Observations on intrauterine oxygen tension measured by fibre-optic microsensors

Ottosen, Lars Ditlev Mørck; Hindkjær, Johnny; Husth, Merete; Petersen, Dorrit Elschner; Kirk, J. E.; Ingerslev, Hans Jakob

doi:10.1016/s1472-6483(10)61443-5

Cited by 83 publications

(47 citation statements)

References 27 publications

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“…The oxygen level in the uterus at the time of implantation is 15-18.9 mm Hg in normal pregnancy (29,30) and the increased number of syncytial knots in the placenta from pregnancies complicated by PE can be replicated in vitro by 1% hypoxia, supporting the idea of 1% hypoxia involvement in the pathogenesis of PE and use in an in vitro trophoblast hypoxia model) (31). PMTs and JEG-3 cells incubated under normoxic conditions (21% O 2 ) served as controls (JEG3 and PMTs have adapted).…”

Section: Hypoxia Of Pmts and Jeg-3 Cellsmentioning

confidence: 99%

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Jiang¹,

Cai

Zhu

et al. 2014

The Journal of Immunology

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High mobility group box 1 (HMGB1) plays an important role in the pathologic processes of endothelial permeability under oxidative stress. Trophoblast oxidative stress has been implicated in the pathophysiology of preeclampsia (PE). HMGB1 serum levels are increased in PE. However, the potential roles of HMGB1 in endothelial permeability in PE remain unclear. We assessed the effects of the hypoxic trophoblast on the permeability of the endothelial monolayer. Our results showed that the hypoxic trophoblast displayed higher HMGB1 mRNA, intracellular HMGB1 protein, and HMGB1 in conditioned medium than those of the normoxic trophoblast did. The hypoxic trophoblast conditioned medium increased the endothelial monolayer permeability and increased TLR 4 and caveolin-1 (CAV-1) protein expression in endothelial cells, which was inhibited by glycyrrhizic acid and HMGB1 small interfering RNA transfection to trophoblasts before hypoxia. The increased endothelial permeability induced by hypoxic trophoblast conditioned medium could be inhibited with TLR4 or CAV-1 gene silencing in endothelial cells. Immunoprecipitation showed that CAV-1 and TLR4 are colocalized in HUVECs and C57BL/6 mouse kidney. TLR4 small interfering RNA suppressed CAV-1 protein expression in endothelial cells upon stimulation of hypoxic trophoblast conditioned medium or HMGB1. We conclude that hypoxic trophoblasts play an important role in the mechanism of general edema (including protein urine) in PE via increasing endothelial monolayer permeability through the HMGB1/TLR4/CAV-1 pathway.

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Section: Hypoxia Of Pmts and Jeg-3 Cellsmentioning

confidence: 99%

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Jiang¹,

Cai

Zhu

et al. 2014

The Journal of Immunology

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“…ES cells are likely to have developed this form of metabolism as an adaptation to the hypoxic in vivo environment of the early embryo [69] . Interestingly, various groups have shown that iPS cell reprogramming is enhanced by hypoxia [70,71] , likely due to the acceleration of this metabolic shift.…”

Section: Bix-01294mentioning

confidence: 99%

Cell signalling pathways underlying induced pluripotent stem cell reprogramming

Hawkins

Joy

McKay

2014

WJSC

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Induced pluripotent stem (iPS) cells, somatic cells reprogrammed to the pluripotent state by forced expression of defined factors, represent a uniquely valuable resource for research and regenerative medicine. However, this methodology remains inefficient due to incomplete mechanistic understanding of the reprogramming process. In recent years, various groups have endeavoured to interrogate the cell signalling that governs the reprogramming process, including LIF/STAT3, BMP, PI3K, FGF2, Wnt, TGFβ and MAPK pathways, with the aim of increasing our understanding and identifying new mechanisms of improving safety, reproducibility and efficiency. This has led to a unified model of reprogramming that consists of 3 stages: initiation, maturation and stabilisation. Initiation of reprogramming occurs in almost all cells that receive the reprogramming transgenes; most commonly Oct4, Sox2, Klf4 and cMyc , and involves a phenotypic mesenchymal-to-epithelial transition. The initiation stage is also characterised by increased proliferation and a metabolic switch from oxidative phosphorylation to glycolysis. The maturation stage is considered the major bottleneck within the process, resulting in very few "stabilisation competent" cells progressing to the final stabilisation phase. To reach this stage in both mouse and human cells, pre-iPS cells must activate endogenous expression of the core circuitry of pluripotency, comprising Oct4, Sox2, and Nanog , and thus reach a state of transgene independence. By the stabilisation stage, iPS cells generally use the same signalling networks that govern pluripotency in embryonic stem cells. These pathways differ between mouse and human cells although recent work has demonstrated that this is context dependent. As iPS cell generation technologies move forward, tools are being developed to interrogate the process in more detail, thus allowing a greater understanding of this intriguing biological phenomenon.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Pluripotency; Reprogramming; Induced pluripotent stem; Cell signalling; Embryonic stem Core tip: Induced pluripotent stem (iPS) cells present great promise, both to research and to medicine. However, we know very little regarding the mechanisms that occur throughout the iPS cell reprogramming process and thus the process remains inefficient. In this review, we discuss the 3 stages of reprogramming, initiation, maturation and stabilisation, and clarify the signalling pathways underlying each phase. We draw together the current knowledge to propose a model for the interactions between the key pathways in iPS cell reprogramming with the aim of illuminating this complex yet fascinating process.Hawkins K, Joy S, McKay T. Cell signalling pathways underlying induced pluripotent stem cell reprogramming. World J Stem Cells

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“…I emailed for more articles. Thirty years after Yedwab's initial description, another report of the uterine O 2 tension in the human was published, and the findings were remarkably similar: 18.9 mmHg or 2.5% [5]. Other mammals, including the rat, hamster, rabbit, and Rhesus monkey likewise have been reported to have uterine O 2 tensions of approximately 2%, as well [4,6].…”

Section: Reading Upmentioning

confidence: 94%

On developing a thesis for Reproductive Endocrinology and Infertility fellowship: a case study of ultra-low (2%) oxygen tension for extended culture of human embryos

Kaser

2017

J Assist Reprod Genet

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Fellows in Reproductive Endocrinology and Infertility training are expected to complete 18 months of clinical, basic, or epidemiological research. The goal of this research is not only to provide the basis for the thesis section of the oral board exam but also to spark interest in reproductive medicine research and to provide the next generation of physician-scientists with a foundational experience in research design and implementation. Incoming fellows often have varying degrees of training in research methodology and, likewise, different career goals. Ideally, selection of a thesis topic and mentor should be geared toward defining an Banswerableq uestion and building a practical skill set for future investigation. This contribution to the JARG Young Investigator's Forum revisits the steps of the scientific method through the lens of one recently graduated fellow and his project aimed to test the hypothesis that Bsequential oxygen exposure (5% from days 1 to 3, then 2% from days 3 to 5) improves blastocyst yield and quality compared to continuous exposure to 5% oxygen among human preimplantation embryos.K

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Observations on intrauterine oxygen tension measured by fibre-optic microsensors

Cited by 83 publications

References 27 publications

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Cell signalling pathways underlying induced pluripotent stem cell reprogramming

On developing a thesis for Reproductive Endocrinology and Infertility fellowship: a case study of ultra-low (2%) oxygen tension for extended culture of human embryos

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