Decorin Protects Retinal Pigment Epithelium Cells from Oxidative Stress and Apoptosis via AMPK-mTOR-Regulated Autophagy
Age-related macular degeneration (AMD) is the leading cause of irreversible visual loss among the elderly worldwide with unidentified pathogenesis and limited therapeutic options. Oxidative stress-induced damage to the retinal pigment epithelium (RPE) is central in the development and progression of...
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| creator | Xie, Xinyi Li, Duo Cui, Yuqing Xie, Tianhua Cai, Jiping Yao, Yong |
| description | Age-related macular degeneration (AMD) is the leading cause of irreversible visual loss among the elderly worldwide with unidentified pathogenesis and limited therapeutic options. Oxidative stress-induced damage to the retinal pigment epithelium (RPE) is central in the development and progression of AMD. Decorin (DCN), a small leucine-rich proteoglycan, possesses powerful antifibrotic, anti-inflammatory, and antiangiogenic properties. DCN has also been reported to serve a cytoprotective role in various cell types, but its protective effects against H2O2-induced oxidative stress and apoptosis in ARPE-19 cells remain unclear. In this study, we showed that DCN significantly attenuated the increase in cell viability loss, apoptosis rate, and reactive oxygen species (ROS) levels in ARPE-19 cells induced by H2O2. Furthermore, DCN activated the AMPK/mTOR pathway to promote autophagy while genetic inhibition of autophagy-related gene 5 (ATG5) hindered autophagic process and diminished the protective role of DCN against oxidative stress in ARPE-19 cells. Collectively, these results suggest that DCN could protect RPE cells from H2O2-induced oxidative stress and apoptosis via autophagy promotion, thus providing the therapeutic potential for AMD prevention and treatment. |
| doi_str_mv | 10.1155/2022/3955748 |
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Oxidative stress-induced damage to the retinal pigment epithelium (RPE) is central in the development and progression of AMD. Decorin (DCN), a small leucine-rich proteoglycan, possesses powerful antifibrotic, anti-inflammatory, and antiangiogenic properties. DCN has also been reported to serve a cytoprotective role in various cell types, but its protective effects against H2O2-induced oxidative stress and apoptosis in ARPE-19 cells remain unclear. In this study, we showed that DCN significantly attenuated the increase in cell viability loss, apoptosis rate, and reactive oxygen species (ROS) levels in ARPE-19 cells induced by H2O2. Furthermore, DCN activated the AMPK/mTOR pathway to promote autophagy while genetic inhibition of autophagy-related gene 5 (ATG5) hindered autophagic process and diminished the protective role of DCN against oxidative stress in ARPE-19 cells. Collectively, these results suggest that DCN could protect RPE cells from H2O2-induced oxidative stress and apoptosis via autophagy promotion, thus providing the therapeutic potential for AMD prevention and treatment.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2022/3955748</identifier><identifier>PMID: 35391926</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Aged ; Aging ; AMP-Activated Protein Kinases - metabolism ; Apoptosis ; Autophagy ; Decorin - metabolism ; Decorin - pharmacology ; Flow cytometry ; Growth factors ; Humans ; Hydrogen Peroxide - metabolism ; Hydrogen Peroxide - toxicity ; Macular degeneration ; Macular Degeneration - pathology ; Membranes ; Older people ; Oxidative Stress ; Pathogenesis ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reagents ; Retinal Pigment Epithelium - metabolism ; TOR Serine-Threonine Kinases - metabolism ; Variance analysis</subject><ispartof>Oxidative medicine and cellular longevity, 2022, Vol.2022, p.3955748-17</ispartof><rights>Copyright © 2022 Xinyi Xie et al.