lipophilic metal chelators DP-109 and DP-460 are neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis
One of the hypotheses for the development of familial amyotrophic lateral sclerosis (ALS) is that mutations in the superoxide dismutase 1 enzyme lead to aberrant properties of the copper within the active site of the enzyme which then causes increased oxidative damage. The lipophilic metal chelators...
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| Veröffentlicht in: | Journal of neurochemistry 2007-08, Vol.102 (3), p.991-1000 |
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| creator | Petri, Susanne Calingasan, Noel Y Alsaied, Osama A Wille, Elizabeth Kiaei, Mahmoud Friedman, Jonathan E Baranova, Oxana Chavez, Juan C Beal, M. Flint |
| description | One of the hypotheses for the development of familial amyotrophic lateral sclerosis (ALS) is that mutations in the superoxide dismutase 1 enzyme lead to aberrant properties of the copper within the active site of the enzyme which then causes increased oxidative damage. The lipophilic metal chelators DP-109 and DP-460 which chelate calcium, copper, and zinc were tested in the G93A-transgenic ALS mouse model. Both compounds significantly extended survival, DP-109 (5 mg/kg/day) by 10%, DP-460 (10 mg/kg/day) by 9%. While the effect on survival was relatively small, chelator treatment also improved motor performance, dramatically reduced cell loss in the lumbar spinal cord and decreased reactive astrocytosis and microgliosis. Markers of oxidative damage, tumor necrosis factor (TNF)-αand α-synuclein were reduced in the lumbar spinal cord of G93A mice treated with DP-109 or DP-460 as compared with vehicle-treated animals. Furthermore, the treatment induced protein expression of the transcription factor hypoxia inducible factor-1α and mRNA levels of vascular endothelial growth factor as a corresponding target gene. In line with previous studies using metal chelators in the G93A animal model, our results suggest that these compounds have neuroprotective capacities in ALS. |
| doi_str_mv | 10.1111/j.1471-4159.2007.04604.x |
| format | Article |
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Flint</creator><creatorcontrib>Petri, Susanne ; Calingasan, Noel Y ; Alsaied, Osama A ; Wille, Elizabeth ; Kiaei, Mahmoud ; Friedman, Jonathan E ; Baranova, Oxana ; Chavez, Juan C ; Beal, M. Flint</creatorcontrib><description>One of the hypotheses for the development of familial amyotrophic lateral sclerosis (ALS) is that mutations in the superoxide dismutase 1 enzyme lead to aberrant properties of the copper within the active site of the enzyme which then causes increased oxidative damage. The lipophilic metal chelators DP-109 and DP-460 which chelate calcium, copper, and zinc were tested in the G93A-transgenic ALS mouse model. Both compounds significantly extended survival, DP-109 (5 mg/kg/day) by 10%, DP-460 (10 mg/kg/day) by 9%. While the effect on survival was relatively small, chelator treatment also improved motor performance, dramatically reduced cell loss in the lumbar spinal cord and decreased reactive astrocytosis and microgliosis. Markers of oxidative damage, tumor necrosis factor (TNF)-αand α-synuclein were reduced in the lumbar spinal cord of G93A mice treated with DP-109 or DP-460 as compared with vehicle-treated animals. Furthermore, the treatment induced protein expression of the transcription factor hypoxia inducible factor-1α and mRNA levels of vascular endothelial growth factor as a corresponding target gene. In line with previous studies using metal chelators in the G93A animal model, our results suggest that these compounds have neuroprotective capacities in ALS.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2007.04604.x</identifier><identifier>PMID: 17630988</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Amyotrophic lateral sclerosis ; Amyotrophic Lateral Sclerosis - drug therapy ; Amyotrophic Lateral Sclerosis - metabolism ; Amyotrophic Lateral Sclerosis - physiopathology ; Animals ; Biological and medical sciences ; Biomarkers - metabolism ; Cell Survival - drug effects ; Cell Survival - physiology ; Central Nervous System - drug effects ; Central Nervous System - metabolism ; Central Nervous System - physiopathology ; Cerebrospinal fluid. Meninges. Spinal cord ; Chelating Agents - pharmacology ; Chelating Agents - therapeutic use ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Disease Models, Animal ; Egtazic Acid - analogs & derivatives ; Egtazic Acid - pharmacology ; Egtazic Acid - therapeutic use ; Female ; Hypoxia-Inducible Factor 1, alpha Subunit - drug effects ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; inflammation ; Inflammatory diseases ; Male ; Medical sciences ; Membrane Lipids - metabolism ; Metals - antagonists & inhibitors ; Metals - metabolism ; Mice ; Mice, Transgenic ; Nerve Degeneration - drug therapy ; Nerve Degeneration - physiopathology ; Nerve Degeneration - prevention & control ; Nervous system (semeiology, syndromes) ; Neurology ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Oxidation ; oxidative stress ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; RNA, Messenger - drug effects ; RNA, Messenger - metabolism ; Rodents ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism ; Superoxide Dismutase-1 ; Transgenic animals ; transition metals ; Treatment Outcome ; tumor necrosis factor-α ; vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics</subject><ispartof>Journal of neurochemistry, 2007-08, Vol.102 (3), p.991-1000</ispartof><rights>2007 INIST-CNRS</rights><rights>2007 The Authors Journal compilation 2007 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5954-98b29969b5660edf3e93dbab7f0e8650f4656a2e01aebbb2f2cb8a9a24d2bb1a3</citedby><cites>FETCH-LOGICAL-c5954-98b29969b5660edf3e93dbab7f0e8650f4656a2e01aebbb2f2cb8a9a24d2bb1a3</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.1471-4159.2007.04604.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2007.04604.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,1432,27922,27923,45572,45573,46407,46831</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18913666$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17630988$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Petri, Susanne</creatorcontrib><creatorcontrib>Calingasan, Noel Y</creatorcontrib><creatorcontrib>Alsaied, Osama A</creatorcontrib><creatorcontrib>Wille, Elizabeth</creatorcontrib><creatorcontrib>Kiaei, Mahmoud</creatorcontrib><creatorcontrib>Friedman, Jonathan E</creatorcontrib><creatorcontrib>Baranova, Oxana</creatorcontrib><creatorcontrib>Chavez, Juan C</creatorcontrib><creatorcontrib>Beal, M. Flint</creatorcontrib><title>lipophilic metal chelators DP-109 and DP-460 are neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>One of the hypotheses for the development of familial amyotrophic lateral sclerosis (ALS) is that mutations in the superoxide dismutase 1 enzyme lead to aberrant properties of the copper within the active site of the enzyme which then causes increased oxidative damage. The lipophilic metal chelators DP-109 and DP-460 which chelate calcium, copper, and zinc were tested in the G93A-transgenic ALS mouse model. Both compounds significantly extended survival, DP-109 (5 mg/kg/day) by 10%, DP-460 (10 mg/kg/day) by 9%. While the effect on survival was relatively small, chelator treatment also improved motor performance, dramatically reduced cell loss in the lumbar spinal cord and decreased reactive astrocytosis and microgliosis. Markers of oxidative damage, tumor necrosis factor (TNF)-αand α-synuclein were reduced in the lumbar spinal cord of G93A mice treated with DP-109 or DP-460 as compared with vehicle-treated animals. Furthermore, the treatment induced protein expression of the transcription factor hypoxia inducible factor-1α and mRNA levels of vascular endothelial growth factor as a corresponding target gene. In line with previous studies using metal chelators in the G93A animal model, our results suggest that these compounds have neuroprotective capacities in ALS.</description><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic Lateral Sclerosis - drug therapy</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Amyotrophic Lateral Sclerosis - physiopathology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - physiology</subject><subject>Central Nervous System - drug effects</subject><subject>Central Nervous System - metabolism</subject><subject>Central Nervous System - physiopathology</subject><subject>Cerebrospinal fluid. Meninges. Spinal cord</subject><subject>Chelating Agents - pharmacology</subject><subject>Chelating Agents - therapeutic use</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Disease