Modulation of DNA base excision repair during neuronal differentiation
Abstract Neurons are terminally differentiated cells with a high rate of metabolism and multiple biological properties distinct from their undifferentiated precursors. Previous studies showed that nucleotide excision DNA repair is downregulated in postmitotic muscle cells and neurons. Here, we chara...
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| Veröffentlicht in: | Neurobiology of aging 2013-07, Vol.34 (7), p.1717-1727 |
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| container_title | Neurobiology of aging |
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| creator | Sykora, Peter Yang, Jenq-Lin Ferrarelli, Leslie K Tian, Jingyan Tadokoro, Takashi Kulkarni, Avanti Weissman, Lior Keijzers, Guido Wilson, David M Mattson, Mark P Bohr, Vilhelm A |
| description | Abstract Neurons are terminally differentiated cells with a high rate of metabolism and multiple biological properties distinct from their undifferentiated precursors. Previous studies showed that nucleotide excision DNA repair is downregulated in postmitotic muscle cells and neurons. Here, we characterize DNA damage susceptibility and base excision DNA repair (BER) capacity in undifferentiated and differentiated human neural cells. The results show that undifferentiated human SH-SY5Y neuroblastoma cells are less sensitive to oxidative damage than their differentiated counterparts, in part because they have robust BER capacity, which is heavily attenuated in postmitotic neurons. The reduction in BER activity in differentiated cells correlates with diminished protein levels of key long patch BER components, flap endonuclease-1, proliferating cell nuclear antigen, and ligase I. Thus, because of their higher BER capacity, proliferative neural progenitor cells are more efficient at repairing DNA damage compared with their neuronally differentiated progeny. |
| doi_str_mv | 10.1016/j.neurobiolaging.2012.12.016 |
| format | Article |
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Previous studies showed that nucleotide excision DNA repair is downregulated in postmitotic muscle cells and neurons. Here, we characterize DNA damage susceptibility and base excision DNA repair (BER) capacity in undifferentiated and differentiated human neural cells. The results show that undifferentiated human SH-SY5Y neuroblastoma cells are less sensitive to oxidative damage than their differentiated counterparts, in part because they have robust BER capacity, which is heavily attenuated in postmitotic neurons. The reduction in BER activity in differentiated cells correlates with diminished protein levels of key long patch BER components, flap endonuclease-1, proliferating cell nuclear antigen, and ligase I. Thus, because of their higher BER capacity, proliferative neural progenitor cells are more efficient at repairing DNA damage compared with their neuronally differentiated progeny.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2012.12.016</identifier><identifier>PMID: 23375654</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aging ; BER ; Cell Differentiation - drug effects ; Cell Differentiation - physiology ; Cell Line, Tumor ; Differentiation ; DNA - metabolism ; DNA - physiology ; DNA damage ; DNA Damage - drug effects ; DNA Damage - physiology ; DNA repair ; DNA Repair - drug effects ; DNA Repair - physiology ; Humans ; Hydrogen Peroxide - toxicity ; Internal Medicine ; Neurology ; Neuron ; Neurons - drug effects ; Neurons - physiology ; Postmitotic</subject><ispartof>Neurobiology of aging, 2013-07, Vol.34 (7), p.1717-1727</ispartof><rights>2013</rights><rights>Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c682t-3bff01cb3bace9a7831ddbd3d745d058ef405586fceb540d4293fe4ef39635873</citedby><cites>FETCH-LOGICAL-c682t-3bff01cb3bace9a7831ddbd3d745d058ef405586fceb540d4293fe4ef39635873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0197458012006471$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23375654$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sykora, Peter</creatorcontrib><creatorcontrib>Yang, Jenq-Lin</creatorcontrib><creatorcontrib>Ferrarelli, Leslie K</creatorcontrib><creatorcontrib>Tian, Jingyan</creatorcontrib><creatorcontrib>Tadokoro, Takashi</creatorcontrib><creatorcontrib>Kulkarni, Avanti</creatorcontrib><creatorcontrib>Weissman, Lior</creatorcontrib><creatorcontrib>Keijzers, Guido</creatorcontrib><creatorcontrib>Wilson, David M</creatorcontrib><creatorcontrib>Mattson, Mark P</creatorcontrib><creatorcontrib>Bohr, Vilhelm A</creatorcontrib><title>Modulation of DNA base excision repair during neuronal differentiation</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>Abstract Neurons are terminally differentiated cells with a high rate of metabolism and multiple biological properties distinct from their undifferentiated precursors. Previous studies showed that nucleotide excision DNA repair is downregulated in postmitotic muscle cells and neurons. Here, we characterize DNA damage susceptibility and base excision DNA repair (BER) capacity in undifferentiated and differentiated human neural cells. The results show that undifferentiated human SH-SY5Y neuroblastoma cells are less sensitive to oxidative damage than their differentiated counterparts, in part because they have robust BER capacity, which is heavily attenuated in postmitotic neurons. The reduction in BER activity in differentiated cells correlates with diminished protein levels of key long patch BER components, flap endonuclease-1, proliferating cell nuclear antigen, and ligase I. Thus, because of their higher BER capacity, proliferative neural progenitor cells are more efficient at repairing DNA damage compared with their neuronally differentiated progeny.