Inhibition of autophagy induces IL-1β release from ARPE-19 cells via ROS mediated NLRP3 inflammasome activation under high glucose stress
Autophagy plays an important role in the development of diabetic retinopathy (DR). Retinal pigment epithelial (RPE) cells are the main cells involved in DR, a process in which hyperglycemia plays a crucial role. This study was conducted to investigate the protective effect of autophagy against high...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2015-08, Vol.463 (4), p.1071-1076 |
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| creator | Shi, Huanqi Zhang, Zhen Wang, Xiaodan Li, Ruishu Hou, Wenwen Bi, Wenjiao Zhang, Xiaomei |
| description | Autophagy plays an important role in the development of diabetic retinopathy (DR). Retinal pigment epithelial (RPE) cells are the main cells involved in DR, a process in which hyperglycemia plays a crucial role. This study was conducted to investigate the protective effect of autophagy against high glucose-induced inflammatory response in ARPE-19 cells and its underlying mechanism. In the present study we subjected ARPE-19 cells to high glucose stress and showed that ARPE-19 cells respond to high glucose with an increase in autophagy. 3-methyladenine (3-MA) inhibited occurrence of autophagy and it leaded to the accumulation of damaged-mitochondria-producing-ROS, and the activation of NLRP3 inflammasome, and subsequently, caused IL-1β secretion.
•Inhibition of autophagy increases IL-1β release in ARPE-19 cells under high glucose stress.•Autophagy-induced cytoprotection is related to ROS mediated NLRP3 inflammasome activation.•Activation autophagy may be a potential therapeutic target for preventing DR. |
| doi_str_mv | 10.1016/j.bbrc.2015.06.060 |
| format | Article |
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•Inhibition of autophagy increases IL-1β release in ARPE-19 cells under high glucose stress.•Autophagy-induced cytoprotection is related to ROS mediated NLRP3 inflammasome activation.•Activation autophagy may be a potential therapeutic target for preventing DR.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2015.06.060</identifier><identifier>PMID: 26102024</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Autophagy ; Autophagy - physiology ; Carrier Proteins - metabolism ; Cell Line ; Diabetic retinopathy ; Glucose - metabolism ; Humans ; Inflammasomes - metabolism ; Interleukin-1beta - metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 inflammasome ; Reactive Oxygen Species - metabolism ; Retinal pigment epithelium ; Retinal Pigment Epithelium - cytology ; Retinal Pigment Epithelium - metabolism ; Stress, Physiological</subject><ispartof>Biochemical and biophysical research communications, 2015-08, Vol.463 (4), p.1071-1076</ispartof><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-f1e1a4f7ea881607d45ab223c58e51f5038d8aa53357cf244f6caa9117dba2863</citedby><cites>FETCH-LOGICAL-c426t-f1e1a4f7ea881607d45ab223c58e51f5038d8aa53357cf244f6caa9117dba2863</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2015.06.060$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26102024$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Huanqi</creatorcontrib><creatorcontrib>Zhang, Zhen</creatorcontrib><creatorcontrib>Wang, Xiaodan</creatorcontrib><creatorcontrib>Li, Ruishu</creatorcontrib><creatorcontrib>Hou, Wenwen</creatorcontrib><creatorcontrib>Bi, Wenjiao</creatorcontrib><creatorcontrib>Zhang, Xiaomei</creatorcontrib><title>Inhibition of autophagy induces IL-1β release from ARPE-19 cells via ROS mediated NLRP3 inflammasome activation under high glucose stress</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Autophagy plays an important role in the development of diabetic retinopathy (DR). Retinal pigment epithelial (RPE) cells are the main cells involved in DR, a process in which hyperglycemia plays a crucial role. This study was conducted to investigate the protective effect of autophagy against high glucose-induced inflammatory response in ARPE-19 cells and its underlying mechanism. In the present study we subjected ARPE-19 cells to high glucose stress and showed that ARPE-19 cells respond to high glucose with an increase in autophagy. 3-methyladenine (3-MA) inhibited occurrence of autophagy and it leaded to the accumulation of damaged-mitochondria-producing-ROS, and the activation of NLRP3 inflammasome, and subsequently, caused IL-1β secretion.
