| http://purl.uniprot.org/citations/26415877 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/26415877 | http://www.w3.org/2000/01/rdf-schema#comment | "Oxidative stress and inflammation are two interrelated biological events implicated in the pathogenesis of many diseases. Reactive oxygen species (ROS) produced under oxidative stress play a key role in pathological conditions. Inhibition of p22phox, an indispensable component of the NADPH oxidase (NOX) complex comprising the main source of ROS, plays a protective role in many ocular conditions by inhibiting the activation of NOXs and the generation of ROS. However, little is understood regarding the role of p22phox in oxidative stress-related inflammation in the eye. We used a p22phox small interfering RNA (siRNA) to transfect the retinal pigment epithelium (RPE)-derived cell line ARPE-19, and human primary RPE (hRPE) cells, then stimulated with Ang II. We observed a potent anti-inflammatory effect and studied the underlying mechanism. Downregulating p22phox resulted in decreased ROS generation, a reduction of NOXs (NOX1, 2, 4) and a decrease in inflammatory cytokine. In addition, p22phox downregulation reduced the activation of the MAPK and NF-κB signaling pathways. We conclude that inhibition of p22phox has an anti-inflammatory effect in Ang II-induced oxidative stress. Suppressing the MAPK and NF-κB pathways is involved in this protective effect. These results suggest that p22phox may provide a promising therapeutic target for oxidative stress-induced ocular inflammation."xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.org/dc/terms/identifier | "doi:10.1038/srep14362"xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/author | "Li Q."xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/author | "Lei B."xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/author | "Qiu Y."xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/author | "Lei C."xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/author | "Tao L."xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/author | "Wang J."xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/author | "Yang P."xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/name | "Sci Rep"xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/pages | "14362"xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/title | "Downregulating p22phox ameliorates inflammatory response in Angiotensin II-induced oxidative stress by regulating MAPK and NF-kappaB pathways in ARPE-19 cells."xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://purl.uniprot.org/core/volume | "5"xsd:string |
| http://purl.uniprot.org/citations/26415877 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26415877 |
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