The role of elevated autophagy on the synaptic plasticity impairment caused by CdSe/ZnS quantum dots
Abstract It is well known that autophagy, a cellular stress response to degrade damaged components, can be activated by many nanoparticles. We have demonstrated that CdSe/ZnS quantum dots (QDs), which are widely applied in vitro for diagnostics and cellular imaging, can impair synaptic transmission...
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| Veröffentlicht in: | Biomaterials 2013-12, Vol.34 (38), p.10172-10181 |
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| container_title | Biomaterials |
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| creator | Chen, Liang Miao, Yanyan Chen, Lin Jin, Peipei Zha, Yingying Chai, Yuming Zheng, Fang Zhang, Yunjiao Zhou, Wei Zhang, Jigui Wen, Longping Wang, Ming |
| description | Abstract It is well known that autophagy, a cellular stress response to degrade damaged components, can be activated by many nanoparticles. We have demonstrated that CdSe/ZnS quantum dots (QDs), which are widely applied in vitro for diagnostics and cellular imaging, can impair synaptic transmission and synaptic plasticity in the dentate gyrus (DG) area, but the mechanism is still unclear. Here we show that elevated autophagy is at least partly responsible for this synaptic dysfunction induced by QDs in vivo . QDs elicited autophagy in the HeLa cells and cultured hippocampal neurons as well, accompanied with GFP-light chain protein 3 (LC3) puncta dots and autophagosome formation, extensive conversion of LC3-I to LC3-II and a significant decrease of p62. Furthermore, we found that autophagy inhibitors (wortmannin, 3-MA or chloroquine) suppressed QDs-induced autophagic flux, partly blocked LTP impairment, coincident with down-regulation of synapsin-I and synapse deficits by QDs in the hippocampal CA1 area. Our studies have important implications in providing a potential clinical remedy for brain damage caused by nanomaterials and in designing safer nanoparticles. |
| doi_str_mv | 10.1016/j.biomaterials.2013.09.048 |
| format | Article |
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We have demonstrated that CdSe/ZnS quantum dots (QDs), which are widely applied in vitro for diagnostics and cellular imaging, can impair synaptic transmission and synaptic plasticity in the dentate gyrus (DG) area, but the mechanism is still unclear. Here we show that elevated autophagy is at least partly responsible for this synaptic dysfunction induced by QDs in vivo . QDs elicited autophagy in the HeLa cells and cultured hippocampal neurons as well, accompanied with GFP-light chain protein 3 (LC3) puncta dots and autophagosome formation, extensive conversion of LC3-I to LC3-II and a significant decrease of p62. Furthermore, we found that autophagy inhibitors (wortmannin, 3-MA or chloroquine) suppressed QDs-induced autophagic flux, partly blocked LTP impairment, coincident with down-regulation of synapsin-I and synapse deficits by QDs in the hippocampal CA1 area. Our studies have important implications in providing a potential clinical remedy for brain damage caused by nanomaterials and in designing safer nanoparticles.</description><identifier>ISSN: 0142-9612</identifier><identifier>EISSN: 1878-5905</identifier><identifier>DOI: 10.1016/j.biomaterials.2013.09.048</identifier><identifier>PMID: 24094936</identifier><language>eng</language><publisher>Netherlands: Elsevier Ltd</publisher><subject>Advanced Basic Science ; Animals ; Autophagy ; Autophagy - physiology ; Blotting, Western ; Cadmium Compounds - adverse effects ; Cadmium Compounds - chemistry ; Dentistry ; HeLa Cells ; Humans ; LC3-I/II ; Male ; Microscopy, Electron, Transmission ; QDs ; Quantum Dots - adverse effects ; Quantum Dots - chemistry ; Rats ; Rats, Wistar ; Reactive Oxygen Species - metabolism ; Selenium Compounds - adverse effects ; Selenium Compounds - chemistry ; Synapse density ; Synapsin-I ; Synaptic plasticity ; Synaptic Transmission - drug effects ; Zinc Compounds - adverse effects ; Zinc Compounds - chemistry</subject><ispartof>Biomaterials, 2013-12, Vol.34 (38), p.10172-10181</ispartof><rights>Elsevier Ltd</rights><rights>2013 Elsevier Ltd</rights><rights>Copyright © 2013 