti Ovarian cancer tissue arr Multiple ovarian cancer t Angiogenesis (Human) Anti Uterus cancer test tissue High density ovarian canc Angiogenesis (Mouse) Anti Endometrial cancer tissue Brain Specific Angiogenes Ovary disease spectrum (o Ovarian cancer tissue arr Angiogenesis (Mouse) Anti

Related Pathways

paperclip

#29452694   // Save this To Up

Chitinase 3 like 1 (CHI3L1) promotes vasculogenic mimicry formation in cervical cancer.

Vasculogenic mimicry (VM) is an alternative microvascular system which tumour cells orchestrate, independent of endothelial cell-mediated angiogenesis. VM develops tumour vascular networks that correlate with tumour growth, metastasis, and short survival time of patients with a number of cancers. However, little is known regarding VM in the vascularisation of cervical cancer. Chitinase 3 like 1 (CHI3L1) has been previously reported to display the ability to induce angiogenesis in cervical cancer. Here, we explored a pathological role of CHI3L1 in tumour cell-mediated vascularisation. Sixty-six samples of cervical cancer were collected to examine CHI3L1 expression and VM formation using immunohistochemistry and CD34-periodic acid-Schiff (PAS) dual staining. CHI3L1 expression was significantly correlated with formation of tumour cell-associated vascular channels in the absence of endothelial cells (p=0.031). Interestingly, tumour samples lacking VM were positively correlated with non-metastasis (p=0.035). Patients with VM positive tumours tended to have decreased overall survival (OS) compared to those with VM negative samples (43.9 versus 64.6 months, p=0.079). In addition, recombinant CHI3L1 enhanced cervical cancer cell lines to form tube-like structures, supporting the notion that CHI3L1 mediates VM in cervical cancer. Our present data reveal the crucial role of CHI3L1 in the formation of VM, which may contribute to tumour aggressiveness. Therefore, targeting CHI3L1 may be a valuable strategy for the reduction of cervical cancer vascularisation and metastasis.

1133 related Products with: Chitinase 3 like 1 (CHI3L1) promotes vasculogenic mimicry formation in cervical cancer.

Cervical cancer tissue ar Cervical cancer tissue ar Uterine cervical cancer t Uterine cervical cancer a Cervical cancer test tiss Cervical cancer tissue ar High density cervical can ASP-3026 Mechanisms: ALK Cervical cancer survey ti Tissue array of uterine c Rabbit Anti-SLC25A6 Polyc Liver cancer tissue array

Related Pathways

paperclip

#29360423   // Save this To Up

Efficacy for lung metastasis induced by the allogeneic bEnd3 vaccine in mice.

The mouse brain microvascular endothelial cell line bEnd.3 was used to develop a vaccine and its anti-tumor effect on lung metastases was observed in immunized mice.

2771 related Products with: Efficacy for lung metastasis induced by the allogeneic bEnd3 vaccine in mice.

Multiple lung carcinoma ( Lung carcinoma and normal Lung cancer and adjacent Lung cancer test tissue a Colon cancer tissue array Non-small cell lung cance Lung cancer tissue array, (7’-Benzyloxy-indolymet Lung cancer tissue array High density (208 cores), FDA Standard Frozen Tissu Jurkat Cell Extract (Indu

Related Pathways

paperclip

#29334762   // Save this To Up

Altered Redox State Modulates Endothelial K2.3 and K3.1 Levels in Normal Pregnancy and Preeclampsia.

Altered redox state has been related to the development of normal pregnancy (NP) and preeclampsia (PE). Endothelial K2.3 and K3.1 (Ks) play an important role in vasodilation, and Ks levels are affected by oxidative stress. We investigated the mechanisms of oxidative stress-mediated Ks expression modulation during NP and PE.

2495 related Products with: Altered Redox State Modulates Endothelial K2.3 and K3.1 Levels in Normal Pregnancy and Preeclampsia.

Rabbit Anti-Human Androge Androgen Receptor (Ab 650 Androgen Receptor , Mouse Androgen Receptor Androsta-3,5,16-trien-17- Androgen Receptor (Phosph Androstane 3a, 17b diol 5 3β-O-Acetyl-androsta-5,1 5α-Androstan-3β-ol � ASP-3026 Mechanisms: ALK Androgen Receptor Antibod ∆1-Androstene-3α,17β-

Related Pathways

paperclip

#29329415   // Save this To Up

Establishment of a three-dimensional model to study human uterine angiogenesis.