</rights><rights>Copyright © 2022 Xinyi Xie et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Xinyi Xie et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-796a04899e318f8d04acc813c7d0a0381df3a913d59d5f1fad97fd4cbcf20cb53</citedby><cites>FETCH-LOGICAL-c514t-796a04899e318f8d04acc813c7d0a0381df3a913d59d5f1fad97fd4cbcf20cb53</cites><orcidid>0000-0002-9280-6356</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8983248/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8983248/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35391926$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Cosentino, Cristina</contributor><contributor>Cristina Cosentino</contributor><creatorcontrib>Xie, Xinyi</creatorcontrib><creatorcontrib>Li, Duo</creatorcontrib><creatorcontrib>Cui, Yuqing</creatorcontrib><creatorcontrib>Xie, Tianhua</creatorcontrib><creatorcontrib>Cai, Jiping</creatorcontrib><creatorcontrib>Yao, Yong</creatorcontrib><title>Decorin Protects Retinal Pigment Epithelium Cells from Oxidative Stress and Apoptosis via AMPK-mTOR-Regulated Autophagy</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Age-related macular degeneration (AMD) is the leading cause of irreversible visual loss among the elderly worldwide with unidentified pathogenesis and limited therapeutic options. Oxidative stress-induced damage to the retinal pigment epithelium (RPE) is central in the development and progression of AMD. Decorin (DCN), a small leucine-rich proteoglycan, possesses powerful antifibrotic, anti-inflammatory, and antiangiogenic properties. DCN has also been reported to serve a cytoprotective role in various cell types, but its protective effects against H2O2-induced oxidative stress and apoptosis in ARPE-19 cells remain unclear. In this study, we showed that DCN significantly attenuated the increase in cell viability loss, apoptosis rate, and reactive oxygen species (ROS) levels in ARPE-19 cells induced by H2O2. Furthermore, DCN activated the AMPK/mTOR pathway to promote autophagy while genetic inhibition of autophagy-related gene 5 (ATG5) hindered autophagic process and diminished the protective role of DCN against oxidative stress in ARPE-19 cells. Collectively, these results suggest that DCN could protect RPE cells from H2O2-induced oxidative stress and apoptosis via autophagy promotion, thus providing the therapeutic potential for AMD prevention and treatment.</description><subject>Aged</subject><subject>Aging</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Decorin - metabolism</subject><subject>Decorin - pharmacology</subject><subject>Flow cytometry</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Hydrogen Peroxide - toxicity</subject><subject>Macular degeneration</subject><subject>Macular Degeneration - pathology</subject><subject>Membranes</subject><subject>Older people</subject><subject>Oxidative Stress</subject><subject>Pathogenesis</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reagents</subject><subject>Retinal Pigment Epithelium - metabolism</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Variance analysis</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kUtvEzEUhS0EoqWwY40ssUGCaf0YZ-wNUhRKi1qUKJS15fiRuJoZD7Ynpf8eRwkRsGB1r3Q_HZ17DgCvMTrHmLELggi5oIKxpuZPwCkWNamQEPXT447QCXiR0j1CE0pq_BycUEYFFmRyCh4-WR2i7-Eihmx1TnBps-9VCxd-3dk-w8vB541t_djBmW3bBF0MHZz_9EZlv7XwW442Jah6A6dDGHJIPsGtV3D6dXFTdXfzZbW067FV2RZizGHYqPXjS_DMqTbZV4d5Br5_vrybXVe386svs-ltpRmuc9WIiUI1F8JSzB03qFZac0x1Y5BClGPjqBKYGiYMc9gpIxpnar3SjiC9YvQMfNzrDuOqs0aXj6Jq5RB9p-KjDMrLvy-938h12EoueAmLF4F3B4EYfow2Zdn5pEsQqrdhTJJMas4FI4gW9O0_6H0YY8nyQGHWiJ2jD3tKx5BStO5oBiO5a1TuGpWHRgv-5s8HjvDvCgvwfg9sfG_Ug_-_3C9Gd6o-</recordid><startdate>2022</startdate><enddate>2022</enddate><creator>Xie, Xinyi</creator><creator>Li, Duo</creator><creator>Cui, Yuqing</creator><creator>Xie, Tianhua</creator><creator>Cai, Jiping</creator><creator>Yao, Yong</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9280-6356</orcidid></search><sort><creationdate>2022</creationdate><title>Decorin Protects Retinal Pigment