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Literature summary for 1.6.3.1 extracted from

  • Chen, J.X.; Zeng, H.; Tuo, Q.H.; Yu, H.; Meyrick, B.; Aschner, J.L.
    NADPH oxidase modulates myocardial Akt, ERK1/2 activation, and angiogenesis after hypoxia-reoxygenation (2007), Am. J. Physiol. Heart Circ. Physiol., 292, H1664-H1674.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 1.6.3.1

Application

Application Comment Organism
medicine exposure of porcine coronary artery endothelial cells, PCAECs, to hypoxia for 2 h followed by 1 h of reoxygenation significantly increases reactive oxygen species formation. Pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium and apocynin, significantly attenuates hypoxia/reoxygenation-induced reactive oxygen species formation. Exposure of PCAECs to hypoxia/reoxygenation causes a significant increase in serine-threonine kinase Akt and ERK1/2 activation. Exposure of PCAEC spheroids to hypoxia/reoxygenation significantly increases endothelial spheroid sprouting and vessel outgrowth, whereas pharmacological inhibition of NADPH oxidase or genetic deletion of the NADPH oxidase subunit p47phox significantly suppresses these changes Sus scrofa
medicine increases in myocardial serine-threonine kinase Akt and ERK1/2 activation and vascular endothelial growth factor expression are markedly blunted in the subunit p47phox-deficient mouse subjected to myocardial ischemia-reperfusion compared with the wild-type mouse Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information genetic deletion of the NADPH oxidase subunit, p47phox, significantly suppresses increased vessel outgrowth induced by hypoxia/reoxygenation. Increases in myocardial serine-threonine kinase Akt and ERK1/2 activation and vascular endothelial growth factor expression are markedly blunted in the subunit p47phox-deficient mouse subjected to myocardial ischemia-reperfusion compared with the wild-type mouse Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
apocynin significantly attenuates hypoxia/reoxygenation-induced reactive oxygen species formation in porcine coronary artery endothelial cells and suppresses the hypoxia/reoxygenation-induced endothelial spheroid sprouting Sus scrofa
diphenyleneiodonium significantly attenuates hypoxia/reoxygenation-induced reactive oxygen species formation in porcine coronary artery endothelial cells and suppresses the hypoxia/reoxygenation-induced endothelial spheroid sprouting Sus scrofa

Organism

Organism UniProt Comment Textmining
Mus musculus
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Sus scrofa
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Source Tissue

Source Tissue Comment Organism Textmining
aorta Exposure of mouse aortic rings to hypoxia/reoxygenation significantly increases vessel outgrowth, whereas pharmacological inhibition of NADPH oxidase or genetic deletion of the NADPH oxidase subunit, p47phox significantly suppresses these changes. Increases in myocardial serine-threonine kinase Akt and ERK1/2 activation and vascular endothelial growth factor expression are markedly blunted in the subunit p47phox-deficient mouse subjected to myocardial ischemia-reperfusion compared with the wild-type mouse Mus musculus
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artery porcine coronary artery endothelial cell, PCAEC. Exposure of cells to hypoxia for 2 h followed by 1 h of reoxygenation significantly increases reactive oxygen species formation. Pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium and apocynin , significantly attenuates hypoxia/reoxygenation-induced reactive oxygen species formation. Exposure of PCAECs to hypoxia/reoxygenation causes a significant increase in serine-threonine kinase Akt and ERK1/2 activation. Exposure of PCAEC spheroids to hypoxia/reoxygenation significantly increases endothelial spheroid sprouting, whereas pharmacological inhibition of NADPH oxidase or genetic deletion of the NADPH oxidase subunit, p47phox (p47phox/), significantly suppresses these changes Sus scrofa
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