Baicalein reduces E46K α-synuclein aggregation in vitro and protects cells against E46K α-synuclein toxicity in cell models of familiar Parkinsonism
J. Neurochem. (2010) 114, 419-429. The E46K is a point mutation in α-synuclein (α-syn) that causes familial Parkinsonism with Lewy body dementia. We have now generated a cell model of Parkinsonism/Parkinson's disease (PD) and demonstrated cell toxicity after expression of E46K in the differenti...
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| creator | Jiang, Mali Porat-Shliom, Yair Pei, Zhong Cheng, Yong Xiang, Lan Sommers, Katherine Li, Qing Gillardon, Frank Hengerer, Bastian Berlinicke, Cynthia Smith, Wanli W Zack, Donald J Poirier, Michelle A Ross, Christopher A Duan, Wenzhen |
| description | J. Neurochem. (2010) 114, 419-429. The E46K is a point mutation in α-synuclein (α-syn) that causes familial Parkinsonism with Lewy body dementia. We have now generated a cell model of Parkinsonism/Parkinson's disease (PD) and demonstrated cell toxicity after expression of E46K in the differentiated PC12 cells. E46K α-syn inhibited proteasome activity and induced mitochondrial depolarization in the cell model. Baicalein has been reported to inhibit fibrillation of wild type α-syn in vitro, and to protect neurons against several chemical-induced models of PD. We now report that baicalein significantly attenuated E46K-induced mitochondrial depolarization and proteasome inhibition, and protected cells against E46K-induced toxicity in a cell model of PD. Baicalein also reduced E46K fibrilization in vitro, with a concentration-dependent decrease in beta sheet conformation, though it increased some oligomeric species, and decreased formation of E46K α-syn-induced aggregates and rescued toxicity in N2A cells. Taken together, these data indicate that mitochondrial dysfunction, proteasome inhibition and specific aspects of abnormal E46K aggregation accompany E46K α-syn-induced cell toxicity, and baicalein can protect as well as altering aggregation properties. Baicalein has potential as a tool to understand the relation between different aggregation species and toxicity, and might be a candidate compound for further validation by using in vivoα-syn genetic PD models. |
| doi_str_mv | 10.1111/j.1471-4159.2010.06752.x |
| format | Article |
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Neurochem. (2010) 114, 419-429. The E46K is a point mutation in α-synuclein (α-syn) that causes familial Parkinsonism with Lewy body dementia. We have now generated a cell model of Parkinsonism/Parkinson's disease (PD) and demonstrated cell toxicity after expression of E46K in the differentiated PC12 cells. E46K α-syn inhibited proteasome activity and induced mitochondrial depolarization in the cell model. Baicalein has been reported to inhibit fibrillation of wild type α-syn in vitro, and to protect neurons against several chemical-induced models of PD. We now report that baicalein significantly attenuated E46K-induced mitochondrial depolarization and proteasome inhibition, and protected cells against E46K-induced toxicity in a cell model of PD. Baicalein also reduced E46K fibrilization in vitro, with a concentration-dependent decrease in beta sheet conformation, though it increased some oligomeric species, and decreased formation of E46K α-syn-induced aggregates and rescued toxicity in N2A cells. Taken together, these data indicate that mitochondrial dysfunction, proteasome inhibition and specific aspects of abnormal E46K aggregation accompany E46K α-syn-induced cell toxicity, and baicalein can protect as well as altering aggregation properties. Baicalein has potential as a tool to understand the relation between different aggregation species and toxicity, and might be a candidate compound for further validation by using in vivoα-syn genetic PD models.