Downregulating p22phox ameliorates inflammatory response in Angiotensin II-induced oxidative stress by regulating MAPK and NF-κB pathways in ARPE-19 cells
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 (...
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| creator | Qiu, Yiguo Tao, Lifei Lei, Chunyan Wang, Jiaming Yang, Peizeng Li, Qiuhong Lei, Bo |
| description | 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 |
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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</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep14362</identifier><identifier>PMID: 26415877</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject><![CDATA[13 ; 13/21 ; 13/31 ; 13/89 ; 13/95 ; 38/77 ; 631/250/256 ; 692/308/1426 ; Angiotensin II - pharmacology ; Cell Line ; Chemokine CCL2 - antagonists & inhibitors ; Chemokine CCL2 - genetics ; Chemokine CCL2 - metabolism ; Epithelial Cells - cytology ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Gene Expression Regulation ; Humanities and Social Sciences ; Humans ; Inflammation ; Interleukin-6 - antagonists & inhibitors ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Interleukin-8 - antagonists & inhibitors ; Interleukin-8 - genetics ; Interleukin-8 - metabolism ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - metabolism ; Mitogen-Activated Protein Kinase 1 - genetics ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - genetics ; Mitogen-Activated Protein Kinase 3 - metabolism ; multidisciplinary ; NADPH Oxidase 1 ; NADPH Oxidase 2 ; NADPH Oxidase 4 ; NADPH Oxidases - antagonists & inhibitors ; NADPH Oxidases - genetics ; NADPH Oxidases - metabolism ; NF-kappa B - antagonists & inhibitors ; NF-kappa B - genetics ; NF-kappa B - metabolism ; Oxidative Stress ; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases - genetics ; p38 Mitogen-Activated Protein Kinases - metabolism ; Primary Cell Culture ; Retinal Pigment Epithelium - cytology ; Retinal Pigment Epithelium - drug effects ; Retinal Pigment Epithelium - metabolism ; RNA, Small Interfering - genetics ; RNA, Small Interfering - metabolism ; Science ; Signal Transduction]]></subject><ispartof>Scientific reports, 2015-09, Vol.5 (1), p.14362-14362, Article 14362</ispartof><rights>The Author(s) 2015</rights><rights>Copyright © 2015, Macmillan Publishers Limited 2015 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c340t-e21308ad67dec74bc41a2acc22ef8bf29899244bc2c244c6def41c514ad147103</citedby><cites>FETCH-LOGICAL-c340t-e21308ad67dec74bc41a2acc22ef8bf29899244bc2c244c6def41c514ad147103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586461/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586461/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26415877$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qiu, Yiguo</creatorcontrib><creatorcontrib>Tao, Lifei</creatorcontrib><creatorcontrib>Lei, Chunyan</creatorcontrib><creatorcontrib>Wang, Jiaming</creatorcontrib><creatorcontrib>Yang, Peizeng</creatorcontrib><creatorcontrib>Li, Qiuhong</creatorcontrib><creatorcontrib>Lei, Bo</creatorcontrib><title>Downregulating p22phox ameliorates inflammatory response in Angiotensin II-induced oxidative stress by regulating MAPK and NF-κB pathways in ARPE-19 cells</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>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</description><subject>13</subject><subject>13/21</subject><subject>13/31</subject><subject>13/89</subject><subject>13/95</subject><subject>38/77</subject><subject>631/250/256</subject><subject>692/308/1426</subject><subject>Angiotensin II - pharmacology</subject><subject>Cell Line</subject><subject>Chemokine CCL2 - antagonists & inhibitors</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interleukin-6 - antagonists & inhibitors</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Interleukin-8 - antagonists & inhibitors</subject><subject>Interleukin-8 - genetics</subject><subject>Interleukin-8 - metabolism</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Mitogen-Activated Protein Kinase 1 - genetics</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - genetics</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>multidisciplinary</subject><subject>NADPH Oxidase 1</subject><subject>NADPH Oxidase 2</subject><subject>NADPH Oxidase 4</subject><subject>NADPH Oxidases - antagonists & inhibitors</subject><subject>NADPH Oxidases - genetics</subject><subject>NADPH Oxidases - metabolism</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-kappa B - genetics</subject><subject>NF-kappa B - metabolism</subject><subject>Oxidative Stress</subject><subject>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>p38 Mitogen-Activated Protein Kinases - genetics</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Primary Cell Culture</subject><subject>Retinal Pigment Epithelium - cytology</subject><subject>Retinal Pigment Epithelium - drug effects</subject><subject>Retinal Pigment Epithelium - metabolism</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Science</subject><subject>Signal