</description><subject>Aging</subject><subject>BER</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - physiology</subject><subject>Cell Line, Tumor</subject><subject>Differentiation</subject><subject>DNA - metabolism</subject><subject>DNA - physiology</subject><subject>DNA damage</subject><subject>DNA Damage - drug effects</subject><subject>DNA Damage - physiology</subject><subject>DNA repair</subject><subject>DNA Repair - drug effects</subject><subject>DNA Repair - physiology</subject><subject>Humans</subject><subject>Hydrogen Peroxide - toxicity</subject><subject>Internal Medicine</subject><subject>Neurology</subject><subject>Neuron</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Postmitotic</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUk1v1DAQtRAVXQp_AeXAgUu2dmzHjoQqVS0LlVo4AGfLsceLF2-82ElF_z1Ot61aLiCNZMnz3puPNwi9JXhJMGmPN8sBphR7H4Ne-2G9bDBpliVK8hlaEM5lTVgnnqMFJp2oGZf4EL3MeYMxFky0L9BhQ6ngLWcLtLqKdgp69HGooqvOP59Wvc5QwW_j8_yZYKd9quyUSq3qtvSgQ2W9c5BgGP0t9xU6cDpkeH33HqHvqw_fzj7Vl18-XpydXtamlc1Y0945TExPe22g00JSYm1vqRWMW8wlOIZL_60z0HOGLWs66oCBo11LuRT0CJ3sdXdTvwVrSgNJB7VLfqvTjYraq6eZwf9Q63itOBet7FgReHcnkOKvCfKotj4bCEEPEKesCG8wFVLI5t9QyiTrCJayQN_voSbFnBO4h44IVrNraqOeuqZm11SJkiz0N4-neiDf21QAqz0Aym6vPSSVjYfBgPUJzKhs9P9b6eQvIRP84I0OP-EG8iZOqbhbZlO5ENTX-YLmAyINxi0ThP4BYk_IIg</recordid><startdate>20130701</startdate><enddate>20130701</enddate><creator>Sykora, Peter</creator><creator>Yang, Jenq-Lin</creator><creator>Ferrarelli, Leslie K</creator><creator>Tian, Jingyan</creator><creator>Tadokoro, Takashi</creator><creator>Kulkarni, Avanti</creator><creator>Weissman, Lior</creator><creator>Keijzers, Guido</creator><creator>Wilson, David M</creator><creator>Mattson, Mark P</creator><creator>Bohr, Vilhelm A</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>7TK</scope><scope>7TM</scope><scope>5PM</scope></search><sort><creationdate>20130701</creationdate><title>Modulation of DNA base excision repair during neuronal differentiation</title><author>Sykora, Peter ; Yang, Jenq-Lin ; Ferrarelli, Leslie K ; Tian, Jingyan ; Tadokoro, Takashi ; Kulkarni, Avanti ; Weissman, Lior ; Keijzers, Guido ; Wilson, David M ; Mattson, Mark P ; Bohr, Vilhelm A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c682t-3bff01cb3bace9a7831ddbd3d745d058ef405586fceb540d4293fe4ef39635873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Aging</topic><topic>BER</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Differentiation - physiology</topic><topic>Cell Line, Tumor</topic><topic>Differentiation</topic><topic>DNA - metabolism</topic><topic>DNA - physiology</topic><topic>DNA damage</topic><topic>DNA Damage - drug effects</topic><topic>DNA Damage - physiology</topic><topic>DNA repair</topic><topic>DNA Repair - drug effects</topic><topic>DNA Repair - physiology</topic><topic>Humans</topic><topic>Hydrogen Peroxide - toxicity</topic><topic>Internal Medicine</topic><topic>Neurology</topic><topic>Neuron</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Postmitotic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sykora, Peter</creatorcontrib><creatorcontrib>Yang, Jenq-Lin</creatorcontrib><creatorcontrib>Ferrarelli, Leslie K</creatorcontrib><creatorcontrib>Tian, Jingyan</creatorcontrib><creatorcontrib>Tadokoro, Takashi</creatorcontrib><creatorcontrib>Kulkarni, Avanti</creatorcontrib><creatorcontrib>Weissman, Lior</creatorcontrib><creatorcontrib>Keijzers, Guido</creatorcontrib><creatorcontrib>Wilson, David M</creatorcontrib><creatorcontrib>Mattson, Mark P</creatorcontrib><creatorcontrib>Bohr, Vilhelm A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sykora, Peter</au><au>Yang, Jenq-Lin</au><au>Ferrarelli, Leslie K</au><au>Tian, Jingyan</au><au>Tadokoro, Takashi</au><au>Kulkarni, Avanti</au><au>Weissman, Lior</au><au>Keijzers, Guido</au><au>Wilson, David M</au><au>Mattson, Mark P</au><au>Bohr, Vilhelm A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of DNA base excision repair during neuronal differentiation</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2013-07-01</date><risdate>2013</risdate><volume>34</volume><issue>7</issue><spage>1717</spage><epage>1727</epage><pages>1717-1727</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><abstract>Abstract Neurons are terminally differentiated cells with a high rate of metabolism and multiple biological properties distinct from their undifferentiated precursors. Previous studies showed that nucleotide excision DNA repair is downregulated in postmitotic muscle cells and neurons. Here, we characterize DNA damage susceptibility and base excision DNA repair (BER) capacity in undifferentiated and differentiated human neural cells. The results show that undifferentiated human SH-SY5Y neuroblastoma cells are less sensitive to oxidative damage than their differentiated counterparts, in part because they have robust BER capacity, which is heavily attenuated in postmitotic neurons. The reduction in BER activity in differentiated cells correlates with diminished protein levels of key long patch BER components, flap endonuclease-1, proliferating cell nuclear antigen, and ligase I. 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| subjects | Aging BER Cell Differentiation - drug effects Cell Differentiation - physiology Cell Line, Tumor Differentiation DNA - metabolism DNA - physiology DNA damage DNA Damage - drug effects DNA Damage - physiology DNA repair DNA Repair - drug effects DNA Repair - physiology Humans Hydrogen Peroxide - toxicity Internal Medicine Neurology Neuron Neurons - drug effects Neurons - physiology Postmitotic |
| title | Modulation of DNA base excision repair during neuronal differentiation |
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