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Neuroprotective role of transgenic PAF-Acetylhydrolase II in mouse models of focal cerebral ischemia
Platelet-activating factor (PAF) and oxidized unsaturated free fatty acids have been postulated to aggravate neuronal damage in the postischemic brain. Type II PAF-acetylhydrolase (PAF-AH II) not only terminates signals by PAF by its PAF-hydrolyzing activity but also protects cells against oxidative...
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Published in: | Stroke (1970) 2007-03, Vol.38 (3), p.1063-1068 |
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creator | UMEMURA, Kimiko KATO, Ichiro ENDO, Shunro ODA, Masaya ARAI, Hiroyuki KINOUCHI, Hiroyuki HIRAGA, Koichi HIRASHIMA, Yutaka ISHII, Yoko INOUE, Takao JUNKEN, Aoki KONO, Nozomu OYA, Takeshi HAYASHI, Nakamasa HAMADA, Hideo |
description | Platelet-activating factor (PAF) and oxidized unsaturated free fatty acids have been postulated to aggravate neuronal damage in the postischemic brain. Type II PAF-acetylhydrolase (PAF-AH II) not only terminates signals by PAF by its PAF-hydrolyzing activity but also protects cells against oxidative stress. We examined whether PAF-AH II can rescue cerebral neurons against ischemic insults.
Transgenic mice overexpressing human PAF-AH II in neurons were generated and enzyme expressions were examined biochemically and histochemically. The mice were subjected to 60 minutes of transient middle cerebral artery occlusion followed by reperfusion for 24 hours. The infarction and apoptosis were estimated by TTC staining and fluorescence TUNEL staining, respectively.
Overexpression of PAF-AH II was found in brains of transgenic mice by Western blot and enzymatic activity analyses. In immunohistochemistry, human PAF-AH II expression was found throughout the central nervous system, especially in neurons of neocortex, hippocampus, and basal ganglia. The neurological deficit scores, cerebral edema index, and relative infarction volume were all significantly (P |
doi_str_mv | 10.1161/01.STR.0000257981.09329.d2 |
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Transgenic mice overexpressing human PAF-AH II in neurons were generated and enzyme expressions were examined biochemically and histochemically. The mice were subjected to 60 minutes of transient middle cerebral artery occlusion followed by reperfusion for 24 hours. The infarction and apoptosis were estimated by TTC staining and fluorescence TUNEL staining, respectively.
Overexpression of PAF-AH II was found in brains of transgenic mice by Western blot and enzymatic activity analyses. In immunohistochemistry, human PAF-AH II expression was found throughout the central nervous system, especially in neurons of neocortex, hippocampus, and basal ganglia. The neurological deficit scores, cerebral edema index, and relative infarction volume were all significantly (P<0.05) lower in transgenic mice (1.30+/-0.72, 1.12+/-0.04, and 14.0+/-7.7%, respectively) than in wild-type mice (2.56+/-0.93, 1.23+/-0.12, and 31.9+/-9.7%, respectively). Percentages of apoptotic cells were also significantly (P<0.001) lower in transgenic mice (cortex, 5.2+/-3.3%; hippocampus, 3.4+/-7.0%) than in wild-type mice (cortex, 41.1+/-16.9%; hippocampus, 58.9+/-15.3%).
