Disease relevance of Cell Hypoxia

• Both ouabain and furosemide attenuated ATP depletion and resulted in higher AEC while acidosis had no effect on these indices of cellular hypoxia [1].
• Moreover, in an in vitro model of cellular hypoxia, BHDP prevented the fall in adenosine triphosphate (ATP) levels caused by 24 h hypoxia in cultured astrocytes [2].
• CONCLUSIONS: Our data demonstrate in a rat model of endotoxemia that epinephrine-induced hyperlactatemia is not related to cellular hypoxia [3].
• BACKGROUND: Hypoxia-inducible factor 1 alpha (HIF-1alpha) is a transcription factor that may play an important role in tumour growth and metastasis by its regulation of angiogenesis and lymphangiogenesis to survive cellular hypoxia [4].
• In peripheral vascular disease, impaired muscle energy metabolism is assumed to be due mainly to defective vascular O2 supply, the resulting cellular hypoxia inhibiting oxidative ATP synthesis [5].

High impact information on Cell Hypoxia

• Results of our studies on rat muscle, liver, heart, brain, and plasma suggest that there is no evidence of bioenergetic failure in these septic tissues and that the increase in lactate production is not necessarily due to cellular hypoxia [6].
• Misonidazole binding in murine liver tissue: a marker for cellular hypoxia in vivo [7].
• An increased apoptotic index of tumor cells in endostatin-treated tumors [3.2 +/- 0.5% versus 1.9 +/- 0.3% (P < 0.05)] was observed in conjunction with a significant decrease in tumor perfused vessels (DiOC7 staining), and an increase in tumor cell hypoxia (EF5 staining) [8].
• S-Nitroso-N-acetyl-D, L-penicillamine (SNAP), a nitric oxide (NO) donor, and desferrioxamine (DFx) and cobalt chloride, mimics of cellular hypoxia, similarly stimulated VEGF mRNA expression and secretion [9].
• Cellular hypoxia induced a time-dependent increase in nuclear p65, suggesting a dominant role for NF-kappaB in hypoxia-elicited induction of proinflammatory gene products [10].

Biological context of Cell Hypoxia

• RESULTS: Exposure of LNCaP cells to acute hypoxia activated a typical cellular hypoxia response characterized by up-regulation of HIF-1alpha and vascular endothelial growth factor protein expression [11].
• Although gram-negative endotoxin and cellular hypoxia independently enhance activation of nuclear factor-kappaB (NF-kappaB) via generation of reactive O(2) species (ROS), the combination of these stimuli downregulates hepatic TNF-alpha gene expression [12].
• First trimester and term placental explants were grown in 5-6% dissolved O(2) (n=10/trimester) and 200 microM cobalt chloride (CoCl(2),n =6/trimester) to simulate environmental and cellular hypoxia respectively, for up to 72 h [13].
• We investigated the toxicity of hemoglobin/myoglobin on endothelial cells under oxidative stress conditions that include cellular hypoxia and reduced antioxidant capacity [14].

Anatomical context of Cell Hypoxia

• Parallel induction of epithelial surface-associated chemokine and proteoglycan by cellular hypoxia: implications for neutrophil activation [15].
• 3) Angiogenesis: cellular hypoxia initially attracts and activates macrophages that express vascular endothelial growth factor and other cytokines, dissolving capillary basement membranes and degrading extracellular matrix, resulting in capillary leakage [16].

Associations of Cell Hypoxia with chemical compounds

• These observed changes, in correlation with a low T(3)/rT(3) ratio, may represent tissue-specific ways to reduce thyroid hormone bioactivity during cellular hypoxia and contribute to the low T(3) syndrome of severe illness [17].
• Measurement of hypoxanthine/xanthine has been suggested to be a useful indicator of cellular hypoxia [18].
• High speed epicardial fluorescence photography using reduced nicotinamide adenosine nucleotide (NADH) was used to identify areas of cell anoxia [19].
• These findings are consistent with a role for E-4031-sensitive K+ current, and possibly HERG-like K+ currents, in the type I cell hypoxia response maturation [20].
• The aim of this study was to compare tumor cell hypoxia assessed by the hypoxic cell marker pimonidazole (PIMO) with expression of the endogenous hypoxia-related marker carbonic anhydrase IX (CAIX) in three human head and neck tumor lines [21].

Gene context of Cell Hypoxia

• Therefore, the expression of HIF-1alpha and p53 proteins is not coupled during the cellular hypoxia response [22].
• In addition, we observed an increase in nNOS expression levels upon mild cellular hypoxia induced by 3-NP in transgenic but not in wild-type animals [23].
• This review discusses the reciprocal relationship between tumor cell hypoxia and EGFR [24].
• An early event in the adaptive response to cellular hypoxia is the binding of hypoxia-inducible factor 1 (HIF-1) to cis-acting regulatory sites in target genes [25].
• In vitro studies have indicated increased endothelial release of endothelin during tissue and cellular hypoxia [26].

References