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Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Biol+Chem 2000 ; 275 (33): 25130-8 Nephropedia Template TP
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Reactive oxygen species generated at mitochondrial complex III stabilize hypoxia-inducible factor-1alpha during hypoxia: a mechanism of O2 sensing #MMPMID10833514
J Biol Chem 2000[Aug]; 275 (33): 25130-8 PMID10833514show ga
During hypoxia, hypoxia-inducible factor-1alpha (HIF-1alpha) is required for induction of a variety of genes including erythropoietin and vascular endothelial growth factor. Hypoxia increases mitochondrial reactive oxygen species (ROS) generation at Complex III, which causes accumulation of HIF-1alpha protein responsible for initiating expression of a luciferase reporter construct under the control of a hypoxic response element. This response is lost in cells depleted of mitochondrial DNA (rho(0) cells). Overexpression of catalase abolishes hypoxic response element-luciferase expression during hypoxia. Exogenous H(2)O(2) stabilizes HIF-1alpha protein during normoxia and activates luciferase expression in wild-type and rho(0) cells. Isolated mitochondria increase ROS generation during hypoxia, as does the bacterium Paracoccus denitrificans. These findings reveal that mitochondria-derived ROS are both required and sufficient to initiate HIF-1alpha stabilization during hypoxia.
|*Hypoxia[MESH]
|*Transcription Factors[MESH]
|Androstadienes/pharmacology[MESH]
|Animals[MESH]
|Cell Line[MESH]
|Cell Nucleus/metabolism[MESH]
|Chelating Agents/pharmacology[MESH]
|Cobalt/pharmacology[MESH]
|Cytosol/chemistry[MESH]
|DNA-Binding Proteins/*metabolism[MESH]
|Deferoxamine/pharmacology[MESH]
|Dose-Response Relationship, Drug[MESH]
|Electron Transport Complex III/*chemistry/*metabolism[MESH]