Disease relevance of Hig1

• Hypoxia-induced VEGF governs both physiological retinal vascular development and pathological retinal neovascularization [1].
• Our results demonstrate that hypoxia-induced pulmonary hypertension is associated with a loss of EDRF activity in pulmonary vessels, with a rapid recovery on return to a normoxic environment [2].
• Hypoxia induced by a low rate of perfusion led to near anoxia confined to centrilobular regions of the liver lobule [3].
• Chronic hypoxia induced the expression and accumulation of BNIP3 mRNA and protein in cardiac myocytes, but acidosis was required to activate the death pathway [4].
• Enhanced sensitivity to hypoxia-induced diastolic dysfunction in pressure-overload left ventricular hypertrophy in the rat: role of high-energy phosphate depletion [5].

Psychiatry related information on Hig1

• Hypoxia-induced amnesia, as assessed with active and passive avoidance behavior tests, was reversed in rats treated with 5 or 10 mg/kg of the drug [6].
• We speculate that NOS-mediated mechanisms may play an important role in hypoxia-induced ventilatory roll-off during wakefulness [7].
• Hypoxia-induced impaired conditioned avoidance learning was improved by ganglioside treatment [8].

High impact information on Hig1

• Prevention of hypoxia-induced cell death by Bcl-2 and Bcl-xL [9].
• The hypoxia-induced shift of PKC delta to the soluble compartment does not prevent subsequent 4-beta phorbol 12-myristate-13-acetate-dependent translocation/activation of PKC delta [10].
• These results suggest that the intracellular signaling pathways activated by p53 might play a critical role in the regulation of hypoxia-induced apoptosis of cardiomyocytes [11].
• Hypoxia-induced exocytosis of endothelial cell Weibel-Palade bodies. A mechanism for rapid neutrophil recruitment after cardiac preservation [12].
• Angiotensin converting enzyme expression is increased in small pulmonary arteries of rats with hypoxia-induced pulmonary hypertension [13].

Chemical compound and disease context of Hig1

• -The increased delivery of serotonin (5-hydroxytryptamine, 5-HT) to the lung aggravates the development of hypoxia-induced pulmonary hypertension in rats, possibly through stimulation of the proliferation of pulmonary artery smooth muscle cells (PA-SMCs) [14].
• Allopurinol (0.2 to 5 mM) delayed the release of lactate dehydrogenase during low-flow hypoxia in a dose-dependent fashion (e.g., 5 mM allopurinol delayed hypoxia-induced lactate dehydrogenase release by about 30 min).(ABSTRACT TRUNCATED AT 250 WORDS)[15]
• Resistance to hypoxia, hypoxia-generated interstitial acidification, and hypoxia-induced electrophysiological damage were absent after pharmacological inhibition of nerve glycolysis with iodoacetate [16].
• Hypoxia-induced transcriptional activation and increased mRNA stability of vascular endothelial growth factor in C6 glioma cells [17].
• This suggests that the modulation of glucose transport and glycolysis by hypoxia may contribute to the development of hypoxia-induced tolerance [18].

Biological context of Hig1

• Measurements of the membrane potentials of intact mitochondria in PC12 cells and of isolated rat liver mitochondria showed that hypoxia induced depolarization of the mitochondrial membrane [19].
• Adenovirus-mediated overexpression of MSRA significantly diminished the hypoxia-induced increase in ROS and facilitated cell survival [19].
• Hypoxia-induced coronary vasodilation as assessed by the change in coronary vascular resistance was similar in the hypertrophied and control hearts (2.9 +/- 0.5 vs. 2.3 +/- 0.9 mm Hg/[(ml/min)/g], NS) [20].
• To investigate the relation between hypoxia-induced vasodilation and smooth muscle oxidative phosphorylation, we monitored changes in arteriolar levels of reduced NADH during exposure to hypoxia [21].
• RNA interference experiments indicate that endogenous Gene 33 reduces Akt and ERK signaling and is required for maximal hypoxia-induced cardiomyocyte death [22].

Anatomical context of Hig1

• In this paper we describe the cloning and characterization of the rat hypoxia induced gene-1 (Hig-1), its expression pattern during spinal cord maturation and in situ localization of its mRNA [23].
• Characterization of hypoxia induced gene 1: expression during rat central nervous system maturation and evidence of antisense RNA expression [23].
• p53 and the hypoxia-induced apoptosis of cultured neonatal rat cardiac myocytes [11].
• To assess the metabolic recovery of mitochondria after injury, we have monitored, in vivo and noninvasively, changes in the redox state of cytochrome (cyt) a,a3 in 35 rats after tissue hypoxia induced by rapid exsanguination to a mean arterial pressure of 30-35 mmHg [24].
• To further investigate the involvement of H2O2 in hypoxia-induced liver cell apoptosis, small pieces of liver in the cultured media were exposed to 0.5 mmol/L of reagent H2O2 and stained with the TUNEL method [25].

