Hypoxia is a signal guiding placental development, and molecular mechanisms directing cellular adaptations to low oxygen tension are integral to trophoblast cell differentiation and placentation. Hypoxia can also be used as an experimental tool to investigate regulatory processes controlling hemochorial placentation.

Intrauterine hypoxia (also known as fetal hypoxia) occurs when the fetus is deprived of an adequate supply of oxygen. It may be due to a variety of reasons such as prolapse or occlusion of the umbilical cord, placental infarction, maternal diabetes (prepregnancy or gestational diabetes) and maternal smoking.

These data suggest that PHD3 plays a critical role in maintaining insulin signalling in a prolyl hydroxylase-independent manner, and that loss of PHD3 impairs insulin signalling at the level of IRS tyrosine phosphorylation. PHD3 depletion impairs insulin signalling associated with NF-κB and JNK activation.

Cells exposed to prolonged chronic hypoxia can also acquire genetic instability through decreased translation of DNA repair proteins leading to defective repair in proliferating cells and an increased mutation rate.

HIF/VHL. Hypoxia-inducible factor (HIF) is a sensor of hypoxia and a regulator of the cellular hypoxic response. HIF is a heterodimeric complex comprised of an α-subunit, usually HIF-1α, and a β-subunit, usually the aryl hydrocarbon receptor nuclear translocator (ARNT).

PHD3 regulates glucose metabolism and lactate production in ccRCC. ccRCC has been suggested to rely on altered glucose metabolism [4, 6,7,8].

Hypoxemia (low oxygen in your blood) can cause hypoxia (low oxygen in your tissues) when your blood doesn’t carry enough oxygen to your tissues to meet your body’s needs. The word hypoxia is sometimes used to describe both problems.

It seems that proteins called hypoxia-inducible factors (HIFs) can affect gene expression in low-oxygen conditions. Changes in gene expression can be mediated by a variety of signals emanating from the environment. One such signal is the amount of oxygen in the atmosphere.

Transcriptional Regulation Controls Angiogenesis in Hypoxia During hypoxia, HIF-1 binds the regulatory region of the VEGF gene, inducing its transcription and initiating its expression [12,15,16]. Such endothelial cells ultimately help to form new blood vessels, supplying the given area with oxygenated blood [14].

Keywords: Hypoxia, Hypoxia-inducible factor, Necrotizing enterocolitis, Neonate, retinopathy of prematurity, Prolyl hydroxylase inhibitor, Respiratory distress syndrome Introduction

HIF expression and transcriptional activity are regulated by the oxygen-sensitive prolyl hydroxylases (PHD1-3), but the role of PHDs in neutrophil survival is unclear. We examined PHD expression in human neutrophils and found that PHD3 was strongly induced in response to hypoxia and inflammatory stimuli in vitro and in vivo.

The regulation of neutrophil lifespan by induction of apoptosis is critical for maintaining an effective host response and preventing excessive inflammation. The hypoxia-inducible factor (HIF) oxygen-sensing pathway has a major effect on the susceptibility of neutrophils to apoptosis, with a marked …