spermine/hypoxia

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Spermine is neuroprotective against anoxia and N-methyl-D-aspartate in hippocampal slices.

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Polyamines were implicated as either neurotoxic or neuroprotective in several models of stroke. Spermine augments the excitotoxicity mediated by the N-methyl-D-aspartate (NMDA) receptor because this receptor is activated at micromolar spermine concentrations. However, at higher concentrations,

Exogenous spermine inhibits the proliferation of human pulmonary artery smooth muscle cells caused by chemically-induced hypoxia via the suppression of the ERK1/2- and PI3K/AKT-associated pathways.

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Pulmonary vascular remodeling is a significant pathological feature of hypoxia-induced pulmonary hypertension (HPH), while pulmonary artery smooth muscle cell (PASMC) proliferation plays a leading role in pulmonary vascular remodeling. Spermine (Sp), a polyamine, plays a critical role in periodic

Spermidine/spermine N(1)-acetyltransferase-1 binds to hypoxia-inducible factor-1alpha (HIF-1alpha) and RACK1 and promotes ubiquitination and degradation of HIF-1alpha.

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Hypoxia-inducible factor-1 (HIF-1) is a master regulator of oxygen homeostasis that controls the expression of genes encoding proteins that play key roles in angiogenesis, erythropoiesis, and glucose/energy metabolism. The stability of the HIF-1alpha subunit is regulated by ubiquitination and

Spermine dependent activation of the N-methyl-D-aspartate receptor and the effect of nitric oxide synthase inhibition during hypoxia in the cerebral cortex of newborn piglets.

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This study tests the hypothesis that brain tissue hypoxia results in modification of spermine-dependent activation of the cerebral N-methyl-D-aspartate (NMDA) receptor ion-channel in newborn piglet brains and that pretreatment with N(omega)-nitro-L-arginine (NNLA), an inhibitor of nitric oxide

Spermine accelerates hypoxia-initiated cancer cell migration.

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Polyamine levels are elevated in the organs and tissues of cancer patients due to increased synthesis and active intercellular transport in cancer cells. Because increased polyamine levels are associated with poor prognosis, the effect of polyamines on the malignant potential of cancer cells was

Exogenous spermine inhibits hypoxia/ischemia-induced myocardial apoptosis via regulation of mitochondrial permeability transition pore and associated pathways.

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Myocardial infarction (MI) is associated with a high mortality rate, which is attributed to the effects of myocyte loss that occurs as a result of ischemia-induced cell death. Very few therapies can effectively prevent or delay the effects of ischemia. Polyamines (PAs) are polycations required for

Regulation of Spermine Oxidase through Hypoxia-Inducible Factor-1α Signaling in Retinal Glial Cells under Hypoxic Conditions

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Purpose: Acrolein, a highly reactive unsaturated aldehyde, is known to facilitate glial cell migration, one of the pathological hallmarks in diabetic retinopathy. However, cellular mechanisms of acrolein generation in retinal glial cells

Spermidine/spermine-N1-acetyltransferase 2 is an essential component of the ubiquitin ligase complex that regulates hypoxia-inducible factor 1alpha.

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Hypoxia-inducible factor 1 (HIF-1) is a heterodimeric transcription factor that functions as a master regulator of oxygen homeostasis. The HIF-1alpha subunit is subjected to O(2)-dependent prolyl hydroxylation leading to ubiquitination by the von Hippel-Lindau protein (VHL)-Elongin C

Hyperglycaemia produced by the polyamines spermine and spermidine.

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1 Intravenous injection of rabbits with the polyamines spermine (10-30 mg/kg) and spermidine (50-90 mg/kg) produced hyperglycaemia.2 Given by intraventricular injection, spermine and spermidine gave rise to hyperglycaemia in doses 250-500 times smaller than those effective intravenously.3

Effects of the polyamine spermine on arterial chemoreception.

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Polyamines modulate many biological functions. Here we report a novel inhibitory modulation by spermine of catecholamine release by the rat carotid body and have identified the molecular mechanism underpinning it. We used molecular (RT-PCR and confocal microscopy) and functional (i.e.,

Acute hypoxia increases ornithine decarboxylase activity and polyamine concentrations in fetal rat brain.

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The cellular responses to hypoxia are poorly understood. To test the hypothesis that ornithine decarboxylase (ODC; L-ornithine carboxy-lyase; EC 4.1.1.17) activity and polyamine concentrations change in response to acute hypoxia, we performed the following studies. Pregnant Sprague-Dawley rats

Spermine attenuates carotid body glomus cell oxygen sensing by inhibiting L-type Ca²(+) channels.

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An increase in intracellular Ca²(+) is crucial to O₂ sensing by the carotid body. Polyamines have been reported to modulate both the extracellular Ca²(+)-sensing receptor (CaR) and voltage-gated Ca²(+) channels in a number of cell types. Using RT-PCR and immunohistochemistry, the predominant

Duplication and diversification of the spermidine/spermine N1-acetyltransferase 1 genes in zebrafish.

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Spermidine/spermine N(1)-acetyltransferase 1 (Ssat1) is a key enzyme in the polyamine interconversion pathway, which maintains polyamine homeostasis. In addition, mammalian Ssat1 is also involved in many physiological and pathological events such as hypoxia, cell migration, and carcinogenesis. Using

[Role of mitochondrial calcium uniporter in myocardial hypoxia/reoxygenation induced injury].

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OBJECTIVE To investigate the role and mechanism of mitochondrial calcium uniporter (MCU) in myocardial hypoxia/reoxygenation injury. METHODS Isolated rat hearts were perfused with Langendorff apparatus. The hypoxia/reoxygenation injury was achieved by ligation of left anterior coronary artery for 30

NMDA receptor modification in the fetal guinea pig brain during hypoxia.

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The effect of maternal hypoxia on the modification of the fetal brain cell membrane N-methyl-D-aspartate (NMDA) receptor and its modulatory sites was investigated. Experiments were conducted in pregnant guinea pigs of 60 days of gestation. Guinea pig fetuses were exposed to maternal hypoxia (FiO2 =

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