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lipoxygenase/hypoxia
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Enzyme 15-lipoxygenase 1 promotes hypoxia-inducible factor 1α turnover and reduces vascular endothelial growth factor expression: implications for angiogenesis.
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Hypoxia-inducible factor 1α (HIF-1α) is the regulatory subunit of the heterodimeric HIF-1 that plays a critical role in transcriptional regulation of genes in angiogenesis and hypoxic adaptation, while fatty acid metabolism mediated by lipoxygenases has been implicated in a variety of pathogeneses,
Influence of hypoxia on 5-lipoxygenase pathway in rat alveolar macrophages.
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The effect of hypoxia was studied on the ionophore A23187-induced leukotriene production by rat alveolar macrophages. The production of LTB4 and LTC4 decreased with reducing oxygenation without change of cell viability. The synthesis of 5-HETE increased during hypoxia and the total production of
15-Lipoxygenase/15-hydroxyeicosanoid and activator protein 1 contribute to hypoxia-induced pulmonary artery smooth muscle cells phenotype alteration.
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We have previously shown that 15-lipoxygenase (15-LOX) and its metabolite 15-hydroxyeicosanoid (15-HETE) play a critical role on hypoxia-triggered pulmonary artery smooth muscle cell (PASMC) phenotype alteration through multifactorial pathways, like extracellular signal-regulated kinase and p38
Expression of 15-lipoxygenases in pulmonary arteries after hypoxia.
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OBJECTIVE
We have previously reported that subacute hypoxia upregulates and activates the steady state expression of pulmonary artery 15-lipoxygenase (15-LOX). However, there are two 15-LOX isoenzymes, 15-LOX-1 and 15-LOX-2, which are expressed in pulmonary arteries that have not been previously
15-Lipoxygenase promotes chronic hypoxia-induced phenotype changes of PASMCs via positive feedback-loop of BMP4.
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Our laboratory has previously demonstrated that 15-lipoxygenase (15-LO)/15-hydroxyeicosatetr-aenoic acid (15-HETE) is involved in hypoxic pulmonary arterial hypertension (PAH). Phenotypical alterations of vascular smooth muscle cells are considered to be an important stage in the development of PAH,
Elk-1-mediated 15-lipoxygenase expression is required for hypoxia-induced pulmonary vascular adventitial fibroblast dynamics.
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15-Lipoxygenase (15-LO) is an important factor in the pathogenesis of pulmonary artery hypertension (PAH). However, the role of 15-LO in the adventitia of the pulmonary arterial wall is unclear. The aim of this study was to explore the role of 15-LO in the modulation of pulmonary adventitial
15-Lipoxygenase-2 is expressed in macrophages in human carotid plaques and regulated by hypoxia-inducible factor-1alpha.
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BACKGROUND
Macrophages are prominent in hypoxic areas of atherosclerotic lesions and their secreted cytokines, growth factors and activity of enzymes are involved in atherogenesis. Previously, we showed that 15-lipoxygenase (LOX)-2 is expressed in human monocyte-derived macrophages and that hypoxia
Adenoviral 15-lipoxygenase-1 gene transfer inhibits hypoxia-induced proliferation of retinal microvascular endothelial cells in vitro.
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OBJECTIVE
To investigate whether 15-Lipoxygenase-1 (15-LOX-1) plays an important role in the regulation of angiogenesis, inhibiting hypoxia-induced proliferation of retinal microvascular endothelial cells (RMVECs) and the underlying mechanism.
METHODS
Primary RMVECs were isolated from the retinas of
[SiRNA-mediated silencing of 5-lipoxygenase gene (ALOX5) reduces necrosis of neonatal cardiomyocytes in anoxia-reoxygenation].
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In experiments on the primary culture of isolated neonatal rat cardiomyocytes it was determined that cardiomyocytes express ALOX5 gene encoding enzyme 5-lipoxygenase. Anoxia-reoxygenation does not affect significantly the expression of 5-lipoxygenase mRNA in cardiomyocytes. Transfection of
15-Lipoxygenase promotes chronic hypoxia-induced pulmonary artery inflammation via positive interaction with nuclear factor-κB.
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OBJECTIVE
Our laboratory has previously demonstrated that 15-lipoxygenase (15-LO)/15-hydroxyeicosatetraenoic acid (15-HETE) is involved in hypoxic pulmonary arterial hypertension. Chronic hypoxia-induced vascular inflammation has been considered as an important stage in the development of pulmonary
Chronic hypoxia activates lung 15-lipoxygenase, which catalyzes production of 15-HETE and enhances constriction in neonatal rabbit pulmonary arteries.
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Hypoxia causes localized pulmonary arterial (PA) constriction to divert blood flow to optimally ventilated regions of the lung. The biochemical mechanisms for this have remained elusive, especially during prolonged exposures to reduced PO2. We have evidence that subacute hypoxia activates
The key role of transforming growth factor-beta receptor I and 15-lipoxygenase in hypoxia-induced proliferation of pulmonary artery smooth muscle cells.
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Our laboratory has proved that 15-hydroxyeicosatetraenoic acid, a product of arachidonic acid catalyzed by 15-lipoxygenase (15-LO), plays a pivotal role in hypoxic pulmonary arterial hypertension. However, the mechanisms of how hypoxia regulates 15-LO expression are still unclear. As the formation
Heme oxygenase-1 induces 15-lipoxygenase expression during hypoxia-induced pulmonary hypertension.
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We previously reported that 15-lipoxygenase (15-LO) induced by hypoxia catalyzed the conversion of arachidonic acid (AA) into 15-hydroxyeicosatetraenoic acid (15-HETE), which plays an essential role in the development of hypoxic pulmonary arterial hypertension (HPH). However, the mechanisms by which
12-Lipoxygenase and the regulation of hypoxia-inducible factor in prostate cancer cells.
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12-Lipoxygenase, an arachidonic acid metabolizing enzyme of the lipoxygenase pathway, has been implicated as a major factor in promoting prostate cancer progression and metastasis. The ability of 12-LOX to aggravate the disease was linked to its proangiogenic role. Recent studies clearly
Chronic hypoxia enhances 15-lipoxygenase-mediated vasorelaxation in rabbit arteries.
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15-Lipoxygenase (15-LO-1) metabolizes arachidonic acid (AA) to 11,12,15-trihydroxyeicosatrienoic acids (THETAs) and 15-hydroxy-11,12-epoxyeicosatrienoic acids (HEETA) that dilate rabbit arteries. Increased endothelial 15-LO-1 expression enhances arterial relaxations to agonists. We tested the effect
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