The protective effect of hepatocyte growth factor against cell death in the hippocampus after transient forebrain ischemia is related to the improvement of apurinic/apyrimidinic endonuclease/redox factor-1 level and inhibition of NADPH oxidase activity
Early oxidative DNA damage is regarded to be an initiator of neuronal apoptotic cell death after cerebral ischemia. Although evidence suggests that HGF has the ability to protect cells from oxidative stress, it remains unclear as to how HGF suppresses oxidative DNA damage after cerebral ischemia. Ap...
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| Veröffentlicht in: | Neuroscience letters 2006-10, Vol.407 (2), p.136-140 |
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| container_title | Neuroscience letters |
| container_volume | 407 |
| creator | Niimura, Makiko Takagi, Norio Takagi, Keiko Mizutani, Reiko Tanonaka, Kouichi Funakoshi, Hiroshi Matsumoto, Kunio Nakamura, Toshikazu Takeo, Satoshi |
| description | Early oxidative DNA damage is regarded to be an initiator of neuronal apoptotic cell death after cerebral ischemia. Although evidence suggests that HGF has the ability to protect cells from oxidative stress, it remains unclear as to how HGF suppresses oxidative DNA damage after cerebral ischemia. Apurinic/apyrimidinic endonuclease/redox factor-1 (APE/Ref-1) is a multifunctional protein in the DNA base repair pathway that is responsible for repairing apurinic/apyrimidinic sites in DNA after oxidation. We demonstrated that both the immunoreactivity and the number of APE/Ref-1-positive cells in the hippocampal CA1 region were decreased after transient forebrain ischemia and that treatment with HGF suppressed this reduction. The expression of Cu/ZnSOD and MnSOD in the hippocampal CA1 region did not change after ischemia, regardless of treatment with or not with HGF. The activity of NADPH oxidase was increased mainly in glia-like cells in the hippocampal CA1 region after ischemia, and this increase was attenuated by HGF treatment. These results suggest that the protective effects of HGF against cerebral ischemia-induced cell death in the hippocampal CA1 region are related to the improvement of neuronal APE/Ref-1 expression and the inhibition of NADPH oxidase activity in glia-like cells. |
| doi_str_mv | 10.1016/j.neulet.2006.08.060 |
| format | Article |
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Although evidence suggests that HGF has the ability to protect cells from oxidative stress, it remains unclear as to how HGF suppresses oxidative DNA damage after cerebral ischemia. Apurinic/apyrimidinic endonuclease/redox factor-1 (APE/Ref-1) is a multifunctional protein in the DNA base repair pathway that is responsible for repairing apurinic/apyrimidinic sites in DNA after oxidation. We demonstrated that both the immunoreactivity and the number of APE/Ref-1-positive cells in the hippocampal CA1 region were decreased after transient forebrain ischemia and that treatment with HGF suppressed this reduction. The expression of Cu/ZnSOD and MnSOD in the hippocampal CA1 region did not change after ischemia, regardless of treatment with or not with HGF. The activity of NADPH oxidase was increased mainly in glia-like cells in the hippocampal CA1 region after ischemia, and this increase was attenuated by HGF treatment. These results suggest that the protective effects of HGF against cerebral ischemia-induced cell death in the hippocampal CA1 region are related to the improvement of neuronal APE/Ref-1 expression and the inhibition of NADPH oxidase activity in glia-like cells.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2006.08.060</identifier><identifier>PMID: 16973282</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Apoptosis - drug effects ; Apurinic/apyrimidinic endonuclease/redox factor-1 ; Biological and medical sciences ; Cerebral ischemia ; DNA Repair - drug effects ; DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism ; Electrophoresis, Polyacrylamide Gel ; Fundamental and applied biological sciences. Psychology ; Hepatocyte growth factor ; Hepatocyte Growth Factor - pharmacology ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - pathology ; Humans ; Immunohistochemistry ; In Situ Nick-End Labeling ; Ischemic Attack, Transient - pathology ; Medical sciences ; NADPH oxidase ; NADPH Oxidases - metabolism ; Neurology ; Recombinant Proteins - pharmacology ; Reperfusion Injury - pathology ; Superoxide Dismutase - metabolism ; Vascular diseases and vascular malformations of the nervous system ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience letters, 2006-10, Vol.407 (2), p.136-140</ispartof><rights>2006 Elsevier Ireland