Models, Animal</subject><subject>Egtazic Acid - analogs & derivatives</subject><subject>Egtazic Acid - pharmacology</subject><subject>Egtazic Acid - therapeutic use</subject><subject>Female</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - drug effects</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>inflammation</subject><subject>Inflammatory diseases</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Lipids - metabolism</subject><subject>Metals - antagonists & inhibitors</subject><subject>Metals - metabolism</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Nerve Degeneration - drug therapy</subject><subject>Nerve Degeneration - physiopathology</subject><subject>Nerve Degeneration - prevention & control</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Oxidation</subject><subject>oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>RNA, Messenger - drug effects</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxide Dismutase-1</subject><subject>Transgenic animals</subject><subject>transition metals</subject><subject>Treatment Outcome</subject><subject>tumor necrosis factor-α</subject><subject>vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EokPhFcBCgl2C7ThOvGCBBsqPKkCCri3buWk98iRTO4HOou_ODTOiEhvIwrHk755z7EMI5azk-L3alFw2vJC81qVgrCmZVEyWN_fI6s_BfbJiTIiiYlKckEc5bxjjSir-kJzwRlVMt-2K3MawG3dXIQZPtzDZSP0VRDuNKdO3XwvONLVDt2zRgdoEdIA5jbs0TuCn8ANoGKilU7JDvoRhURnnDLh2EOnYU7vdj1NaLDxFXUhokX2ENOaQH5MHvY0Znhz_p-Ti7N339Yfi_Mv7j-s354WvdS0L3TqhtdKuVopB11egq85Z1_QMWlWzXqpaWQGMW3DOiV5411ptheyEc9xWp-TlQRdzX8-QJ7MN2UOMdgCMaxrWCMG1_ifI8dEUhkDw-V_gZpzTgJcwgqlatkIsau0B8njbnKA3uxS2Nu0NZ2Yp0mzM0pdZ-jJLkeZ3keYGR58e9We3he5u8NgcAi-OgM3exh4L8CHfca3mFSZF7vWB-xki7P87gPn0eb3scP7ZYb63o7GXCT0uvgnGK4RbNGmqX1gNwmw</recordid><startdate>200708</startdate><enddate>200708</enddate><creator>Petri, Susanne</creator><creator>Calingasan, Noel Y</creator><creator>Alsaied, Osama A</creator><creator>Wille, Elizabeth</creator><creator>Kiaei, Mahmoud</creator><creator>Friedman, Jonathan E</creator><creator>Baranova, Oxana</creator><creator>Chavez, Juan C</creator><creator>Beal, M. Flint</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><general>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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7QO</scope><scope>7X8</scope></search><sort><creationdate>200708</creationdate><title>lipophilic metal chelators DP-109 and DP-460 are neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis</title><author>Petri, Susanne ; Calingasan, Noel Y ; Alsaied, Osama A ; Wille, Elizabeth ; Kiaei, Mahmoud ; Friedman, Jonathan E ; Baranova, Oxana ; Chavez, Juan C ; Beal, M. Flint</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5954-98b29969b5660edf3e93dbab7f0e8650f4656a2e01aebbb2f2cb8a9a24d2bb1a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Amyotrophic lateral sclerosis</topic><topic>Amyotrophic Lateral Sclerosis - drug therapy</topic><topic>Amyotrophic Lateral Sclerosis - metabolism</topic><topic>Amyotrophic Lateral Sclerosis - physiopathology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - metabolism</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - physiology</topic><topic>Central Nervous System - drug effects</topic><topic>Central Nervous System - metabolism</topic><topic>Central Nervous System - physiopathology</topic><topic>Cerebrospinal fluid. Meninges. Spinal cord</topic><topic>Chelating Agents - pharmacology</topic><topic>Chelating Agents - therapeutic use</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Disease Models, Animal</topic><topic>Egtazic Acid - analogs & derivatives</topic><topic>Egtazic Acid - pharmacology</topic><topic>Egtazic Acid - therapeutic use</topic><topic>Female</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - drug effects</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>inflammation</topic><topic>Inflammatory diseases</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Lipids - metabolism</topic><topic>Metals - antagonists & inhibitors</topic><topic>Metals - metabolism</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Nerve Degeneration - drug therapy</topic><topic>Nerve Degeneration - physiopathology</topic><topic>Nerve Degeneration - prevention & control</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Oxidation</topic><topic>oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>RNA, Messenger - drug