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10.1167/iovs.15-16466 http://scihub22266oqcxt.onion/10.1167/iovs.15-16466 C4432552!4432552 !26024084     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26024084 &cmd=llinks): Failed to open stream: HTTP request failed! 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Lipotoxicity augments glucotoxicity-induced mitochondrial damage in the development of diabetic retinopathy |pdf=|usr=}}{{26024084 }} gab.com Text Lipotoxicity augments glucotoxicity-induced mitochondrial damage in the development of diabetic retinopathy JO: Invest Ophthalmol Vis Sci http://www.kidney.de/pget.php?&tw=1&pmid=26024084 #FOAvip PURPOSE: Although hyperglycemia is the main instigator in the development of diabetic retinopathy, dyslipidemia is also considered to play an important role. In the pathogenesis of diabetic retinopathy, cytosolic NADPH oxidase 2 (Nox2) is activated before retinal mitochondria are damaged. Our aim was to investigate the effect of lipids in the development of diabetic retinopathy. METHODS: Reactive oxygen species (ROS, by 2',7'-dichlorofluorescein diacetate) and activities of Nox2 (by a lucigenin-based method) and Rac1 (by G-LISA) were quantified in retinal endothelial cells incubated with 50 ?M palmitate in 5 mM glucose (lipotoxicity) or 20 mM glucose (glucolipotoxicity) for 6 to 96 hours. Mitochondrial DNA (mtDNA) damage was evaluated by extended-length PCR and its transcription by quantifying cytochrome b transcripts. RESULTS: Within 6 hours of exposure of endothelial cells to lipotoxicity, or glucotoxicity (20 mM glucose, without palmitate), significant increase in ROS, Nox2, and Rac1 was observed, which was exacerbated by glucolipotoxic insult. At 48 hours, neither lipotoxicity nor glucotoxicity had any effect on mtDNA and its transcription, but glucolipotoxicity significantly damaged mtDNA and decreased cytochrome b transcripts, and at 96 hours, glucotoxicity and glucolipotoxicity produced similar detrimental effects on mitochondrial damage. CONCLUSIONS: Although during initial exposure, lipotoxic or glucotoxic insult produces similar increase in ROS, addition of lipotoxicity in a glucotoxic environment further exacerbates ROS production, and also accelerates their damaging effects on mitochondrial homeostasis. Thus, modulation of Nox2 by pharmacological agents in prediabetic patients with dyslipidemia could retard the development of retinopathy before their hyperglycemia is observable. Twit Text FOAVip Lipotoxicity augments glucotoxicity-induced mitochondrial damage in the development of diabetic retinopathy ????Invest Ophthalmol Vis Sci http://www.kidney.de/pget.php?&tw=1&pmid=26024084 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26024084 #FOAvip English Wikipedia <ref>{{Cite pmid|26024084 }}</ref> Lipotoxicity augments glucotoxicity-induced mitochondrial damage in the development of diabetic retinopathy #MMPMID26024084 Kumar B ; Kowluru A ; Kowluru RA Invest Ophthalmol Vis Sci 2015[May]; 56 (5 ): 2985-92 PMID26024084 show ga PURPOSE: Although hyperglycemia is the main instigator in the development of diabetic retinopathy, dyslipidemia is also considered to play an important role. In the pathogenesis of diabetic retinopathy, cytosolic NADPH oxidase 2 (Nox2) is activated before retinal mitochondria are damaged. Our aim was to investigate the effect of lipids in the development of diabetic retinopathy. METHODS: Reactive oxygen species (ROS, by 2',7'-dichlorofluorescein diacetate) and activities of Nox2 (by a lucigenin-based method) and Rac1 (by G-LISA) were quantified in retinal endothelial cells incubated with 50 ?M palmitate in 5 mM glucose (lipotoxicity) or 20 mM glucose (glucolipotoxicity) for 6 to 96 hours. Mitochondrial DNA (mtDNA) damage was evaluated by extended-length PCR and its transcription by quantifying cytochrome b transcripts. RESULTS: Within 6 hours of exposure of endothelial cells to lipotoxicity, or glucotoxicity (20 mM glucose, without palmitate), significant increase in ROS, Nox2, and Rac1 was observed, which was exacerbated by glucolipotoxic insult. At 48 hours, neither lipotoxicity nor glucotoxicity had any effect on mtDNA and its transcription, but glucolipotoxicity significantly damaged mtDNA and decreased cytochrome b transcripts, and at 96 hours, glucotoxicity and glucolipotoxicity produced similar detrimental effects on mitochondrial damage. CONCLUSIONS: Although during initial exposure, lipotoxic or glucotoxic insult produces similar increase in ROS, addition of lipotoxicity in a glucotoxic environment further exacerbates ROS production, and also accelerates their damaging effects on mitochondrial homeostasis. Thus, modulation of Nox2 by pharmacological agents in prediabetic patients with dyslipidemia could retard the development of retinopathy before their hyperglycemia is observable. |Animals [MESH] |Cytochromes b [MESH] |DNA Damage [MESH] |DNA, Mitochondrial/genetics [MESH] |Diabetic Retinopathy/*etiology/metabolism/pathology [MESH] |Drug Synergism [MESH] |Endothelium, Vascular/drug effects/metabolism [MESH] |Glucose/*toxicity [MESH] |Humans [MESH] |Hyperglycemia/metabolism [MESH] |Membrane Glycoproteins/metabolism [MESH] |Mitochondria/*drug effects/genetics [MESH] |NADPH Oxidase 2 [MESH] |NADPH Oxidases/metabolism [MESH] |Palmitic Acid/*toxicity [MESH] |Polymerase Chain Reaction [MESH] |Reactive Oxygen Species/metabolism [MESH] |Retina/*drug effects/metabolism [MESH]Lipotoxicity augments glucotoxicity-induced mitochondrial damage in th(epmc).pdf DeepDyve Pubget Overpricing