•Inhibition of autophagy increases IL-1β release in ARPE-19 cells under high glucose stress.•Autophagy-induced cytoprotection is related to ROS mediated NLRP3 inflammasome activation.•Activation autophagy may be a potential therapeutic target for preventing DR.</description><subject>Autophagy</subject><subject>Autophagy - physiology</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell Line</subject><subject>Diabetic retinopathy</subject><subject>Glucose - metabolism</subject><subject>Humans</subject><subject>Inflammasomes - metabolism</subject><subject>Interleukin-1beta - metabolism</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein</subject><subject>NLRP3 inflammasome</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Retinal pigment epithelium</subject><subject>Retinal Pigment Epithelium - cytology</subject><subject>Retinal Pigment Epithelium - metabolism</subject><subject>Stress, Physiological</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2O00AQhVsIxISBC7BAvWTjUNW227bEZjQaIFLEjAJI7FrldnXSkX9Ctx1prsBxOAhnwpkMLJFKqs17X6neE-I1whIB9bv9sq6DXSrAfAl6HngiFggVJAoheyoWAKATVeH3C_Eixj0AYqar5-JCaQQFKluIn6t-52s_-qGXg5M0jcNhR9t76ftmshzlap3g718ycMsUWbowdPJqc3eTYCUtt22UR09yc_tFdtx4GrmRn9ebu3QGuJa6juLQsSQ7-iM9XJn6hoPc-e1ObtvJDjM0joFjfCmeOWojv3rcl-Lbh5uv15-S9e3H1fXVOrGZ0mPikJEyVzCVJWoomiynWqnU5iXn6HJIy6YkytM0L6xTWea0JaoQi6YmVer0Urw9cw9h-DFxHE3n4-kV6nmYokFd5VikxYNUnaU2DDEGduYQfEfh3iCYUwdmb04dmFMHBvQ8MJvePPKnes7kn-Vv6LPg_VnA85dHz8FE67m3c36B7Wiawf-P_wcX9JjD</recordid><startdate>20150807</startdate><enddate>20150807</enddate><creator>Shi, Huanqi</creator><creator>Zhang, Zhen</creator><creator>Wang, Xiaodan</creator><creator>Li, Ruishu</creator><creator>Hou, Wenwen</creator><creator>Bi, Wenjiao</creator><creator>Zhang, Xiaomei</creator><general>Elsevier Inc</general><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></search><sort><creationdate>20150807</creationdate><title>Inhibition of autophagy induces IL-1β release from ARPE-19 cells via ROS mediated NLRP3 inflammasome activation under high glucose stress</title><author>Shi, Huanqi ; Zhang, Zhen ; Wang, Xiaodan ; Li, Ruishu ; Hou, Wenwen ; Bi, Wenjiao ; Zhang, Xiaomei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-f1e1a4f7ea881607d45ab223c58e51f5038d8aa53357cf244f6caa9117dba2863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Autophagy</topic><topic>Autophagy - physiology</topic><topic>Carrier Proteins - metabolism</topic><topic>Cell Line</topic><topic>Diabetic retinopathy</topic><topic>Glucose - metabolism</topic><topic>Humans</topic><topic>Inflammasomes - metabolism</topic><topic>Interleukin-1beta - metabolism</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein</topic><topic>NLRP3 inflammasome</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Retinal pigment epithelium</topic><topic>Retinal Pigment Epithelium - cytology</topic><topic>Retinal Pigment Epithelium - metabolism</topic><topic>Stress, Physiological</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Huanqi</creatorcontrib><creatorcontrib>Zhang, Zhen</creatorcontrib><creatorcontrib>Wang, Xiaodan</creatorcontrib><creatorcontrib>Li, Ruishu</creatorcontrib><creatorcontrib>Hou, Wenwen</creatorcontrib><creatorcontrib>Bi, Wenjiao</creatorcontrib><creatorcontrib>Zhang, Xiaomei</creatorcontrib><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><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Huanqi</au><au>Zhang, Zhen</au><au>Wang, Xiaodan</au><au>Li, Ruishu</au><au>Hou, Wenwen</au><au>Bi, Wenjiao</au><au>Zhang, Xiaomei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of autophagy induces IL-1β release from ARPE-19 cells via ROS mediated NLRP3 inflammasome activation under high glucose stress</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2015-08-07</date><risdate>2015</risdate><volume>463</volume><issue>4</issue><spage>1071</spage><epage>1076</epage><pages>1071-1076</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Autophagy plays an important role in the development of diabetic retinopathy (DR). Retinal pigment epithelial (RPE) cells are the main cells involved in DR, a process in which hyperglycemia plays a crucial role. This study was conducted to investigate the protective effect of autophagy against high glucose-induced inflammatory response in ARPE-19 cells and its underlying mechanism. In the present study we subjected ARPE-19 cells to high glucose stress and showed that ARPE-19 cells respond to high glucose with an increase in autophagy. 3-methyladenine (3-MA) inhibited occurrence of autophagy and it leaded to the accumulation of damaged-mitochondria-producing-ROS, and the activation of NLRP3 inflammasome, and subsequently, caused IL-1β secretion.
•Inhibition of autophagy increases IL-1β release in ARPE-19 cells under high glucose stress.•Autophagy-induced cytoprotection is related to ROS mediated NLRP3 inflammasome activation.•Activation autophagy may be a potential therapeutic target for preventing DR.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26102024</pmid><doi>10.1016/j.bbrc.2015.06.060</doi><tpages>6</tpages></addata></record> |
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| subjects | Autophagy Autophagy - physiology Carrier Proteins - metabolism Cell Line Diabetic retinopathy Glucose - metabolism Humans Inflammasomes - metabolism Interleukin-1beta - metabolism NLR Family, Pyrin Domain-Containing 3 Protein NLRP3 inflammasome Reactive Oxygen Species - metabolism Retinal pigment epithelium Retinal Pigment Epithelium - cytology Retinal Pigment Epithelium - metabolism Stress, Physiological |
| title | Inhibition of autophagy induces IL-1β release from ARPE-19 cells via ROS mediated NLRP3 inflammasome activation under high glucose stress |
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