DNA damage preceding dopamine neuron degeneration in A53T human α-synuclein transgenic mice
Defective DNA repair has been linked with age-associated neurodegenerative disorders. Parkinson's disease (PD) is a progressive neurodegenerative disorder caused by genetic and environmental factors. Whether damages to nuclear DNA contribute to neurodegeneration of PD still remain obscure. in t...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2016-12, Vol.481 (1-2), p.104-110 |
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| creator | Wang, Degui Yu, Tianyu Liu, Yongqiang Yan, Jun Guo, Yingli Jing, Yuhong Yang, Xuguang Song, Yanfeng Tian, Yingxia |
| description | Defective DNA repair has been linked with age-associated neurodegenerative disorders. Parkinson's disease (PD) is a progressive neurodegenerative disorder caused by genetic and environmental factors. Whether damages to nuclear DNA contribute to neurodegeneration of PD still remain obscure. in this study we aim to explore whether nuclear DNA damage induce dopamine neuron degeneration in A53T human α-Synuclein over expressed mouse model. We investigated the effects of X-ray irradiation on A53T-α-Syn MEFs and A53T-α-Syn transgene mice. Our results indicate that A53T-α-Syn MEFs show a prolonged DNA damage repair process and senescense phenotype. DNA damage preceded onset of motor phenotype in A53T-α-Syn transgenic mice and decrease the number of nigrostriatal dopaminergic neurons. Neurons of A53T-α-Syn transgenic mice are more fragile to DNA damages.
•This study explore contribution of DNA damage to neurodegeneration in Parkinson's disease mice.•A53T-α-Syn MEF cells show a prolonged DNA damage repair process and senescense phenotype.•DNA damage preceded onset of motor phenotype in A53T-α-Syn transgenic mice.•DNA damage decrease the number of nigrostriatal dopaminergic neurons.•Neurons of A53T-α-Syn transgenic mice are more fragile to DNA damages. |
| doi_str_mv | 10.1016/j.bbrc.2016.11.008 |
| format | Article |
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•This study explore contribution of DNA damage to neurodegeneration in Parkinson's disease mice.•A53T-α-Syn MEF cells show a prolonged DNA damage repair process and senescense phenotype.•DNA damage preceded onset of motor phenotype in A53T-α-Syn transgenic mice.•DNA damage decrease the number of nigrostriatal dopaminergic neurons.•Neurons of A53T-α-Syn transgenic mice are more fragile to DNA damages.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2016.11.008</identifier><identifier>PMID: 27818201</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; alpha-Synuclein - genetics ; Animals ; Cell Line ; DNA damage ; DNA Damage - genetics ; DNA DAMAGES ; DNA REPAIR ; DOPAMINE ; Dopaminergic Neurons ; Humans ; Mice ; Mice, Transgenic ; Mouse ; NERVE CELLS ; Nerve Degeneration - genetics ; Nerve Degeneration - pathology ; Neurodegeneration ; Parkinson Disease - genetics ; Parkinson Disease - pathology ; Parkinson's disease ; PHENOTYPE ; TRANSGENIC MICE ; X RADIATION ; α-Synuclein</subject><ispartof>Biochemical and biophysical research communications, 2016-12, Vol.481 (1-2), p.104-110</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-7fe0caf8585866597f029f8a6dc507dc46254a4409e8162dce0cd13ac8e7a05c3</citedby><cites>FETCH-LOGICAL-c417t-7fe0caf8585866597f029f8a6dc507dc46254a4409e8162dce0cd13ac8e7a05c3</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.2016.11.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27818201$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22696722$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Degui</creatorcontrib><creatorcontrib>Yu, Tianyu</creatorcontrib><creatorcontrib>Liu, Yongqiang</creatorcontrib><creatorcontrib>Yan, Jun</creatorcontrib><creatorcontrib>Guo, Yingli</creatorcontrib><creatorcontrib>Jing, Yuhong</creatorcontrib><creatorcontrib>Yang, Xuguang</creatorcontrib><creatorcontrib>Song, Yanfeng</creatorcontrib><creatorcontrib>Tian, Yingxia</creatorcontrib><title>DNA damage preceding dopamine neuron degeneration in A53T human α-synuclein transgenic mice</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Defective DNA repair has been linked with age-associated neurodegenerative disorders. Parkinson's disease (PD) is a progressive neurodegenerative disorder caused by genetic and environmental factors. Whether damages to nuclear DNA contribute to neurodegeneration of PD still remain obscure. in this study we aim to explore whether nuclear DNA damage induce dopamine neuron degeneration in A53T human α-Synuclein over expressed mouse model. We investigated the effects of X-ray irradiation on A53T-α-Syn MEFs and A53T-α-Syn transgene mice. Our results indicate that A53T-α-Syn MEFs show a prolonged DNA damage repair process and senescense phenotype. DNA damage preceded onset of motor phenotype in A53T-α-Syn transgenic mice and decrease the number of nigrostriatal dopaminergic neurons. Neurons of A53T-α-Syn transgenic mice are more fragile to DNA damages.