These results indicate that PAF-AH II exerts strong neuroprotective effects against ischemic injury and suggest a possibility for clinical use of this enzyme in cerebral ischemia.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.STR.0000257981.09329.d2</identifier><identifier>PMID: 17272759</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>1-Alkyl-2-acetylglycerophosphocholine Esterase - biosynthesis ; 1-Alkyl-2-acetylglycerophosphocholine Esterase - genetics ; 1-Alkyl-2-acetylglycerophosphocholine Esterase - therapeutic use ; Animals ; Biological and medical sciences ; Brain Ischemia - enzymology ; Brain Ischemia - genetics ; Brain Ischemia - prevention & control ; Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges ; Disease Models, Animal ; Female ; Fundamental and applied biological sciences. Psychology ; Humans ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neurology ; Neuropharmacology ; Neuroprotective agent ; Neuroprotective Agents - metabolism ; Pharmacology. Drug treatments ; Vascular diseases and vascular malformations of the nervous system ; Vertebrates: nervous system and sense organs</subject><ispartof>Stroke (1970), 2007-03, Vol.38 (3), p.1063-1068</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c532t-b0455e06f055209655c09f7e44853db4bc0483744b121a56321887500e6500673</citedby><cites>FETCH-LOGICAL-c532t-b0455e06f055209655c09f7e44853db4bc0483744b121a56321887500e6500673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18581970$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17272759$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>UMEMURA, Kimiko</creatorcontrib><creatorcontrib>KATO, Ichiro</creatorcontrib><creatorcontrib>ENDO, Shunro</creatorcontrib><creatorcontrib>ODA, Masaya</creatorcontrib><creatorcontrib>ARAI, Hiroyuki</creatorcontrib><creatorcontrib>KINOUCHI, Hiroyuki</creatorcontrib><creatorcontrib>HIRAGA, Koichi</creatorcontrib><creatorcontrib>HIRASHIMA, Yutaka</creatorcontrib><creatorcontrib>ISHII, Yoko</creatorcontrib><creatorcontrib>INOUE, Takao</creatorcontrib><creatorcontrib>JUNKEN, Aoki</creatorcontrib><creatorcontrib>KONO, Nozomu</creatorcontrib><creatorcontrib>OYA, Takeshi</creatorcontrib><creatorcontrib>HAYASHI, Nakamasa</creatorcontrib><creatorcontrib>HAMADA, Hideo</creatorcontrib><title>Neuroprotective role of transgenic PAF-Acetylhydrolase II in mouse models of focal cerebral ischemia</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Platelet-activating factor (PAF) and oxidized unsaturated free fatty acids have been postulated to aggravate neuronal damage in the postischemic brain. Type II PAF-acetylhydrolase (PAF-AH II) not only terminates signals by PAF by its PAF-hydrolyzing activity but also protects cells against oxidative stress. We examined whether PAF-AH II can rescue cerebral neurons against ischemic insults.
Transgenic mice overexpressing human PAF-AH II in neurons were generated and enzyme expressions were examined biochemically and histochemically. The mice were subjected to 60 minutes of transient middle cerebral artery occlusion followed by reperfusion for 24 hours. The infarction and apoptosis were estimated by TTC staining and fluorescence TUNEL staining, respectively.
Overexpression of PAF-AH II was found in brains of transgenic mice by Western blot and enzymatic activity analyses. In immunohistochemistry, human PAF-AH II expression was found throughout the central nervous system, especially in neurons of neocortex, hippocampus, and basal ganglia. The neurological deficit scores, cerebral edema index, and relative infarction volume were all significantly (P<0.05) lower in transgenic mice (1.30+/-0.72, 1.12+/-0.04, and 14.0+/-7.7%, respectively) than in wild-type mice (2.56+/-0.93, 1.23+/-0.12, and 31.9+/-9.7%, respectively). Percentages of apoptotic cells were also significantly (P<0.001) lower in transgenic mice (cortex, 5.2+/-3.3%; hippocampus, 3.4+/-7.0%) than in wild-type mice (cortex, 41.1+/-16.9%; hippocampus, 58.9+/-15.3%).