Can primary human uterine microvascular endothelial cells (UtMVECs) be used as a model to study uterine angiogenic responses in vitro that are relevant in pregnancy?

1014 related Products with: Establishment of a three-dimensional model to study human uterine angiogenesis.

Angiogenesis (Human) Quan Human Antithrombin III to Angiogenesis (Human) Anti Human Angiogenesis Array Goat Anti-Human TOM1L2, ( Human Angiogenesis Array Recombinant Human Interfe Goat Anti-Human TEM8 Anth Rabbit Anti-Human TOSO (C In vitro Human Glomerular Hsp90 total Monoclonals A Rabbit Anti-Human Toll In

Related Pathways

paperclip

#29136193   // Save this To Up

Early first trimester uteroplacental flow and the progressive disintegration of spiral artery plugs: new insights from contrast-enhanced ultrasound and tissue histopathology.

Does the use of a vascular contrast agent facilitate earlier detection of maternal flow to the placental intervillous space (IVS) in the first trimester of pregnancy?

1367 related Products with: Early first trimester uteroplacental flow and the progressive disintegration of spiral artery plugs: new insights from contrast-enhanced ultrasound and tissue histopathology.

FDA Standard Frozen Tissu Androgen Receptor Androgen Receptor (Phosph Androgen Receptor , Mouse (5α,16β)-N-Acetyl-16-[2 (5α)-Androst-2-en-17-one Normal rat multiple organ 1,4 Androstadiene 3,17 di ELISA 5α-Androstane-3α, ∆1-Androstene-3α,17β- Androstenedione-19 Antibo FDA Standard Frozen Tissu

Related Pathways

  •  
  • No related Items
paperclip

#29055792   // Save this To Up

The effect of acetyl salicylic acid (Aspirin) on trophoblast-endothelial interaction in vitro.

Early administration of low dose acetyl salicylic acid (Aspirin) in high risk women reduces the risk of early onset preeclampsia. This study aims to investigate the effect of aspirin on trophoblast integration and the its effect on angiogenic and invasive pathways in an in-vitro model of preeclampsia. 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 were co-cultured with the endothelial networks with/without TNF-a (0.5ng/mL) and/or aspirin (0.1mM) for 24h. Fluorescent images were captured and quantified by Image J to examine the effects of TNF-a and aspirin on the trophoblast-endothelial integration. Conditioned media were collected to measure free VEGF, PlGF and sFlt-1 by ELISA and PGF1a by Enzyme immunoassay (EIA). Cells were retrieved to examine mRNA expression of angiogenic factors (VEGF, PlGF and sFlt-1), invasion markers (MMP-2 and TIMP-1), endothelial cell activation markers (E-selectin and VCAM), eNOS and cyclooxygenase (COX)-2 by quantitative PCR. Aspirin reversed the inhibitory effect of TNF-a on trophoblast cell integration into endothelial cellular networks. TNF-a increased PGF1a production (128±11%, p<0.05), whilst aspirin reversed the TNF-a effect on PGF1a production (19±4%, p<0.01). TNF-a decreased the mRNA expression of PlGF, eNOS, MMP-2 and TIMP-1, and stimulated COX2, E-selectin and VCAM mRNA expression. Aspirin did not reverse the TNF-a effect on these molecules. Aspirin improves trophoblast cell integration into endothelial cellular networks by inhibiting the effect of TNF-a via PGI with no significant effect on antiangiogenic, invasive or endothelial activation markers.

1165 related Products with: The effect of acetyl salicylic acid (Aspirin) on trophoblast-endothelial interaction in vitro.

Cultrex In Vitro Angiogen N-Acetyl-2-O-(5-bromo-1H- Anti-Conjugated Acetyl Sa BID & BAX Protein Protein TNFRSF1A & HSA Protein Pr 4-Acetylamino-2,6-anhydro 3-Acetylthio-2-methylprop MAPK3 & DAPK1 Protein Pro BIRC3 & TRAF2 Protein Pro HNF4A & FOXO1 Protein Pro Rabbit Anti-IAA (Indole-3 AKT1 & MAPKAPK2 Protein P

Related Pathways