•This study explore contribution of DNA damage to neurodegeneration in Parkinson's disease mice.•A53T-α-Syn MEF cells show a prolonged DNA damage repair process and senescense phenotype.•DNA damage preceded onset of motor phenotype in A53T-α-Syn transgenic mice.•DNA damage decrease the number of nigrostriatal dopaminergic neurons.•Neurons of A53T-α-Syn transgenic mice are more fragile to DNA damages.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>alpha-Synuclein - genetics</subject><subject>Animals</subject><subject>Cell Line</subject><subject>DNA damage</subject><subject>DNA Damage - genetics</subject><subject>DNA DAMAGES</subject><subject>DNA REPAIR</subject><subject>DOPAMINE</subject><subject>Dopaminergic Neurons</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mouse</subject><subject>NERVE CELLS</subject><subject>Nerve Degeneration - genetics</subject><subject>Nerve Degeneration - pathology</subject><subject>Neurodegeneration</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson Disease - pathology</subject><subject>Parkinson's disease</subject><subject>PHENOTYPE</subject><subject>TRANSGENIC MICE</subject><subject>X RADIATION</subject><subject>α-Synuclein</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9u1DAQhy0EotvCC3BAlrhwSZhxEseRuKwKBaSKXlqJA5LltSdbrzbOYidIfSxepM-Ew5YeEfLBf_TNbzT-GHuFUCKgfLcrN5toS5HPJWIJoJ6wFUIHhUCon7IVAMhCdPjthJ2mtANArGX3nJ2IVqHKdSv2_cPXNXdmMFvih0iWnA9b7saDGXwgHmiOY-COthQomsnniw983VTX_HYeTOD3v4p0F2a7p_w-RRNSRr3lg7f0gj3rzT7Ry4f9jN1cfLw-_1xcXn36cr6-LGyN7VS0PYE1vWrykrLp2h5E1ysjnW2gdbaWoqlNXUNHCqVwNuMOK2MVtQYaW52xN8fcMU1eJ-snsrd2DIHspIWQnWyFyNTbI3WI44-Z0qQHnyzt9ybQOCeNKndTNVbNf6BVCxV0f1BxRG0cU4rU60P0g4l3GkEvmvROL5r0okkj6qwpF71-yJ83A7nHkr9eMvD-CFD-tp-e4jIVhUVPXIZyo_9X_m9E3aKY</recordid><startdate>20161202</startdate><enddate>20161202</enddate><creator>Wang, Degui</creator><creator>Yu, Tianyu</creator><creator>Liu, Yongqiang</creator><creator>Yan, Jun</creator><creator>Guo, Yingli</creator><creator>Jing, Yuhong</creator><creator>Yang, Xuguang</creator><creator>Song, Yanfeng</creator><creator>Tian, Yingxia</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><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>OTOTI</scope></search><sort><creationdate>20161202</creationdate><title>DNA damage preceding dopamine neuron degeneration in A53T human α-synuclein transgenic mice</title><author>Wang, Degui ; Yu, Tianyu ; Liu, Yongqiang ; Yan, Jun ; Guo, Yingli ; Jing, Yuhong ; Yang, Xuguang ; Song, Yanfeng ; Tian, Yingxia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-7fe0caf8585866597f029f8a6dc507dc46254a4409e8162dce0cd13ac8e7a05c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>alpha-Synuclein - genetics</topic><topic>Animals</topic><topic>Cell Line</topic><topic>DNA damage</topic><topic>DNA Damage - genetics</topic><topic>DNA DAMAGES</topic><topic>DNA REPAIR</topic><topic>DOPAMINE</topic><topic>Dopaminergic Neurons</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mouse</topic><topic>NERVE CELLS</topic><topic>Nerve Degeneration - genetics</topic><topic>Nerve Degeneration - pathology</topic><topic>Neurodegeneration</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson Disease - pathology</topic><topic>Parkinson's