Autophagy Protects Advanced Glycation End Product-Induced Apoptosis and Expression of MMP-3 and MMP-13 in Rat Chondrocytes
Aging is one of the most prominent risk factors for the pathological progression of osteoarthritis (OA). One feature of age-related changes in OA is advanced glycation end products (AGEs) accumulation in articular cartilage. Autophagy plays a cellular housekeeping role by removing dysfunctional cell...
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| Veröffentlicht in: | BioMed research international 2017-01, Vol.2017 (2017), p.1-9 |
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| creator | Cheng, Xigao Yin, Changchang Deng, Zhongbo Xu, Libiao Wu, Tianlong Li, Jian Ao, Peng Huang, Wenzhou Chen, Wenjie |
| description | Aging is one of the most prominent risk factors for the pathological progression of osteoarthritis (OA). One feature of age-related changes in OA is advanced glycation end products (AGEs) accumulation in articular cartilage. Autophagy plays a cellular housekeeping role by removing dysfunctional cellular organelles and proteins. However, the relationship between autophagy and AGE-associated OA is unknown. The aim of this study is to determine whether autophagy participates in the pathology of AGE-treated chondrocytes and to investigate the exact role of autophagy in AGE-induced cell apoptosis and expression of matrix metalloproteinase- (MMP-) 3 and MMP-13. AGEs induced notable apoptosis that was detected by Annexin V/PI double-staining, and the upregulation of MMP-3 and MMP-13 was confirmed by Western blotting. Autophagy-related proteins were also determined by Western blotting, and chondrocytes were transfected with mCherry-GFP-LC3B-adenovirus to monitor autophagic flux. As a result, autophagy significantly increased in chondrocytes and peaked at 6 h. Furthermore, rapamycin (RA) attenuated AGE-induced apoptosis and expression of MMP-3 and MMP-13 by autophagy activation. In contrast, pretreatment with autophagy inhibitor 3-methyladenine (3-MA) enhanced the abovementioned effects of AGEs. We therefore demonstrated that autophagy is linked with AGE-related pathology in rat chondrocytes and plays a protective role in AGE-induced apoptosis and expression of MMP-3 and MMP-13. |
| doi_str_mv | 10.1155/2017/6341919 |
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One feature of age-related changes in OA is advanced glycation end products (AGEs) accumulation in articular cartilage. Autophagy plays a cellular housekeeping role by removing dysfunctional cellular organelles and proteins. However, the relationship between autophagy and AGE-associated OA is unknown. The aim of this study is to determine whether autophagy participates in the pathology of AGE-treated chondrocytes and to investigate the exact role of autophagy in AGE-induced cell apoptosis and expression of matrix metalloproteinase- (MMP-) 3 and MMP-13. AGEs induced notable apoptosis that was detected by Annexin V/PI double-staining, and the upregulation of MMP-3 and MMP-13 was confirmed by Western blotting. Autophagy-related proteins were also determined by Western blotting, and chondrocytes were transfected with mCherry-GFP-LC3B-adenovirus to monitor autophagic flux. As a result, autophagy significantly increased in chondrocytes and peaked at 6 h. Furthermore, rapamycin (RA) attenuated AGE-induced apoptosis and expression of MMP-3 and MMP-13 by autophagy activation. In contrast, pretreatment with autophagy inhibitor 3-methyladenine (3-MA) enhanced the abovementioned effects of AGEs. We therefore demonstrated that autophagy is linked with AGE-related pathology in rat chondrocytes and plays a protective role in AGE-induced apoptosis and expression of MMP-3 and MMP-13.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2017/6341919</identifier><identifier>PMID: 28265573</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Adenoviruses ; Age ; Aging ; Animals ; Apoptosis ; Apoptosis - drug effects ; Autophagy ; Autophagy - drug effects ; Biomedical research ; Care and treatment ; Cells, Cultured ; Chondrocytes - cytology ; Chondrocytes - enzymology ; Collagen ; Development and progression ; Extracellular matrix ; Gene expression ; Gene Expression Regulation, Enzymologic - drug effects ; Glycation End Products, Advanced - pharmacology ; Health aspects ; Homeostasis ; Laboratories ; Matrix Metalloproteinase 13 - biosynthesis ; Matrix Metalloproteinase 3 - biosynthesis ; Osteoarthritis ; Rats ; Rats, Sprague-Dawley</subject><ispartof>BioMed research international, 2017-01, Vol.2017 (2017), p.1-9</ispartof><rights>Copyright © 2017 Wenzhou Huang et al.