Epithelium Cells from Oxidative Stress and Apoptosis via AMPK-mTOR-Regulated Autophagy</title><author>Xie, Xinyi ; Li, Duo ; Cui, Yuqing ; Xie, Tianhua ; Cai, Jiping ; Yao, Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-796a04899e318f8d04acc813c7d0a0381df3a913d59d5f1fad97fd4cbcf20cb53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Aged</topic><topic>Aging</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Decorin - metabolism</topic><topic>Decorin - pharmacology</topic><topic>Flow cytometry</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Hydrogen Peroxide - toxicity</topic><topic>Macular degeneration</topic><topic>Macular Degeneration - pathology</topic><topic>Membranes</topic><topic>Older people</topic><topic>Oxidative Stress</topic><topic>Pathogenesis</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Reagents</topic><topic>Retinal Pigment Epithelium - metabolism</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xie, Xinyi</creatorcontrib><creatorcontrib>Li, Duo</creatorcontrib><creatorcontrib>Cui, Yuqing</creatorcontrib><creatorcontrib>Xie, Tianhua</creatorcontrib><creatorcontrib>Cai, Jiping</creatorcontrib><creatorcontrib>Yao, Yong</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xie, Xinyi</au><au>Li, Duo</au><au>Cui, Yuqing</au><au>Xie, Tianhua</au><au>Cai, Jiping</au><au>Yao, Yong</au><au>Cosentino, Cristina</au><au>Cristina Cosentino</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decorin Protects Retinal Pigment Epithelium Cells from Oxidative Stress and Apoptosis via AMPK-mTOR-Regulated Autophagy</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2022</date><risdate>2022</risdate><volume>2022</volume><spage>3955748</spage><epage>17</epage><pages>3955748-17</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Age-related macular degeneration (AMD) is the leading cause of irreversible visual loss among the elderly worldwide with unidentified pathogenesis and limited therapeutic options. Oxidative stress-induced damage to the retinal pigment epithelium (RPE) is central in the development and progression of AMD. Decorin (DCN), a small leucine-rich proteoglycan, possesses powerful antifibrotic, anti-inflammatory, and antiangiogenic properties. DCN has also been reported to serve a cytoprotective role in various cell types, but its protective effects against H2O2-induced oxidative stress and apoptosis in ARPE-19 cells remain unclear. In this study, we showed that DCN significantly attenuated the increase in cell viability loss, apoptosis rate, and reactive oxygen species (ROS) levels in ARPE-19 cells induced by H2O2. Furthermore, DCN activated the AMPK/mTOR pathway to promote autophagy while genetic inhibition of autophagy-related gene 5 (ATG5) hindered autophagic process and diminished the protective role of DCN against oxidative stress in ARPE-19 cells. Collectively, these results suggest that DCN could protect RPE cells from H2O2-induced oxidative stress and apoptosis via autophagy promotion, thus providing the therapeutic potential for AMD prevention and treatment.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>35391926</pmid><doi>10.1155/2022/3955748</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-9280-6356</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Aging AMP-Activated Protein Kinases - metabolism Apoptosis Autophagy Decorin - metabolism Decorin - pharmacology Flow cytometry Growth factors Humans Hydrogen Peroxide - metabolism Hydrogen Peroxide - toxicity Macular degeneration Macular Degeneration - pathology Membranes Older people Oxidative Stress Pathogenesis Reactive oxygen species Reactive Oxygen Species - metabolism Reagents Retinal Pigment Epithelium - metabolism TOR Serine-Threonine Kinases - metabolism Variance analysis |
| title | Decorin Protects Retinal Pigment Epithelium Cells from Oxidative Stress and Apoptosis via AMPK-mTOR-Regulated Autophagy |
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