Ltd</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-81eb80f597cb1163896b9da377009085a48892cd8d2c3313121b8d2326dcf89d3</citedby><cites>FETCH-LOGICAL-c456t-81eb80f597cb1163896b9da377009085a48892cd8d2c3313121b8d2326dcf89d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0304394006008342$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18207272$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16973282$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Niimura, Makiko</creatorcontrib><creatorcontrib>Takagi, Norio</creatorcontrib><creatorcontrib>Takagi, Keiko</creatorcontrib><creatorcontrib>Mizutani, Reiko</creatorcontrib><creatorcontrib>Tanonaka, Kouichi</creatorcontrib><creatorcontrib>Funakoshi, Hiroshi</creatorcontrib><creatorcontrib>Matsumoto, Kunio</creatorcontrib><creatorcontrib>Nakamura, Toshikazu</creatorcontrib><creatorcontrib>Takeo, Satoshi</creatorcontrib><title>The protective effect of hepatocyte growth factor against cell death in the hippocampus after transient forebrain ischemia is related to the improvement of apurinic/apyrimidinic endonuclease/redox factor-1 level and inhibition of NADPH oxidase activity</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Early oxidative DNA damage is regarded to be an initiator of neuronal apoptotic cell death after cerebral ischemia. Although evidence suggests that HGF has the ability to protect cells from oxidative stress, it remains unclear as to how HGF suppresses oxidative DNA damage after cerebral ischemia. Apurinic/apyrimidinic endonuclease/redox factor-1 (APE/Ref-1) is a multifunctional protein in the DNA base repair pathway that is responsible for repairing apurinic/apyrimidinic sites in DNA after oxidation. We demonstrated that both the immunoreactivity and the number of APE/Ref-1-positive cells in the hippocampal CA1 region were decreased after transient forebrain ischemia and that treatment with HGF suppressed this reduction. The expression of Cu/ZnSOD and MnSOD in the hippocampal CA1 region did not change after ischemia, regardless of treatment with or not with HGF. The activity of NADPH oxidase was increased mainly in glia-like cells in the hippocampal CA1 region after ischemia, and this increase was attenuated by HGF treatment. These results suggest that the protective effects of HGF against cerebral ischemia-induced cell death in the hippocampal CA1 region are related to the improvement of neuronal APE/Ref-1 expression and the inhibition of NADPH oxidase activity in glia-like cells.</description><subject>Apoptosis - drug effects</subject><subject>Apurinic/apyrimidinic endonuclease/redox factor-1</subject><subject>Biological and medical sciences</subject><subject>Cerebral ischemia</subject><subject>DNA Repair - drug effects</subject><subject>DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hepatocyte growth factor</subject><subject>Hepatocyte Growth Factor - pharmacology</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - pathology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Ischemic Attack, Transient - pathology</subject><subject>Medical sciences</subject><subject>NADPH oxidase</subject><subject>NADPH Oxidases - metabolism</subject><subject>Neurology</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Reperfusion Injury - pathology</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9Uk1v1DAUjBCILoV_gJAvcMuunU_nglSVjyJVwKGcLcd-brxK7GA72-5_58ALu1JvnPwsz4xm3jjL3jK6ZZQ1u_3WwTJC2haUNlvKt7Shz7IN422Rt11bPM82tKRVXnYVvchexbinlNasrl5mF6zp2rLgxSb7czcAmYNPoJI9AAFjcCLekAFmmbw6JiD3wT-kgRipkg9E3kvrYiIKxpFokPhiHUmoM9h59kpO8xKJNAkCSUG6aMElYnyAPiCT2KgGmKzEgQQYZQJNkv8nYCe0coBpJaAFOS_BOqt2cj4GO1m9Xgg47d2iRpARdgG0fzw7yxkZ4QAjkU6jpcH2NlnvVqXvV59-3hD_aDWSiFyz2nR8nb0wcozw5nxeZr--fL67vslvf3z9dn11m6uqblLOGfScmrprVc9YU_Ku6Tsty7altKO8lhXnXaE014UqS1aygvU4l0WjleGdLi-zDyddTPd7gZjEhEvA9UkHfomiQT6tG4bA6gRUwccYwIgZc8twFIyKtXWxF6fWxdq6oFxg60h7d9Zf-gn0E-lcMwLenwEyKjkabEXZ-ITjBW2LdsV9POEAt3GwEERU2J4CbQN-C6G9_b-Tv75m0-o</recordid><startdate>20061023</startdate><enddate>20061023</enddate><creator>Niimura, Makiko</creator><creator>Takagi, Norio</creator><creator>Takagi, Keiko</creator><creator>Mizutani, Reiko</creator><creator>Tanonaka, Kouichi</creator><creator>Funakoshi, Hiroshi</creator><creator>Matsumoto, Kunio</creator><creator>Nakamura, Toshikazu</creator><creator>Takeo, Satoshi</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><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></search><sort><creationdate>20061023</creationdate><title>The protective effect of hepatocyte growth factor against cell death in the hippocampus after transient forebrain ischemia is related to the improvement of apurinic/apyrimidinic endonuclease/redox factor-1 level and inhibition of NADPH oxidase activity</title><author>Niimura, Makiko ; Takagi, Norio ; Takagi, Keiko ; Mizutani, Reiko ; Tanonaka, Kouichi ; Funakoshi, Hiroshi ; Matsumoto, Kunio ; Nakamura, Toshikazu ; Takeo, Satoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-81eb80f597cb1163896b9da377009085a48892cd8d2c3313121b8d2326dcf89d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Apoptosis - drug effects</topic><topic>Apurinic/apyrimidinic endonuclease/redox factor-1</topic><topic>Biological and medical sciences</topic><topic>Cerebral ischemia</topic><topic>DNA Repair - drug effects</topic><topic>DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hepatocyte growth factor</topic><topic>Hepatocyte Growth Factor - pharmacology</topic><topic>Hippocampus</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - pathology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>Ischemic Attack, Transient - pathology</topic><topic>Medical sciences</topic><topic>NADPH oxidase</topic><topic>NADPH Oxidases - metabolism</topic><topic>Neurology</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Reperfusion Injury - pathology</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Niimura, Makiko</creatorcontrib><creatorcontrib>Takagi, Norio</creatorcontrib><creatorcontrib>Takagi, Keiko</creatorcontrib><creatorcontrib>Mizutani, Reiko</creatorcontrib><creatorcontrib>Tanonaka, Kouichi</creatorcontrib><creatorcontrib>Funakoshi, Hiroshi</creatorcontrib><creatorcontrib>Matsumoto, Kunio</creatorcontrib><creatorcontrib>Nakamura, Toshikazu</creatorcontrib><creatorcontrib>Takeo, Satoshi</creatorcontrib><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><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Niimura, Makiko</au><au>Takagi, Norio</au><au>Takagi, Keiko</au><au>Mizutani, Reiko</au><au>Tanonaka, Kouichi</au><au>Funakoshi, Hiroshi</au><au>Matsumoto, Kunio</au><au>Nakamura, Toshikazu</au><au>Takeo, Satoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The protective effect of hepatocyte growth factor against cell death in the hippocampus after transient forebrain ischemia is related to the improvement of apurinic/apyrimidinic endonuclease/redox factor-1 level and inhibition of NADPH oxidase activity</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2006-10-23</date><risdate>2006</risdate><volume>407</volume><issue>2</issue><spage>136</spage><epage>140</epage><pages>136-140</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>Early oxidative DNA damage is regarded to be an initiator of neuronal apoptotic cell death after cerebral ischemia. Although evidence suggests that HGF has the ability to protect cells from oxidative stress, it remains unclear as to how HGF suppresses oxidative DNA damage after cerebral ischemia. Apurinic/apyrimidinic endonuclease/redox factor-1 (APE/Ref-1) is a multifunctional protein in the DNA base repair pathway that is responsible for repairing apurinic/apyrimidinic sites in DNA after oxidation. We demonstrated that both the immunoreactivity and the number of APE/Ref-1-positive cells in the hippocampal CA1 region were decreased after transient forebrain ischemia and that treatment with HGF suppressed this reduction. The expression of Cu/ZnSOD and MnSOD in the hippocampal CA1 region did not change after ischemia, regardless of treatment with or not with HGF. The activity of NADPH oxidase was increased mainly in glia-like cells in the hippocampal CA1 region after ischemia, and this increase was attenuated by HGF treatment. These results suggest that the protective effects of HGF against cerebral ischemia-induced cell death in the hippocampal CA1 region are related to the improvement of neuronal APE/Ref-1 expression and the inhibition of NADPH oxidase activity in glia-like cells.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>16973282</pmid><doi>10.1016/j.neulet.2006.08.060</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Neuroscience letters, 2006-10, Vol.407 (2), p.136-140 |
| issn | 0304-3940 1872-7972 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Apoptosis - drug effects Apurinic/apyrimidinic endonuclease/redox factor-1 Biological and medical sciences Cerebral ischemia DNA Repair - drug effects DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism Electrophoresis, Polyacrylamide Gel Fundamental and applied biological sciences. Psychology Hepatocyte growth factor Hepatocyte Growth Factor - pharmacology Hippocampus Hippocampus - drug effects Hippocampus - pathology Humans Immunohistochemistry In Situ Nick-End Labeling Ischemic Attack, Transient - pathology Medical sciences NADPH oxidase NADPH Oxidases - metabolism Neurology Recombinant Proteins - pharmacology Reperfusion Injury - pathology Superoxide Dismutase - metabolism Vascular diseases and vascular malformations of the nervous system Vertebrates: nervous system and sense organs |
| title | The protective effect of hepatocyte growth factor against cell death in the hippocampus after transient forebrain ischemia is related to the improvement of apurinic/apyrimidinic endonuclease/redox factor-1 level and inhibition of NADPH oxidase activity |
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