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2010.06752.x</identifier><identifier>PMID: 20412383</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>aggregation ; alpha-Synuclein - biosynthesis ; alpha-Synuclein - genetics ; Animals ; baicalein ; Biological and medical sciences ; Cell Death ; Cell Differentiation ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Flavanones - pharmacology ; Medical sciences ; Membrane Potential, Mitochondrial - drug effects ; mitochondria depolarization ; Mutation ; Nervous system (semeiology, syndromes) ; Nervous system as a whole ; Neurology ; Neurons - metabolism ; Neurons - ultrastructure ; Parkinson disease ; Parkinsonian Disorders - genetics ; Parkinsonian Disorders - metabolism ; Parkinson’s disease ; PC12 Cells ; proteasome inhibition ; Proteasome Inhibitors ; Rats ; α-synuclein</subject><ispartof>Journal of neurochemistry, 2010-07, Vol.114 (2), p.419-429</ispartof><rights>2010 The Authors. Journal Compilation © 2010 International Society for Neurochemistry</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5592-75a494781369a6f75d600fea842a49f914fae657d11bb624dfcc7b3eaffcde33</citedby><cites>FETCH-LOGICAL-c5592-75a494781369a6f75d600fea842a49f914fae657d11bb624dfcc7b3eaffcde33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1471-4159.2010.06752.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2010.06752.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22997120$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20412383$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Mali</creatorcontrib><creatorcontrib>Porat-Shliom, Yair</creatorcontrib><creatorcontrib>Pei, Zhong</creatorcontrib><creatorcontrib>Cheng, Yong</creatorcontrib><creatorcontrib>Xiang, Lan</creatorcontrib><creatorcontrib>Sommers, Katherine</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><creatorcontrib>Gillardon, Frank</creatorcontrib><creatorcontrib>Hengerer, Bastian</creatorcontrib><creatorcontrib>Berlinicke, Cynthia</creatorcontrib><creatorcontrib>Smith, Wanli W</creatorcontrib><creatorcontrib>Zack, Donald J</creatorcontrib><creatorcontrib>Poirier, Michelle A</creatorcontrib><creatorcontrib>Ross, Christopher A</creatorcontrib><creatorcontrib>Duan, Wenzhen</creatorcontrib><title>Baicalein reduces E46K α-synuclein aggregation in vitro and protects cells against E46K α-synuclein toxicity in cell models of familiar Parkinsonism</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>J. Neurochem. (2010) 114, 419-429. The E46K is a point mutation in α-synuclein (α-syn) that causes familial Parkinsonism with Lewy body dementia. We have now generated a cell model of Parkinsonism/Parkinson's disease (PD) and demonstrated cell toxicity after expression of E46K in the differentiated PC12 cells. E46K α-syn inhibited proteasome activity and induced mitochondrial depolarization in the cell model. Baicalein has been reported to inhibit fibrillation of wild type α-syn in vitro, and to protect neurons against several chemical-induced models of PD. We now report that baicalein significantly attenuated E46K-induced mitochondrial depolarization and proteasome inhibition, and protected cells against E46K-induced toxicity in a cell model of PD. Baicalein also reduced E46K fibrilization in vitro, with a concentration-dependent decrease in beta sheet conformation, though it increased some oligomeric species, and decreased formation of E46K α-syn-induced aggregates and rescued toxicity in N2A cells. Taken together, these data indicate that mitochondrial dysfunction, proteasome inhibition and specific aspects of abnormal E46K aggregation accompany E46K α-syn-induced cell toxicity, and baicalein can protect as well as altering aggregation properties. Baicalein has potential as a tool to understand the relation between different aggregation species and toxicity, and might be a candidate compound for further validation by using in vivoα-syn genetic PD models.