Inducible Nitric Oxide Synthase Mediates Hypoxia-Induced Hypoxia-Inducible Factor-1α Activation and Vascular Endothelial Growth Factor Expression in Oxygen-Induced Retinopathy
Author(s) -
Tao He,
Ming Ai,
Xiaohui Zhao,
Yiqiao Xing
Publication year - 2007
Publication title -
pathobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.941
H-Index - 53
eISSN - 1423-0291
pISSN - 1015-2008
DOI - 10.1159/000110027
Subject(s) - protein kinase b , nitric oxide synthase , hypoxia inducible factors , vascular endothelial growth factor , pi3k/akt/mtor pathway , hypoxia (environmental) , retinopathy of prematurity , vascular endothelial growth factor a , angiogenesis , nitric oxide , endocrinology , medicine , biology , signal transduction , chemistry , cancer research , microbiology and biotechnology , biochemistry , vegf receptors , oxygen , gene , pregnancy , genetics , organic chemistry , gestational age
Previous studies provided evidence that many factors contribute to retinal angiogenesis, including inducible nitric oxide synthase (iNOS), hypoxia-inducible factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF). But the role of nitric oxide generated by iNOS in the regulation of expression of hypoxia-inducible genes in retinopathy of prematurity remains unclear. So we sought to better define the molecular basis of this iNOS-dependent regulation.
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