These results indicate that PAF-AH II exerts strong neuroprotective effects against ischemic injury and suggest a possibility for clinical use of this enzyme in cerebral ischemia.</description><subject>1-Alkyl-2-acetylglycerophosphocholine Esterase - biosynthesis</subject><subject>1-Alkyl-2-acetylglycerophosphocholine Esterase - genetics</subject><subject>1-Alkyl-2-acetylglycerophosphocholine Esterase - therapeutic use</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain Ischemia - enzymology</subject><subject>Brain Ischemia - genetics</subject><subject>Brain Ischemia - prevention & control</subject><subject>Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Neurology</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Neuroprotective Agents - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNqFkd1u1DAQhS0EokvhFVCEBHdJZ_yT2NytqhZWqqAq5dpynAkNSjbFzlbat2eWrrSX2JI9kr8zM54jxAeECrHGC8Dqx_1dBbykaZzFCpySrurkC7FCI3Wpa2lfihWAcqXUzp2JNzn_PvDKmtfiDBvJ27iV6L7RLs2PaV4oLsMTFWkeqZj7Yklhm3_RdojF7fq6XEda9uPDvuP3kKnYbIphW0zzjuNp7mjMB1E_xzAWkRK1iYMhxweahvBWvOrDmOnd8T4XP6-v7i-_ljffv2wu1zdlNEouZQvaGIK6B2MkuNqYCK5vSGtrVNfqNoK2qtG6RYnB1EqitY0BoJqPulHn4tNzXv7Pnx3lxU_cAo1j2BJ36huQaFj_XxAd13GoGPz8DMY055yo949pmELaewR_MMMDejbDn8zw_8zwnWTx-2OVXTtRd5Iep8_AxyMQMg-u55HHIZ84ayy6BtRfe6-Rgg</recordid><startdate>20070301</startdate><enddate>20070301</enddate><creator>UMEMURA, Kimiko</creator><creator>KATO, Ichiro</creator><creator>ENDO, Shunro</creator><creator>ODA, Masaya</creator><creator>ARAI, Hiroyuki</creator><creator>KINOUCHI, Hiroyuki</creator><creator>HIRAGA, Koichi</creator><creator>HIRASHIMA, Yutaka</creator><creator>ISHII, Yoko</creator><creator>INOUE, Takao</creator><creator>JUNKEN, Aoki</creator><creator>KONO, Nozomu</creator><creator>OYA, Takeshi</creator><creator>HAYASHI, Nakamasa</creator><creator>HAMADA, Hideo</creator><general>Lippincott Williams & Wilkins</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>7QO</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20070301</creationdate><title>Neuroprotective role of transgenic PAF-Acetylhydrolase II in mouse models of focal cerebral ischemia</title><author>UMEMURA, Kimiko ; KATO, Ichiro ; ENDO, Shunro ; ODA, Masaya ; ARAI, Hiroyuki ; KINOUCHI, Hiroyuki ; HIRAGA, Koichi ; HIRASHIMA, Yutaka ; ISHII, Yoko ; INOUE, Takao ; JUNKEN, Aoki ; KONO, Nozomu ; OYA, Takeshi ; HAYASHI, Nakamasa ; HAMADA, Hideo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c532t-b0455e06f055209655c09f7e44853db4bc0483744b121a56321887500e6500673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>1-Alkyl-2-acetylglycerophosphocholine Esterase - biosynthesis</topic><topic>1-Alkyl-2-acetylglycerophosphocholine Esterase - genetics</topic><topic>1-Alkyl-2-acetylglycerophosphocholine Esterase - therapeutic use</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain Ischemia - enzymology</topic><topic>Brain Ischemia - genetics</topic><topic>Brain Ischemia - prevention & control</topic><topic>Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Neurology</topic><topic>Neuropharmacology</topic><topic>Neuroprotective agent</topic><topic>Neuroprotective Agents - metabolism</topic><topic>Pharmacology. Drug treatments</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>UMEMURA, Kimiko</creatorcontrib><creatorcontrib>KATO, Ichiro</creatorcontrib><creatorcontrib>ENDO, Shunro</creatorcontrib><creatorcontrib>ODA, Masaya</creatorcontrib><creatorcontrib>ARAI, Hiroyuki</creatorcontrib><creatorcontrib>KINOUCHI, Hiroyuki</creatorcontrib><creatorcontrib>HIRAGA, Koichi</creatorcontrib><creatorcontrib>HIRASHIMA, Yutaka</creatorcontrib><creatorcontrib>ISHII, Yoko</creatorcontrib><creatorcontrib>INOUE, Takao</creatorcontrib><creatorcontrib>JUNKEN, Aoki</creatorcontrib><creatorcontrib>KONO, Nozomu</creatorcontrib><creatorcontrib>OYA, Takeshi</creatorcontrib><creatorcontrib>HAYASHI, Nakamasa</creatorcontrib><creatorcontrib>HAMADA, Hideo</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>Biotechnology