</description><subject>aggregation</subject><subject>alpha-Synuclein - biosynthesis</subject><subject>alpha-Synuclein - genetics</subject><subject>Animals</subject><subject>baicalein</subject><subject>Biological and medical sciences</subject><subject>Cell Death</subject><subject>Cell Differentiation</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Flavanones - pharmacology</subject><subject>Medical sciences</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>mitochondria depolarization</subject><subject>Mutation</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Nervous system as a whole</subject><subject>Neurology</subject><subject>Neurons - metabolism</subject><subject>Neurons - ultrastructure</subject><subject>Parkinson disease</subject><subject>Parkinsonian Disorders - genetics</subject><subject>Parkinsonian Disorders - metabolism</subject><subject>Parkinson’s disease</subject><subject>PC12 Cells</subject><subject>proteasome inhibition</subject><subject>Proteasome Inhibitors</subject><subject>Rats</subject><subject>α-synuclein</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcuO0zAUhiMEYsrAK4A3iFWK704WIEE1XEeAxLC2Th27uCRxsZOhfRHegxfhmXCmpYCEBN74cr7_9zn6iwIRPCd5PVzPCVek5ETUc4rzK5ZK0Pn2WjE7Fq4XM4wpLRnm9KS4ldIaYyK5JDeLE4o5oaxis-LrU_AGWut7FG0zGpvQGZev0fdvZdr1o7mqwGoV7QoGH3qUr5d-iAFB36BNDIM1Q0LGtm3KHPg-DX9xGMLWGz_sJvnEoi40NiuCQw4633qI6B3ET1keep-628UNB22ydw77aXHx7Oxi8aI8f_v85eLJeWmEqGmpBPCaq4owWYN0SjQSY2eh4jQXXE24AyuFaghZLiXljTNGLZkF50xjGTstHu9tN-Oys42x_RCh1ZvoO4g7HcDrPyu9_6hX4VLTmmAiZDZ4cDCI4fNo06A7n6YBobdhTFpxqoTElP2bZBwTojDOZLUnTQwpReuO_RCsp_j1Wk8p6yllPcWvr-LX2yy9-_s8R-HPvDNw_wBAyrG7CL3x6RdH61oROvXwaM998a3d_XcD-tWbxXTK-nt7vYOgYRXzHx_eZ5JhUolKSMF-AJ2x2QY</recordid><startdate>201007</startdate><enddate>201007</enddate><creator>Jiang, Mali</creator><creator>Porat-Shliom, Yair</creator><creator>Pei, Zhong</creator><creator>Cheng, Yong</creator><creator>Xiang, Lan</creator><creator>Sommers, Katherine</creator><creator>Li, Qing</creator><creator>Gillardon, Frank</creator><creator>Hengerer, Bastian</creator><creator>Berlinicke, Cynthia</creator><creator>Smith, Wanli W</creator><creator>Zack, Donald J</creator><creator>Poirier, Michelle A</creator><creator>Ross, Christopher A</creator><creator>Duan, Wenzhen</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</general><scope>FBQ</scope><scope>IQODW</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>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>201007</creationdate><title>Baicalein reduces E46K α-synuclein aggregation in vitro and protects cells against E46K α-synuclein toxicity in cell models of familiar Parkinsonism</title><author>Jiang, Mali ; Porat-Shliom, Yair ; Pei, Zhong ; Cheng, Yong ; Xiang, Lan ; Sommers, Katherine ; Li, Qing ; Gillardon, Frank ; Hengerer, Bastian ; Berlinicke, Cynthia ; Smith, Wanli W ; Zack, Donald J ; Poirier, Michelle A ; Ross, Christopher A ; Duan, Wenzhen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5592-75a494781369a6f75d600fea842a49f914fae657d11bb624dfcc7b3eaffcde33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>aggregation</topic><topic>alpha-Synuclein - biosynthesis</topic><topic>alpha-Synuclein - genetics</topic><topic>Animals</topic><topic>baicalein</topic><topic>Biological and medical sciences</topic><topic>Cell Death</topic><topic>Cell Differentiation</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Flavanones - pharmacology</topic><topic>Medical sciences</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>mitochondria depolarization</topic><topic>Mutation</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Nervous system as a whole</topic><topic>Neurology</topic><topic>Neurons - metabolism</topic><topic>Neurons - ultrastructure</topic><topic>Parkinson disease</topic><topic>Parkinsonian Disorders - genetics</topic><topic>Parkinsonian Disorders - metabolism</topic><topic>Parkinson’s disease</topic><topic>PC12 Cells</topic><topic>proteasome inhibition</topic><topic>Proteasome