effects</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Superoxide Dismutase-1</topic><topic>Transgenic animals</topic><topic>transition metals</topic><topic>Treatment Outcome</topic><topic>tumor necrosis factor-α</topic><topic>vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Petri, Susanne</creatorcontrib><creatorcontrib>Calingasan, Noel Y</creatorcontrib><creatorcontrib>Alsaied, Osama A</creatorcontrib><creatorcontrib>Wille, Elizabeth</creatorcontrib><creatorcontrib>Kiaei, Mahmoud</creatorcontrib><creatorcontrib>Friedman, Jonathan E</creatorcontrib><creatorcontrib>Baranova, Oxana</creatorcontrib><creatorcontrib>Chavez, Juan C</creatorcontrib><creatorcontrib>Beal, M. 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Flint</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>lipophilic metal chelators DP-109 and DP-460 are neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2007-08</date><risdate>2007</risdate><volume>102</volume><issue>3</issue><spage>991</spage><epage>1000</epage><pages>991-1000</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>One of the hypotheses for the development of familial amyotrophic lateral sclerosis (ALS) is that mutations in the superoxide dismutase 1 enzyme lead to aberrant properties of the copper within the active site of the enzyme which then causes increased oxidative damage. The lipophilic metal chelators DP-109 and DP-460 which chelate calcium, copper, and zinc were tested in the G93A-transgenic ALS mouse model. Both compounds significantly extended survival, DP-109 (5 mg/kg/day) by 10%, DP-460 (10 mg/kg/day) by 9%. While the effect on survival was relatively small, chelator treatment also improved motor performance, dramatically reduced cell loss in the lumbar spinal cord and decreased reactive astrocytosis and microgliosis. Markers of oxidative damage, tumor necrosis factor (TNF)-αand α-synuclein were reduced in the lumbar spinal cord of G93A mice treated with DP-109 or DP-460 as compared with vehicle-treated animals. Furthermore, the treatment induced protein expression of the transcription factor hypoxia inducible factor-1α and mRNA levels of vascular endothelial growth factor as a corresponding target gene. In line with previous studies using metal chelators in the G93A animal model, our results suggest that these compounds have neuroprotective capacities in ALS.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>17630988</pmid><doi>10.1111/j.1471-4159.2007.04604.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Wiley Free Content; IngentaConnect Free/Open Access Journals; EZB-FREE-00999 freely available EZB journals; Free Full-Text Journals in Chemistry |
| subjects | Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - drug therapy Amyotrophic Lateral Sclerosis - metabolism Amyotrophic Lateral Sclerosis - physiopathology Animals Biological and medical sciences Biomarkers - metabolism Cell Survival - drug effects Cell Survival - physiology Central Nervous System - drug effects Central Nervous System - metabolism Central Nervous System - physiopathology Cerebrospinal fluid. Meninges. Spinal cord Chelating Agents - pharmacology Chelating Agents - therapeutic use Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Egtazic Acid - analogs & derivatives Egtazic Acid - pharmacology Egtazic Acid - therapeutic use Female Hypoxia-Inducible Factor 1, alpha Subunit - drug effects Hypoxia-Inducible Factor 1, alpha Subunit - metabolism inflammation Inflammatory diseases Male Medical sciences Membrane Lipids - metabolism Metals - antagonists & inhibitors Metals - metabolism Mice Mice, Transgenic Nerve Degeneration - drug therapy Nerve Degeneration - physiopathology Nerve Degeneration - prevention & control Nervous system (semeiology, syndromes) Neurology Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Oxidation oxidative stress Oxidative Stress - drug effects Oxidative Stress - physiology RNA, Messenger - drug effects RNA, Messenger - metabolism Rodents Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Superoxide Dismutase-1 Transgenic animals transition metals Treatment Outcome tumor necrosis factor-α vascular endothelial growth factor Vascular Endothelial Growth Factor A - genetics |
| title | lipophilic metal chelators DP-109 and DP-460 are neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis |
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