disease</topic><topic>PHENOTYPE</topic><topic>TRANSGENIC MICE</topic><topic>X RADIATION</topic><topic>α-Synuclein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Degui</creatorcontrib><creatorcontrib>Yu, Tianyu</creatorcontrib><creatorcontrib>Liu, Yongqiang</creatorcontrib><creatorcontrib>Yan, Jun</creatorcontrib><creatorcontrib>Guo, Yingli</creatorcontrib><creatorcontrib>Jing, Yuhong</creatorcontrib><creatorcontrib>Yang, Xuguang</creatorcontrib><creatorcontrib>Song, Yanfeng</creatorcontrib><creatorcontrib>Tian, Yingxia</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><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Degui</au><au>Yu, Tianyu</au><au>Liu, Yongqiang</au><au>Yan, Jun</au><au>Guo, Yingli</au><au>Jing, Yuhong</au><au>Yang, Xuguang</au><au>Song, Yanfeng</au><au>Tian, Yingxia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA damage preceding dopamine neuron degeneration in A53T human α-synuclein transgenic mice</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2016-12-02</date><risdate>2016</risdate><volume>481</volume><issue>1-2</issue><spage>104</spage><epage>110</epage><pages>104-110</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Defective DNA repair has been linked with age-associated neurodegenerative disorders. Parkinson's disease (PD) is a progressive neurodegenerative disorder caused by genetic and environmental factors. Whether damages to nuclear DNA contribute to neurodegeneration of PD still remain obscure. in this study we aim to explore whether nuclear DNA damage induce dopamine neuron degeneration in A53T human α-Synuclein over expressed mouse model. We investigated the effects of X-ray irradiation on A53T-α-Syn MEFs and A53T-α-Syn transgene mice. Our results indicate that A53T-α-Syn MEFs show a prolonged DNA damage repair process and senescense phenotype. DNA damage preceded onset of motor phenotype in A53T-α-Syn transgenic mice and decrease the number of nigrostriatal dopaminergic neurons. Neurons of A53T-α-Syn transgenic mice are more fragile to DNA damages.
•This study explore contribution of DNA damage to neurodegeneration in Parkinson's disease mice.•A53T-α-Syn MEF cells show a prolonged DNA damage repair process and senescense phenotype.•DNA damage preceded onset of motor phenotype in A53T-α-Syn transgenic mice.•DNA damage decrease the number of nigrostriatal dopaminergic neurons.•Neurons of A53T-α-Syn transgenic mice are more fragile to DNA damages.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>27818201</pmid><doi>10.1016/j.bbrc.2016.11.008</doi><tpages>7</tpages></addata></record> |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | 60 APPLIED LIFE SCIENCES alpha-Synuclein - genetics Animals Cell Line DNA damage DNA Damage - genetics DNA DAMAGES DNA REPAIR DOPAMINE Dopaminergic Neurons Humans Mice Mice, Transgenic Mouse NERVE CELLS Nerve Degeneration - genetics Nerve Degeneration - pathology Neurodegeneration Parkinson Disease - genetics Parkinson Disease - pathology Parkinson's disease PHENOTYPE TRANSGENIC MICE X RADIATION α-Synuclein |
| title | DNA damage preceding dopamine neuron degeneration in A53T human α-synuclein transgenic mice |
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