Inhibitors</topic><topic>Rats</topic><topic>α-synuclein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Mali</creatorcontrib><creatorcontrib>Porat-Shliom, Yair</creatorcontrib><creatorcontrib>Pei, Zhong</creatorcontrib><creatorcontrib>Cheng, Yong</creatorcontrib><creatorcontrib>Xiang, Lan</creatorcontrib><creatorcontrib>Sommers, Katherine</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><creatorcontrib>Gillardon, Frank</creatorcontrib><creatorcontrib>Hengerer, Bastian</creatorcontrib><creatorcontrib>Berlinicke, Cynthia</creatorcontrib><creatorcontrib>Smith, Wanli W</creatorcontrib><creatorcontrib>Zack, Donald J</creatorcontrib><creatorcontrib>Poirier, Michelle A</creatorcontrib><creatorcontrib>Ross, Christopher A</creatorcontrib><creatorcontrib>Duan, Wenzhen</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</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>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Mali</au><au>Porat-Shliom, Yair</au><au>Pei, Zhong</au><au>Cheng, Yong</au><au>Xiang, Lan</au><au>Sommers, Katherine</au><au>Li, Qing</au><au>Gillardon, Frank</au><au>Hengerer, Bastian</au><au>Berlinicke, Cynthia</au><au>Smith, Wanli W</au><au>Zack, Donald J</au><au>Poirier, Michelle A</au><au>Ross, Christopher A</au><au>Duan, Wenzhen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Baicalein reduces E46K α-synuclein aggregation in vitro and protects cells against E46K α-synuclein toxicity in cell models of familiar Parkinsonism</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2010-07</date><risdate>2010</risdate><volume>114</volume><issue>2</issue><spage>419</spage><epage>429</epage><pages>419-429</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>J. Neurochem. (2010) 114, 419-429. The E46K is a point mutation in α-synuclein (α-syn) that causes familial Parkinsonism with Lewy body dementia. We have now generated a cell model of Parkinsonism/Parkinson's disease (PD) and demonstrated cell toxicity after expression of E46K in the differentiated PC12 cells. E46K α-syn inhibited proteasome activity and induced mitochondrial depolarization in the cell model. Baicalein has been reported to inhibit fibrillation of wild type α-syn in vitro, and to protect neurons against several chemical-induced models of PD. We now report that baicalein significantly attenuated E46K-induced mitochondrial depolarization and proteasome inhibition, and protected cells against E46K-induced toxicity in a cell model of PD. Baicalein also reduced E46K fibrilization in vitro, with a concentration-dependent decrease in beta sheet conformation, though it increased some oligomeric species, and decreased formation of E46K α-syn-induced aggregates and rescued toxicity in N2A cells. Taken together, these data indicate that mitochondrial dysfunction, proteasome inhibition and specific aspects of abnormal E46K aggregation accompany E46K α-syn-induced cell toxicity, and baicalein can protect as well as altering aggregation properties. Baicalein has potential as a tool to understand the relation between different aggregation species and toxicity, and might be a candidate compound for further validation by using in vivoα-syn genetic PD models.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>20412383</pmid><doi>10.1111/j.1471-4159.2010.06752.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | aggregation alpha-Synuclein - biosynthesis alpha-Synuclein - genetics Animals baicalein Biological and medical sciences Cell Death Cell Differentiation Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Flavanones - pharmacology Medical sciences Membrane Potential, Mitochondrial - drug effects mitochondria depolarization Mutation Nervous system (semeiology, syndromes) Nervous system as a whole Neurology Neurons - metabolism Neurons - ultrastructure Parkinson disease Parkinsonian Disorders - genetics Parkinsonian Disorders - metabolism Parkinson’s disease PC12 Cells proteasome inhibition Proteasome Inhibitors Rats α-synuclein |
| title | Baicalein reduces E46K α-synuclein aggregation in vitro and protects cells against E46K α-synuclein toxicity in cell models of familiar Parkinsonism |
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