</rights><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 Wenzhou Huang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2017 Wenzhou Huang et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c598t-ce54c8d683cbe0189e8b3401d356f0f58902e3a7b2e49ddf4f45223b529fafbb3</citedby><cites>FETCH-LOGICAL-c598t-ce54c8d683cbe0189e8b3401d356f0f58902e3a7b2e49ddf4f45223b529fafbb3</cites><orcidid>0000-0001-5970-3569 ; 0000-0001-7999-0104 ; 0000-0001-5879-9482 ; 0000-0001-7566-2613 ; 0000-0002-4317-9755 ; 0000-0002-6105-1499 ; 0000-0001-9941-9837 ; 0000-0001-7863-2479</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/PMC5318618/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5318618/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28265573$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Camins, Antoni</contributor><creatorcontrib>Cheng, Xigao</creatorcontrib><creatorcontrib>Yin, Changchang</creatorcontrib><creatorcontrib>Deng, Zhongbo</creatorcontrib><creatorcontrib>Xu, Libiao</creatorcontrib><creatorcontrib>Wu, Tianlong</creatorcontrib><creatorcontrib>Li, Jian</creatorcontrib><creatorcontrib>Ao, Peng</creatorcontrib><creatorcontrib>Huang, Wenzhou</creatorcontrib><creatorcontrib>Chen, Wenjie</creatorcontrib><title>Autophagy Protects Advanced Glycation End Product-Induced Apoptosis and Expression of MMP-3 and MMP-13 in Rat Chondrocytes</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Aging is one of the most prominent risk factors for the pathological progression of osteoarthritis (OA). One feature of age-related changes in OA is advanced glycation end products (AGEs) accumulation in articular cartilage. Autophagy plays a cellular housekeeping role by removing dysfunctional cellular organelles and proteins. However, the relationship between autophagy and AGE-associated OA is unknown. The aim of this study is to determine whether autophagy participates in the pathology of AGE-treated chondrocytes and to investigate the exact role of autophagy in AGE-induced cell apoptosis and expression of matrix metalloproteinase- (MMP-) 3 and MMP-13. AGEs induced notable apoptosis that was detected by Annexin V/PI double-staining, and the upregulation of MMP-3 and MMP-13 was confirmed by Western blotting. Autophagy-related proteins were also determined by Western blotting, and chondrocytes were transfected with mCherry-GFP-LC3B-adenovirus to monitor autophagic flux. As a result, autophagy significantly increased in chondrocytes and peaked at 6 h. Furthermore, rapamycin (RA) attenuated AGE-induced apoptosis and expression of MMP-3 and MMP-13 by autophagy activation. In contrast, pretreatment with autophagy inhibitor 3-methyladenine (3-MA) enhanced the abovementioned effects of AGEs. We therefore demonstrated that autophagy is linked with AGE-related pathology in rat chondrocytes and plays a protective role in AGE-induced apoptosis and expression of MMP-3 and MMP-13.</description><subject>Adenoviruses</subject><subject>Age</subject><subject>Aging</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Biomedical research</subject><subject>Care and treatment</subject><subject>Cells, Cultured</subject><subject>Chondrocytes - cytology</subject><subject>Chondrocytes - enzymology</subject><subject>Collagen</subject><subject>Development and progression</subject><subject>Extracellular matrix</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Enzymologic - drug effects</subject><subject>Glycation End Products, Advanced - pharmacology</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Laboratories</subject><subject>Matrix Metalloproteinase 13 - biosynthesis</subject><subject>Matrix Metalloproteinase 3 - biosynthesis</subject><subject>Osteoarthritis</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkktv1DAUhSMEolXpjjWKxAaphPode4MUjYa2UisqBGvL8WMmVcYOsVMYfj1OZ5gCq3pzr3w-HV1fn6J4DcEHCCk9RwDW5wwTKKB4VhwjDEnFIIHPDz3GR8VpjHcgHw4ZEOxlcYQ4YpTW-Lj41UwpDGu12pa3Y0hWp1g25l55bU150W-1Sl3w5dKbWTeTTtWVzyWrzRCGFGIXS5XV5c9htDHOcHDlzc1thR_u5w7isvPlF5XKxTp4Mwa9TTa-Kl441Ud7uq8nxbdPy6-Ly-r688XVormuNBU8VdpSorlhHOvWAsiF5S0mABpMmQOOcgGQxapukSXCGEccoQjhliLhlGtbfFJ83PkOU7uxRlufRtXLYew2atzKoDr5r-K7tVyFe0kx5AzybPBubzCG75ONSW66qG3fK2_DFCXkdc0JIxw_BaWQIFKzjL79D70L0-jzJjLFhKCC1uCRWqneys67kEfUs6ls5h8EiJDZ6_2O0mOIcbTu8DoI5BwUOQdF7oOS8Td_b-QA_4lFBs52wLrzRv3onmhnM2OdeqQh5oAi_BtA3c1t</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Cheng, Xigao</creator><creator>Yin, Changchang</creator><creator>Deng, Zhongbo</creator><creator>Xu, Libiao</creator><creator>Wu, Tianlong</creator><creator>Li, Jian</creator><creator>Ao, Peng</creator><creator>Huang, Wenzhou</creator><creator>Chen, Wenjie</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5970-3569</orcidid><orcidid>https://orcid.org/0000-0001-7999-0104</orcidid><orcidid>https://orcid.org/0000-0001-5879-9482</orcidid><orcidid>https://orcid.org/0000-0001-7566-2613</orcidid><orcidid>https://orcid.org/0000-0002-4317-9755</orcidid><orcidid>https://orcid.org/0000-0002-6105-1499</orcidid><orcidid>https://orcid.org/0000-0001-9941-9837</orcidid><orcidid>https://orcid.org/0000-0001-7863-2479</orcidid></search><sort><creationdate>20170101</creationdate><title>Autophagy