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Pro-inflammatory cytokines increase reactive oxygen species through mitochondria and NADPH oxidase in cultured RPE cells.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Yang, Dongli Bian, Z. M. |
| Copyright Year | 2007 |
| Abstract | Reactive oxygen species (ROS) generated during inflammation are believed to play critical roles in various ocular diseases. However, the underlying mechanisms remain poorly understood. We investigated if pro-inflammatory cytokines, tumor necrosis factor (TNF)-alpha, interleukin-1 beta (IL-1 beta), and interferon-gamma (IFN-gamma), induce ROS in human retinal pigment epithelial (RPE) cells. TNF-alpha, IL-1 beta and IFN-gamma increased both intracellular and extracellular ROS production in a time- and dose-dependent manner. Thenoyltrifluoroacetone (TTFA), an inhibitor of mitochondrial respiratory chain, blocked TNF-alpha- and IFN-gamma-, but not IL-1 beta-induced ROS, whereas other two mitochondrial respiratory chain inhibitors, rotenone and antimycin A, had no effect. NADPH oxidase inhibitor (diphenylene iodinium) abolished the ROS production induced by IL-1 beta or IFN-gamma, but not by TNF-alpha, whereas 6-aminonicotinamide (6AN), an inhibitor of the hexose monophosphate shunt (HMS), had no significant effects on the ROS induced by all three cytokines. ROS scavengers, pyrrolidinedithiocarbamate (PDTC) and N-acetyl-cysteine (NAC), reduced the levels of ROS induced by TNF-alpha, IL-1 beta and IFN-gamma (P<0.05). Collectively, these results demonstrate that TNF-alpha, IL-1 beta and IFN-gamma increase mitochondrial- and NADPH oxidase-generated ROS in human RPE cells. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://www.uccs.edu/Documents/rmelamed/yang_et_al_2007_17765224.pdf |
| PubMed reference number | 17765224v1 |
| Volume Number | 85 |
| Issue Number | 4 |
| Journal | Experimental eye research |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | 6-Aminonicotinamide Acetylcysteine Amine Oxidase (Copper-Containing) Antimycin A Hematological Disease Hexoses Inosine Monophosphate Interferon Type II Interleukin-1 beta Interleukin-18 Lethrinidae Mitochondrial Diseases Mitochondrial electron transport chain NADPH Oxidase Pentose Phosphate Pathway Pyrrolidinedithiocarbamate Reactive Oxygen Species Recombinant Interferon-gamma Retina Retinal Pigments Rotenone TNF gene Thenoyltrifluoroacetone Tumor Necrosis Factors alpha-Mannosidosis diphenyleneiodonium |
| Content Type | Text |
| Resource Type | Article |