Associations of Hig1 with chemical compounds

• Dexamethasone (0.5 or 0.05 mg/kg per 12 h) started 12 h before and continued during 48 h of altitude exposure prevented the hypoxia-induced increases in transvascular protein escape and lung water [26].
• Since prostaglandin E1 has no oxyradical-scavenging action, the preventive effect of this reagent on the hypoxia-induced oxidative cell injury is attributable to the attenuation of mitochondrial dysfunction [27].
• Hypoxia induced the expression of nitric oxide (NO) synthase, and the inactivation of methionine adenosyltransferase was prevented by the NO synthase inhibitor N(G)-monomethyl-L-arginine methyl ester [28].
• We also imaged hyperoxia- and hypoxia-induced cerebral hemodynamic changes [29].
• The role of cysteine proteases in hypoxia-induced rat renal proximal tubular injury [30].

Physical interactions of Hig1

• As a possible mechanism of this synergistic action on CAM expression, hypoxia induced a time-dependent increase in the DNA binding activity of both NF-kappaB and activator protein-1 (AP-1), two transcription factors important for cell adhesion molecule expression [31].
• CONCLUSION: The rapid enhancement in CXCR4 chemokine receptor binding in the affected brain areas suggests that SDF-1 alpha/CXCR4 may play a role in the hypoxia-induced inflammatory reaction in the neonatal brain [32].
• Hypoxia-induced protein binding to O2-responsive sequences on the tyrosine hydroxylase gene [33].
• Blocade of NMDA receptor-channel complex by MK-801 was not sufficient to prevent hypoxia-induced neuronal damage [34].

Enzymatic interactions of Hig1

• In addition, studies with rat primary-cultured cardiomyocytes demonstrated that acetylcholine effectively prevented the hypoxia-induced loss of phosphorylated Cx43 and ameliorated the loss of cell-to-cell communication as determined by Lucifer Yellow dye transfer assay, which supports the in vivo results [35].

Regulatory relationships of Hig1

• Hypoxia-induced ischemic tolerance in neonatal rat brain involves enhanced ERK1/2 signaling [36].
• Finally, they suggest that protein kinase C may prime hypoxia induced gene regulation by inducing expression of HIF-1 alpha mRNAs [37].
• The p38 stress-activated kinase inhibitor SB203580 was the most potent in suppressing hypoxia-induced HO-1 [38].
• VEGF and VEGF receptor expression are upregulated by hypoxia in vivo and the role of VEGF in hypoxia-induced angiogenesis has been extensively studied in a variety of disease entities [39].
• In this study, we examined whether hypoxia induces hypertrophy of cardiomyocytes in vitro and whether hypoxia-induced hypertrophy is inhibited by an endothelin A receptor antagonist (BQ123) [40].

Other interactions of Hig1

• We further show that hypoxia-induced trans-activation of EPAS1 is independent of Ras [41].
• These findings suggest that activation of ERK1/2 signaling may contribute to hypoxia-induced tolerance in neonatal rat brain in part by preserving vascular and white matter integrity after HI [36].
• MK-801 attenuated hypoxia-induced SEK1, SAPK/JNK-2, and AP-1 binding in the nucleus tractus solitarii, and the widespread activation of all MAP kinases in the cortex was also attenuated [42].
• These data suggest that a product of HO activity, most likely CO, inhibits hypoxia-induced pulmonary vasoconstriction by reducing ET-1 vascular levels and sensitivity [43].
• Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) have previously been shown to ameliorate ethanol-, hypoglycemia- and hypoxia-induced neurotoxicity [44].

Analytical, diagnostic and therapeutic context of Hig1

• To study the dynamics and spatial heterogeneity of hypoxia-inducible factor-1 (HIF-1)-specific transcriptional activity in tumors, we used repetitive noninvasive positron emission tomography (PET) imaging of hypoxia-induced HIF-1 transcriptional activity in tumors in living mice [45].
• The severity of hypoxia-induced epileptiform EEG changes was highest in the animals subjected to moderately hypoxic conditions (3% and 4% oxygen) at postnatal days 10 to 12 [46].
• Gel shift analysis of this 14-bp region confirms a hypoxia-induced shift independent of direct hypoxia-inducible factor binding [47].
• Hypoxia-induced gene expression in human macrophages: implications for ischemic tissues and hypoxia-regulated gene therapy [48].
• Hypoxia-induced regulation of MAPK phosphatase-1 as identified by subtractive suppression hybridization and cDNA microarray analysis [49].

References