Effects of hyperbaric oxygen on GDNF expression and apoptosis in spinal cord injury
The effects of hyperbaric oxygen treatment on the progress of secondary damage following traumatic spinal cord injury were investigated. The early onset of hyperbaric oxygen treatment significantly diminished the number of apoptotic cells 1 day after the injury. However, hyperbaric oxygen did not in...
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| Veröffentlicht in: | Neuroreport 2004-10, Vol.15 (15), p.2369-2373 |
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| creator | Yu, Yimin Matsuyama, Yukihiro Yanase, Makoto Ito, Sachiko Adachi, Kayo Satake, Kotaro Ishiguro, Noki Kiuchi, Kazutoshi |
| description | The effects of hyperbaric oxygen treatment on the progress of secondary damage following traumatic spinal cord injury were investigated. The early onset of hyperbaric oxygen treatment significantly diminished the number of apoptotic cells 1 day after the injury. However, hyperbaric oxygen did not influence the proliferation of macrophages or activated microglia. The gene expression of glial cell line-derived neurotrophic factor (GDNF) and inducible nitric oxide synthetase (iNOS) was significantly attenuated 1 day after the injury in the hyperbaric oxygen groups compared with the control group. The down-regulation was confirmed by immunohistochemical staining. Early hyperbaric oxygen treatment was shown to effectively suppress the progress of apoptosis perhaps via the inhibition of iNOS gene despite the down-regulation of the GDNF gene. |
| doi_str_mv | 10.1097/00001756-200410250-00014 |
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The early onset of hyperbaric oxygen treatment significantly diminished the number of apoptotic cells 1 day after the injury. However, hyperbaric oxygen did not influence the proliferation of macrophages or activated microglia. The gene expression of glial cell line-derived neurotrophic factor (GDNF) and inducible nitric oxide synthetase (iNOS) was significantly attenuated 1 day after the injury in the hyperbaric oxygen groups compared with the control group. The down-regulation was confirmed by immunohistochemical staining. Early hyperbaric oxygen treatment was shown to effectively suppress the progress of apoptosis perhaps via the inhibition of iNOS gene despite the down-regulation of the GDNF gene.</description><identifier>ISSN: 0959-4965</identifier><identifier>EISSN: 1473-558X</identifier><identifier>DOI: 10.1097/00001756-200410250-00014</identifier><identifier>PMID: 15640758</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Animals ; Apoptosis ; Biological and medical sciences ; Cell Count - methods ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - physiology ; Glial Cell Line-Derived Neurotrophic Factor ; Hyperbaric Oxygenation - methods ; Immunohistochemistry - methods ; In Situ Nick-End Labeling - methods ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Male ; Medical sciences ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Nerve Growth Factors - genetics ; Nerve Growth Factors - metabolism ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Oxygen - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - metabolism ; Spinal Cord Injuries - metabolism ; Spinal Cord Injuries - pathology ; Time Factors ; Traumas. Diseases due to physical agents</subject><ispartof>Neuroreport, 2004-10, Vol.15 (15), p.2369-2373</ispartof><rights>2004 Lippincott Williams & Wilkins, Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4174-6f95b7ce99a670611eb6c56c0b562e30695641ea290f9c5d2266cc1ede2d285a3</citedby><cites>FETCH-LOGICAL-c4174-6f95b7ce99a670611eb6c56c0b562e30695641ea290f9c5d2266cc1ede2d285a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16224170$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15640758$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Yimin</creatorcontrib><creatorcontrib>Matsuyama, Yukihiro</creatorcontrib><creatorcontrib>Yanase, Makoto</creatorcontrib><creatorcontrib>Ito, Sachiko</creatorcontrib><creatorcontrib>Adachi, Kayo</creatorcontrib><creatorcontrib>Satake, Kotaro</creatorcontrib><creatorcontrib>Ishiguro, Noki</creatorcontrib><creatorcontrib>Kiuchi, Kazutoshi</creatorcontrib><title>Effects of hyperbaric oxygen on GDNF expression and apoptosis in spinal cord injury</title><title>Neuroreport</title><addtitle>Neuroreport</addtitle><description>The effects of hyperbaric oxygen treatment on the progress of secondary damage following traumatic spinal cord injury were investigated. The early onset of hyperbaric oxygen treatment significantly diminished the number of apoptotic cells 1 day after the injury. However, hyperbaric oxygen did not influence the proliferation of macrophages or activated microglia. The gene expression of glial cell line-derived neurotrophic factor (GDNF) and inducible nitric oxide synthetase (iNOS) was significantly attenuated 1 day after the injury in the hyperbaric oxygen groups compared with the control group. The down-regulation was confirmed by immunohistochemical staining. Early hyperbaric oxygen treatment was shown to effectively suppress the progress of apoptosis perhaps via the inhibition of iNOS gene despite the down-regulation of the GDNF gene.