Protects Advanced Glycation End Product-Induced Apoptosis and Expression of MMP-3 and MMP-13 in Rat Chondrocytes</title><author>Cheng, Xigao ; Yin, Changchang ; Deng, Zhongbo ; Xu, Libiao ; Wu, Tianlong ; Li, Jian ; Ao, Peng ; Huang, Wenzhou ; Chen, Wenjie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c598t-ce54c8d683cbe0189e8b3401d356f0f58902e3a7b2e49ddf4f45223b529fafbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenoviruses</topic><topic>Age</topic><topic>Aging</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheng, Xigao</au><au>Yin, Changchang</au><au>Deng, Zhongbo</au><au>Xu, Libiao</au><au>Wu, Tianlong</au><au>Li, Jian</au><au>Ao, Peng</au><au>Huang, Wenzhou</au><au>Chen, Wenjie</au><au>Camins, Antoni</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autophagy Protects Advanced Glycation End Product-Induced Apoptosis and Expression of MMP-3 and MMP-13 in Rat Chondrocytes</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>2017</volume><issue>2017</issue><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Aging is one of the most prominent risk factors for the pathological progression of osteoarthritis (OA). One feature of age-related changes in OA is advanced glycation end products (AGEs) accumulation in articular cartilage. Autophagy plays a cellular housekeeping role by removing dysfunctional cellular organelles and proteins. However, the relationship between autophagy and AGE-associated OA is unknown. The aim of this study is to determine whether autophagy participates in the pathology of AGE-treated chondrocytes and to investigate the exact role of autophagy in AGE-induced cell apoptosis and expression of matrix metalloproteinase- (MMP-) 3 and MMP-13. AGEs induced notable apoptosis that was detected by Annexin V/PI double-staining, and the upregulation of MMP-3 and MMP-13 was confirmed by Western blotting. Autophagy-related proteins were also determined by Western blotting, and chondrocytes were transfected with mCherry-GFP-LC3B-adenovirus to monitor autophagic flux. As a result, autophagy significantly increased in chondrocytes and peaked at 6 h. Furthermore, rapamycin (RA) attenuated AGE-induced apoptosis and expression of MMP-3 and MMP-13 by autophagy activation. In contrast, pretreatment with autophagy inhibitor 3-methyladenine (3-MA) enhanced the abovementioned effects of AGEs. We therefore demonstrated that autophagy is linked with AGE-related pathology in rat chondrocytes and plays a protective role in AGE-induced apoptosis and expression of MMP-3 and MMP-13.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>28265573</pmid><doi>10.1155/2017/6341919</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-5970-3569</orcidid><orcidid>https://orcid.org/0000-0001-7999-0104</orcidid><orcidid>https://orcid.org/0000-0001-5879-9482</orcidid><orcidid>https://orcid.org/0000-0001-7566-2613</orcidid><orcidid>https://orcid.org/0000-0002-4317-9755</orcidid><orcidid>https://orcid.org/0000-0002-6105-1499</orcidid><orcidid>https://orcid.org/0000-0001-9941-9837</orcidid><orcidid>https://orcid.org/0000-0001-7863-2479</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenoviruses Age Aging Animals Apoptosis Apoptosis - drug effects Autophagy Autophagy - drug effects Biomedical research Care and treatment Cells, Cultured Chondrocytes - cytology Chondrocytes - enzymology Collagen Development and progression Extracellular matrix Gene expression Gene Expression Regulation, Enzymologic - drug effects Glycation End Products, Advanced - pharmacology Health aspects Homeostasis Laboratories Matrix Metalloproteinase 13 - biosynthesis Matrix Metalloproteinase 3 - biosynthesis Osteoarthritis Rats Rats, Sprague-Dawley |
| title | Autophagy Protects Advanced Glycation End Product-Induced Apoptosis and Expression of MMP-3 and MMP-13 in Rat Chondrocytes |
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