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-e42a6053e51356d0fffcd96533838b267335c1f9f73efd32786b5efa1377a6c83</citedby><cites>FETCH-LOGICAL-c435t-e42a6053e51356d0fffcd96533838b267335c1f9f73efd32786b5efa1377a6c83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0142961213011319$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24094936$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Liang</creatorcontrib><creatorcontrib>Miao, Yanyan</creatorcontrib><creatorcontrib>Chen, Lin</creatorcontrib><creatorcontrib>Jin, Peipei</creatorcontrib><creatorcontrib>Zha, Yingying</creatorcontrib><creatorcontrib>Chai, Yuming</creatorcontrib><creatorcontrib>Zheng, Fang</creatorcontrib><creatorcontrib>Zhang, Yunjiao</creatorcontrib><creatorcontrib>Zhou, Wei</creatorcontrib><creatorcontrib>Zhang, Jigui</creatorcontrib><creatorcontrib>Wen, Longping</creatorcontrib><creatorcontrib>Wang, Ming</creatorcontrib><title>The role of elevated autophagy on the synaptic plasticity impairment caused by CdSe/ZnS quantum dots</title><title>Biomaterials</title><addtitle>Biomaterials</addtitle><description>Abstract It is well known that autophagy, a cellular stress response to degrade damaged components, can be activated by many nanoparticles. We have demonstrated that CdSe/ZnS quantum dots (QDs), which are widely applied in vitro for diagnostics and cellular imaging, can impair synaptic transmission and synaptic plasticity in the dentate gyrus (DG) area, but the mechanism is still unclear. Here we show that elevated autophagy is at least partly responsible for this synaptic dysfunction induced by QDs in vivo . QDs elicited autophagy in the HeLa cells and cultured hippocampal neurons as well, accompanied with GFP-light chain protein 3 (LC3) puncta dots and autophagosome formation, extensive conversion of LC3-I to LC3-II and a significant decrease of p62. Furthermore, we found that autophagy inhibitors (wortmannin, 3-MA or chloroquine) suppressed QDs-induced autophagic flux, partly blocked LTP impairment, coincident with down-regulation of synapsin-I and synapse deficits by QDs in the hippocampal CA1 area. Our studies have important implications in providing a potential clinical remedy for brain damage caused by nanomaterials and in designing safer nanoparticles.</description><subject>Advanced Basic Science</subject><subject>Animals</subject><subject>Autophagy</subject><subject>Autophagy - physiology</subject><subject>Blotting, Western</subject><subject>Cadmium Compounds - adverse effects</subject><subject>Cadmium Compounds - chemistry</subject><subject>Dentistry</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>LC3-I/II</subject><subject>Male</subject><subject>Microscopy, Electron, Transmission</subject><subject>QDs</subject><subject>Quantum Dots - adverse effects</subject><subject>Quantum Dots - chemistry</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Selenium Compounds - adverse effects</subject><subject>Selenium Compounds - chemistry</subject><subject>Synapse density</subject><subject>Synapsin-I</subject><subject>Synaptic plasticity</subject><subject>Synaptic Transmission - drug effects</subject><subject>Zinc Compounds - adverse effects</subject><subject>Zinc Compounds - chemistry</subject><issn>0142-9612</issn><issn>1878-5905</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhi0EokvhLyCLE5ek_oiTmAMSWj6lShy2XLhYXntMvSRxajuV8u9xtAUhTpxGIz3vOzPvIPSKkpoS2l6d6qMPo84QvR5SzQjlNZE1afpHaEf7rq-EJOIx2hHasEq2lF2gZymdSOlJw56iC9YQ2Uje7pC9uQUcwwA4OAwD3Bdbi_WSw3yrf6w4TDgXIq2TnrM3eB50KtXnFftx1j6OMGVs9JKK7LjivT3A1ffpgO8WPeVlxDbk9Bw9cWVTePFQL9G3jx9u9p-r66-fvuzfXVem4SJX0DDdEsFBUC5aS5xzxspWcN7z_sjajnNhqJOu4-AsZ13fHgU4TXnX6db0_BK9PvvOMdwtkLIafTIwDHqCsCRFm4Y3TLJOFPTNGTUxpBTBqTn6UcdVUaK2lNVJ_Z2y2lJWRKqSchG_fJizHEewf6S_Yy3A-zMA5dp7D1El42EyYH0Ek5UN_v_mvP3Hxgx-8kYPP2GFdApLnDYNVYkpog7bv7d3U04o5VTyX1-Zqow</recordid><startdate>20131201</startdate><enddate>20131201</enddate><creator>Chen, Liang</creator><creator>Miao, Yanyan</creator><creator>Chen, Lin</creator><creator>Jin, Peipei</creator><creator>Zha, Yingying</creator><creator>Chai, Yuming</creator><creator>Zheng, Fang</creator><creator>Zhang, Yunjiao</creator><creator>Zhou, Wei</creator><creator>Zhang, Jigui</creator><creator>Wen, Longping</creator><creator>Wang, Ming</creator><general>Elsevier Ltd</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>20131201</creationdate><title>The role of elevated autophagy on the synaptic plasticity impairment caused by CdSe/ZnS quantum dots</title><author>Chen, Liang ; Miao, Yanyan ; Chen, Lin ; Jin, Peipei ; Zha, Yingying ; Chai, Yuming ; Zheng, Fang ; Zhang, Yunjiao ; Zhou, Wei ; Zhang, Jigui ; Wen, Longping ; Wang, Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c435t-e42a6053e51356d0fffcd96533838b267335c1f9f73efd32786b5efa1377a6c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Advanced Basic Science</topic><topic>Animals</topic><topic>Autophagy</topic><topic>Autophagy - physiology</topic><topic>Blotting, Western</topic><topic>Cadmium Compounds - adverse effects</topic><topic>Cadmium Compounds - chemistry</topic><topic>Dentistry</topic><topic>HeLa Cells</topic><topic>Humans</topic><topic>LC3-I/II</topic><topic>Male</topic><topic>Microscopy, Electron, Transmission</topic><topic>QDs</topic><topic>Quantum Dots - adverse effects</topic><topic>Quantum Dots - chemistry</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Selenium Compounds - adverse effects</topic><topic>Selenium Compounds - chemistry</topic><topic>Synapse density</topic><topic>Synapsin-I</topic><topic>Synaptic plasticity</topic><topic>Synaptic Transmission - drug effects</topic><topic>Zinc Compounds - adverse effects</topic><topic>Zinc Compounds - chemistry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Liang</creatorcontrib><creatorcontrib>Miao, Yanyan</creatorcontrib><creatorcontrib>Chen, Lin</creatorcontrib><creatorcontrib>Jin, Peipei</creatorcontrib><creatorcontrib>Zha, Yingying</creatorcontrib><creatorcontrib>Chai, Yuming</creatorcontrib><creatorcontrib>Zheng, Fang</creatorcontrib><creatorcontrib>Zhang, Yunjiao</creatorcontrib><creatorcontrib>Zhou, Wei</creatorcontrib><creatorcontrib>Zhang, Jigui</creatorcontrib><creatorcontrib>Wen, Longping</creatorcontrib><creatorcontrib>Wang, Ming</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>Biomaterials</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Liang</au><au>Miao, Yanyan</au><au>Chen, Lin</au><au>Jin, Peipei</au><au>Zha, Yingying</au><au>Chai, Yuming</au><au>Zheng, Fang</au><au>Zhang, Yunjiao</au><au>Zhou, Wei</au><au>Zhang, Jigui</au><au>Wen, Longping</au><au>Wang, Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of elevated autophagy on the synaptic plasticity impairment caused by CdSe/ZnS quantum dots</atitle><jtitle>Biomaterials</jtitle><addtitle>Biomaterials</addtitle><date>2013-12-01</date><risdate>2013</risdate><volume>34</volume><issue>38</issue><spage>10172</spage><epage>10181</epage><pages>10172-10181</pages><issn>0142-9612</issn><eissn>1878-5905</eissn><abstract>Abstract It is well known that autophagy, a cellular stress response to degrade damaged components, can be activated by many nanoparticles. We have demonstrated that CdSe/ZnS quantum dots (QDs), which are widely applied in vitro for diagnostics and cellular imaging, can impair synaptic transmission and synaptic plasticity in the dentate gyrus (DG) area, but the mechanism is still unclear. Here we show that elevated autophagy is at least partly responsible for this synaptic dysfunction induced by QDs in vivo . QDs elicited autophagy in the HeLa cells and cultured hippocampal neurons as well, accompanied with GFP-light chain protein 3 (LC3) puncta dots and autophagosome formation, extensive conversion of LC3-I to LC3-II and a significant decrease of p62. Furthermore, we found that autophagy inhibitors (wortmannin, 3-MA or chloroquine) suppressed QDs-induced autophagic flux, partly blocked LTP impairment, coincident with down-regulation of synapsin-I and synapse deficits by QDs in the hippocampal CA1 area. Our studies have important implications in providing a potential clinical remedy for brain damage caused by nanomaterials and in designing safer nanoparticles.</abstract><cop>Netherlands</cop><pub>Elsevier Ltd</pub><pmid>24094936</pmid><doi>10.1016/j.biomaterials.2013.09.048</doi><tpages>10</tpages></addata></record> |
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| subjects | Advanced Basic Science Animals Autophagy Autophagy - physiology Blotting, Western Cadmium Compounds - adverse effects Cadmium Compounds - chemistry Dentistry HeLa Cells Humans LC3-I/II Male Microscopy, Electron, Transmission QDs Quantum Dots - adverse effects Quantum Dots - chemistry Rats Rats, Wistar Reactive Oxygen Species - metabolism Selenium Compounds - adverse effects Selenium Compounds - chemistry Synapse density Synapsin-I Synaptic plasticity Synaptic Transmission - drug effects Zinc Compounds - adverse effects Zinc Compounds - chemistry |
| title | The role of elevated autophagy on the synaptic plasticity impairment caused by CdSe/ZnS quantum dots |
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