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Cell Count - methods</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - physiology</subject><subject>Glial Cell Line-Derived Neurotrophic Factor</subject><subject>Hyperbaric Oxygenation - methods</subject><subject>Immunohistochemistry - methods</subject><subject>In Situ Nick-End Labeling - methods</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Nerve Growth Factors - genetics</subject><subject>Nerve Growth Factors - metabolism</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Oxygen - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - metabolism</subject><subject>Spinal Cord Injuries - metabolism</subject><subject>Spinal Cord Injuries - pathology</subject><subject>Time Factors</subject><subject>Traumas. Diseases due to physical agents</subject><issn>0959-4965</issn><issn>1473-558X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EokvhLyBfyi1l7MR2fKxKP5Cq9gBI3CzHmbAp2Th4ErX77-uyCz1V9cWa0fN6Ro8Z4wKOBVjzGfIRRulCAlQCpILisVO9YitRmbJQqv75mq3AKltUVqsD9o7oNiMWRP2WHQilKzCqXrFvZ12HYSYeO77eTpgan_rA4_32F448jvziy_U5x_spIVGfaz-23E9xmiP1xPuR09SPfuAhpjaXt0vavmdvOj8Qftjfh-zH-dn308vi6ubi6-nJVREqYapCd1Y1JqC1XhvQQmCjg9IBGqUllqBt3lKglxY6G1QrpdYhCGxRtrJWvjxkn3bvTin-WZBmt-kp4DD4EeNCThsJNRj9IihBiVqYMoP1DgwpEiXs3JT6jU9bJ8A9mnf_zLv_5t1f8zn6cT9jaTbYPgX3qjNwtAc8BT90yY-hpydOS5m1QOaqHXcXhxkT_R6WO0xujX6Y1-65ny8fAEhlmgk</recordid><startdate>20041025</startdate><enddate>20041025</enddate><creator>Yu, Yimin</creator><creator>Matsuyama, Yukihiro</creator><creator>Yanase, Makoto</creator><creator>Ito, Sachiko</creator><creator>Adachi, Kayo</creator><creator>Satake, Kotaro</creator><creator>Ishiguro, Noki</creator><creator>Kiuchi, Kazutoshi</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams and 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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20041025</creationdate><title>Effects of hyperbaric oxygen on GDNF expression and apoptosis in spinal cord injury</title><author>Yu, Yimin ; Matsuyama, Yukihiro ; Yanase, Makoto ; Ito, Sachiko ; Adachi, Kayo ; Satake, Kotaro ; Ishiguro, Noki ; Kiuchi, Kazutoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4174-6f95b7ce99a670611eb6c56c0b562e30695641ea290f9c5d2266cc1ede2d285a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Cell Count - methods</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - physiology</topic><topic>Glial Cell Line-Derived Neurotrophic Factor</topic><topic>Hyperbaric Oxygenation - methods</topic><topic>Immunohistochemistry - methods</topic><topic>In Situ Nick-End Labeling - methods</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Nerve Growth Factors - genetics</topic><topic>Nerve Growth Factors - metabolism</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Oxygen - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - metabolism</topic><topic>Spinal Cord Injuries - metabolism</topic><topic>Spinal Cord Injuries - pathology</topic><topic>Time Factors</topic><topic>Traumas. Diseases due to physical agents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Yimin</creatorcontrib><creatorcontrib>Matsuyama, Yukihiro</creatorcontrib><creatorcontrib>Yanase, Makoto</creatorcontrib><creatorcontrib>Ito, Sachiko</creatorcontrib><creatorcontrib>Adachi, Kayo</creatorcontrib><creatorcontrib>Satake, Kotaro</creatorcontrib><creatorcontrib>Ishiguro, Noki</creatorcontrib><creatorcontrib>Kiuchi, Kazutoshi</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroreport</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Yimin</au><au>Matsuyama, Yukihiro</au><au>Yanase, Makoto</au><au>Ito, Sachiko</au><au>Adachi, Kayo</au><au>Satake, Kotaro</au><au>Ishiguro, Noki</au><au>Kiuchi, Kazutoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of hyperbaric oxygen on GDNF expression and apoptosis in spinal cord injury</atitle><jtitle>Neuroreport</jtitle><addtitle>Neuroreport</addtitle><date>2004-10-25</date><risdate>2004</risdate><volume>15</volume><issue>15</issue><spage>2369</spage><epage>2373</epage><pages>2369-2373</pages><issn>0959-4965</issn><eissn>1473-558X</eissn><abstract>The effects of hyperbaric oxygen treatment on the progress of secondary damage following traumatic spinal cord injury were investigated. The early onset of hyperbaric oxygen treatment significantly diminished the number of apoptotic cells 1 day after the injury. However, hyperbaric oxygen did not influence the proliferation of macrophages or activated microglia. The gene expression of glial cell line-derived neurotrophic factor (GDNF) and inducible nitric oxide synthetase (iNOS) was significantly attenuated 1 day after the injury in the hyperbaric oxygen groups compared with the control group. The down-regulation was confirmed by immunohistochemical staining. Early hyperbaric oxygen treatment was shown to effectively suppress the progress of apoptosis perhaps via the inhibition of iNOS gene despite the down-regulation of the GDNF gene.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>15640758</pmid><doi>10.1097/00001756-200410250-00014</doi><tpages>5</tpages></addata></record> |
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| subjects | Animals Apoptosis Biological and medical sciences Cell Count - methods Gene Expression Regulation - drug effects Gene Expression Regulation - physiology Glial Cell Line-Derived Neurotrophic Factor Hyperbaric Oxygenation - methods Immunohistochemistry - methods In Situ Nick-End Labeling - methods Injuries of the nervous system and the skull. Diseases due to physical agents Male Medical sciences Membrane Proteins - genetics Membrane Proteins - metabolism Nerve Growth Factors - genetics Nerve Growth Factors - metabolism Nitric Oxide Synthase - genetics Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Oxygen - pharmacology Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - metabolism Spinal Cord Injuries - metabolism Spinal Cord Injuries - pathology Time Factors Traumas. Diseases due to physical agents |
| title | Effects of hyperbaric oxygen on GDNF expression and apoptosis in spinal cord injury |
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