Transduction</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNptkc9u1DAQxi0EolXpgRdAPgJSIJ44_y5IS2lhRYEKwdny2pOsq8RObaftPgtvwkPwTHjZsioSvsxo5udv7PkIecryVywvmtfB48R4UcEDcgg5LzMoAB7eyw_IcQiXeToltJy1j8kBVJyVTV0fkh_v3I312M-DjMb2dAKY1u6WyhEH47yMGKix3SDHUUbnN9RjmJwNmKp0YXvjItqQ8uUyM1bPCjV1t0YntWukISY80NX22n7Ep8XFRyqtpp_Psl8_39JJxvWN3IQ_il8vTjPWUoXDEJ6QR50cAh7fxSPy_ez028mH7PzL--XJ4jxTBc9jhsCKvJG6qjWqmq8UZxKkUgDYNasO2qZtgac6qBRUpbHjTJWMS814nXZ4RN7sdKd5NaJWaKOXg5i8GaXfCCeN-LdjzVr07lrwsql4xZLA8zsB765mDFGMJmy_IC26OQhWsyavq5JBQl_sUOVdSNZ1-zEsF1s_xd7PxD67_649-de9BLzcASG1bI9eXLrZ27Sr_6j9BjSgrbI</recordid><startdate>20150929</startdate><enddate>20150929</enddate><creator>Qiu, Yiguo</creator><creator>Tao, Lifei</creator><creator>Lei, Chunyan</creator><creator>Wang, Jiaming</creator><creator>Yang, Peizeng</creator><creator>Li, Qiuhong</creator><creator>Lei, Bo</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150929</creationdate><title>Downregulating p22phox ameliorates inflammatory response in Angiotensin II-induced oxidative stress by regulating MAPK and NF-κB pathways in ARPE-19 cells</title><author>Qiu, Yiguo ; Tao, Lifei ; Lei, Chunyan ; Wang, Jiaming ; Yang, Peizeng ; Li, Qiuhong ; Lei, Bo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c340t-e21308ad67dec74bc41a2acc22ef8bf29899244bc2c244c6def41c514ad147103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>13</topic><topic>13/21</topic><topic>13/31</topic><topic>13/89</topic><topic>13/95</topic><topic>38/77</topic><topic>631/250/256</topic><topic>692/308/1426</topic><topic>Angiotensin II - pharmacology</topic><topic>Cell Line</topic><topic>Chemokine CCL2 - antagonists & inhibitors</topic><topic>Chemokine CCL2 - genetics</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Interleukin-6 - antagonists & inhibitors</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Interleukin-8 - antagonists & inhibitors</topic><topic>Interleukin-8 - genetics</topic><topic>Interleukin-8 - metabolism</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Mitogen-Activated Protein Kinase 1 - genetics</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - genetics</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>multidisciplinary</topic><topic>NADPH Oxidase 1</topic><topic>NADPH Oxidase 2</topic><topic>NADPH Oxidase 4</topic><topic>NADPH Oxidases - antagonists & inhibitors</topic><topic>NADPH Oxidases - genetics</topic><topic>NADPH Oxidases - metabolism</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>NF-kappa B - genetics</topic><topic>NF-kappa B - metabolism</topic><topic>Oxidative Stress</topic><topic>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>p38 Mitogen-Activated Protein Kinases - genetics</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Primary Cell Culture</topic><topic>Retinal Pigment Epithelium - cytology</topic><topic>Retinal Pigment Epithelium - drug effects</topic><topic>Retinal Pigment Epithelium - metabolism</topic><topic>RNA, Small Interfering - genetics</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Science</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qiu, Yiguo</creatorcontrib><creatorcontrib>Tao, Lifei</creatorcontrib><creatorcontrib>Lei, Chunyan</creatorcontrib><creatorcontrib>Wang, Jiaming</creatorcontrib><creatorcontrib>Yang, Peizeng</creatorcontrib><creatorcontrib>Li, Qiuhong</creatorcontrib><creatorcontrib>Lei, Bo</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qiu, Yiguo</au><au>Tao, Lifei</au><au>Lei, Chunyan</au><au>Wang, Jiaming</au><au>Yang, Peizeng</au><au>Li, Qiuhong</au><au>Lei, Bo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulating p22phox ameliorates inflammatory response in Angiotensin II-induced oxidative stress by regulating MAPK and NF-κB pathways in ARPE-19 cells</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2015-09-29</date><risdate>2015</risdate><volume>5</volume><issue>1</issue><spage>14362</spage><epage>14362</epage><pages>14362-14362</pages><artnum>14362</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>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</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26415877</pmid><doi>10.1038/srep14362</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13 13/21 13/31 13/89 13/95 38/77 631/250/256 692/308/1426 Angiotensin II - pharmacology Cell Line Chemokine CCL2 - antagonists & inhibitors Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Epithelial Cells - cytology Epithelial Cells - drug effects Epithelial Cells - metabolism Gene Expression Regulation Humanities and Social Sciences Humans Inflammation Interleukin-6 - antagonists & inhibitors Interleukin-6 - genetics Interleukin-6 - metabolism Interleukin-8 - antagonists & inhibitors Interleukin-8 - genetics Interleukin-8 - metabolism Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism Mitogen-Activated Protein Kinase 1 - genetics Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - genetics Mitogen-Activated Protein Kinase 3 - metabolism multidisciplinary NADPH Oxidase 1 NADPH Oxidase 2 NADPH Oxidase 4 NADPH Oxidases - antagonists & inhibitors NADPH Oxidases - genetics NADPH Oxidases - metabolism NF-kappa B - antagonists & inhibitors NF-kappa B - genetics NF-kappa B - metabolism Oxidative Stress p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - genetics p38 Mitogen-Activated Protein Kinases - metabolism Primary Cell Culture Retinal Pigment Epithelium - cytology Retinal Pigment Epithelium - drug effects Retinal Pigment Epithelium - metabolism RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Science Signal Transduction |
| title | Downregulating p22phox ameliorates inflammatory response in Angiotensin II-induced oxidative stress by regulating MAPK and NF-κB pathways in ARPE-19 cells |
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