Research Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>UMEMURA, Kimiko</au><au>KATO, Ichiro</au><au>ENDO, Shunro</au><au>ODA, Masaya</au><au>ARAI, Hiroyuki</au><au>KINOUCHI, Hiroyuki</au><au>HIRAGA, Koichi</au><au>HIRASHIMA, Yutaka</au><au>ISHII, Yoko</au><au>INOUE, Takao</au><au>JUNKEN, Aoki</au><au>KONO, Nozomu</au><au>OYA, Takeshi</au><au>HAYASHI, Nakamasa</au><au>HAMADA, Hideo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective role of transgenic PAF-Acetylhydrolase II in mouse models of focal cerebral ischemia</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2007-03-01</date><risdate>2007</risdate><volume>38</volume><issue>3</issue><spage>1063</spage><epage>1068</epage><pages>1063-1068</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Platelet-activating factor (PAF) and oxidized unsaturated free fatty acids have been postulated to aggravate neuronal damage in the postischemic brain. Type II PAF-acetylhydrolase (PAF-AH II) not only terminates signals by PAF by its PAF-hydrolyzing activity but also protects cells against oxidative stress. We examined whether PAF-AH II can rescue cerebral neurons against ischemic insults.
Transgenic mice overexpressing human PAF-AH II in neurons were generated and enzyme expressions were examined biochemically and histochemically. The mice were subjected to 60 minutes of transient middle cerebral artery occlusion followed by reperfusion for 24 hours. The infarction and apoptosis were estimated by TTC staining and fluorescence TUNEL staining, respectively.
Overexpression of PAF-AH II was found in brains of transgenic mice by Western blot and enzymatic activity analyses. In immunohistochemistry, human PAF-AH II expression was found throughout the central nervous system, especially in neurons of neocortex, hippocampus, and basal ganglia. The neurological deficit scores, cerebral edema index, and relative infarction volume were all significantly (P<0.05) lower in transgenic mice (1.30+/-0.72, 1.12+/-0.04, and 14.0+/-7.7%, respectively) than in wild-type mice (2.56+/-0.93, 1.23+/-0.12, and 31.9+/-9.7%, respectively). Percentages of apoptotic cells were also significantly (P<0.001) lower in transgenic mice (cortex, 5.2+/-3.3%; hippocampus, 3.4+/-7.0%) than in wild-type mice (cortex, 41.1+/-16.9%; hippocampus, 58.9+/-15.3%).
These results indicate that PAF-AH II exerts strong neuroprotective effects against ischemic injury and suggest a possibility for clinical use of this enzyme in cerebral ischemia.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>17272759</pmid><doi>10.1161/01.STR.0000257981.09329.d2</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 1-Alkyl-2-acetylglycerophosphocholine Esterase - biosynthesis 1-Alkyl-2-acetylglycerophosphocholine Esterase - genetics 1-Alkyl-2-acetylglycerophosphocholine Esterase - therapeutic use Animals Biological and medical sciences Brain Ischemia - enzymology Brain Ischemia - genetics Brain Ischemia - prevention & control Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges Disease Models, Animal Female Fundamental and applied biological sciences. Psychology Humans Male Medical sciences Mice Mice, Inbred C57BL Mice, Transgenic Neurology Neuropharmacology Neuroprotective agent Neuroprotective Agents - metabolism Pharmacology. Drug treatments Vascular diseases and vascular malformations of the nervous system Vertebrates: nervous system and sense organs |
title | Neuroprotective role of transgenic PAF-Acetylhydrolase II in mouse models of focal cerebral ischemia |
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