Blockade of interleukin‐6 signaling aggravates ischemic cerebral damage in mice: possible involvement of Stat3 activation in the protection of neurons
Interleukin (IL)‐6 expression transiently increases in the acute phase of cerebral ischemia. To investigate the physiological significance of endogenous IL‐6 expression and to identify the main signal pathway for the action of IL‐6, we administered anti‐mouse IL‐6 receptor monoclonal antibody (IL‐6R...
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| Veröffentlicht in: | Journal of neurochemistry 2005-07, Vol.94 (2), p.459-468 |
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| creator | Yamashita, Toru Sawamoto, Kazunobu Suzuki, Shigeaki Suzuki, Norihiro Adachi, Kazuhide Kawase, Takeshi Mihara, Masahiko Ohsugi, Yoshiyuki Abe, Koji Okano, Hideyuki |
| description | Interleukin (IL)‐6 expression transiently increases in the acute phase of cerebral ischemia. To investigate the physiological significance of endogenous IL‐6 expression and to identify the main signal pathway for the action of IL‐6, we administered anti‐mouse IL‐6 receptor monoclonal antibody (IL‐6RA), which blocks IL‐6 signaling, to mice immediately after a 45‐min period of middle cerebral artery occlusion (MCAO). At 6 h after MCAO, IL‐6RA administration had resulted in a significant reduction in the amount of phosphorylated signal transducer and activator of transcription‐3 (Stat3) protein in the peri‐infarct area of the cortex. At 24 h after MCAO, blockade of IL‐6 signaling had led to an increase in number of apoptotic cells in the peri‐infarct area and enlargement of the size of the infarct, and it had adversely affected neurological function. These results suggest that endogenous IL‐6 plays a critical role in preventing damaged neurons from undergoing apoptosis in the acute phase of cerebral ischemia and that its role may be mediated by Stat3 activation. |
| doi_str_mv | 10.1111/j.1471-4159.2005.03227.x |
| format | Article |
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To investigate the physiological significance of endogenous IL‐6 expression and to identify the main signal pathway for the action of IL‐6, we administered anti‐mouse IL‐6 receptor monoclonal antibody (IL‐6RA), which blocks IL‐6 signaling, to mice immediately after a 45‐min period of middle cerebral artery occlusion (MCAO). At 6 h after MCAO, IL‐6RA administration had resulted in a significant reduction in the amount of phosphorylated signal transducer and activator of transcription‐3 (Stat3) protein in the peri‐infarct area of the cortex. At 24 h after MCAO, blockade of IL‐6 signaling had led to an increase in number of apoptotic cells in the peri‐infarct area and enlargement of the size of the infarct, and it had adversely affected neurological function. These results suggest that endogenous IL‐6 plays a critical role in preventing damaged neurons from undergoing apoptosis in the acute phase of cerebral ischemia and that its role may be mediated by Stat3 activation.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2005.03227.x</identifier><identifier>PMID: 15998296</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Anatomy & physiology ; Animals ; Antibodies, Monoclonal - pharmacology ; Apoptosis - drug effects ; Behavior, Animal ; Biological and medical sciences ; Blotting, Western - methods ; Brain Ischemia - etiology ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Caspase 3 ; Caspases - metabolism ; Cell Count - methods ; Cell physiology ; Cerebral Cortex - cytology ; Cerebral Cortex - pathology ; Chi-Square Distribution ; Cytokines ; DNA-Binding Proteins - metabolism ; Enzyme Activation - drug effects ; Enzyme-Linked Immunosorbent Assay - methods ; Extracellular Signal-Regulated MAP Kinases - metabolism ; focal cerebral ischemia ; Fundamental and applied biological sciences. Psychology ; Histocytochemistry - methods ; Infarction, Middle Cerebral Artery - complications ; Interleukin-6 - antagonists & inhibitors ; Interleukin-6 - metabolism ; interleukin‐6 ; interleukin‐6 receptor antibody ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Molecular and cellular biology ; Neurology ; Neurons ; Neurons - drug effects ; neuroprotection ; Phosphorylation - drug effects ; Protein-Serine-Threonine Kinases - metabolism ; Proteins ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-akt ; Receptors, Interleukin-6 - antagonists & inhibitors ; Receptors, Interleukin-6 - immunology ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - metabolism ; Rodents ; signal transducer and activation of transcription‐3 ; Signal transduction ; Signal Transduction - drug effects ; STAT3 Transcription Factor ; Suppressor of Cytokine Signaling 3 Protein ; Suppressor of Cytokine Signaling Proteins ; Time Factors ; Trans-Activators - metabolism ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of neurochemistry, 2005-07, Vol.94 (2), p.459-468</ispartof><rights>2006 INIST-CNRS</rights><rights>2005 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5407-1f16b2655242622da6aa58041ea7fde778da6150df23b5ba0bc1df2535b058b83</citedby><cites>FETCH-LOGICAL-c5407-1f16b2655242622da6aa58041ea7fde778da6150df23b5ba0bc1df2535b058b83</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.1471-4159.2005.03227.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2005.03227.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16897770$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15998296$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamashita, Toru</creatorcontrib><creatorcontrib>Sawamoto, Kazunobu</creatorcontrib><creatorcontrib>Suzuki, Shigeaki</creatorcontrib><creatorcontrib>Suzuki, Norihiro</creatorcontrib><creatorcontrib>Adachi, Kazuhide</creatorcontrib><creatorcontrib>Kawase, Takeshi</creatorcontrib><creatorcontrib>Mihara, Masahiko</creatorcontrib><creatorcontrib>Ohsugi, Yoshiyuki</creatorcontrib><creatorcontrib>Abe, Koji</creatorcontrib><creatorcontrib>Okano, Hideyuki</creatorcontrib><title>Blockade of interleukin‐6 signaling aggravates ischemic cerebral damage in mice: possible involvement of Stat3 activation in the protection of neurons</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Interleukin (IL)‐6 expression transiently increases in the acute phase of cerebral ischemia. To investigate the physiological significance of endogenous IL‐6 expression and to identify the main signal pathway for the action of IL‐6, we administered anti‐mouse IL‐6 receptor monoclonal antibody (IL‐6RA), which blocks IL‐6 signaling, to mice immediately after a 45‐min period of middle cerebral artery occlusion (MCAO). At 6 h after MCAO, IL‐6RA administration had resulted in a significant reduction in the amount of phosphorylated signal transducer and activator of transcription‐3 (Stat3) protein in the peri‐infarct area of the cortex. At 24 h after MCAO, blockade of IL‐6 signaling had led to an increase in number of apoptotic cells in the peri‐infarct area and enlargement of the size of the infarct, and it had adversely affected neurological function. These results suggest that endogenous IL‐6 plays a critical role in preventing damaged neurons from undergoing apoptosis in the acute phase of cerebral ischemia and that its role may be mediated by Stat3 activation.</description><subject>Anatomy & physiology</subject><subject>Animals</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Behavior, Animal</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western - methods</subject><subject>Brain Ischemia - etiology</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>Cell Count - methods</subject><subject>Cell physiology</subject><subject>Cerebral Cortex - cytology</subject><subject>Cerebral Cortex - pathology</subject><subject>Chi-Square Distribution</subject><subject>Cytokines</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme-Linked Immunosorbent Assay - methods</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>focal cerebral ischemia</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Histocytochemistry - methods</subject><subject>Infarction, Middle Cerebral Artery - complications</subject><subject>Interleukin-6 - antagonists & inhibitors</subject><subject>Interleukin-6 - metabolism</subject><subject>interleukin‐6</subject><subject>interleukin‐6 receptor antibody</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular and cellular biology</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>neuroprotection</subject><subject>Phosphorylation - drug effects</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Receptors, Interleukin-6 - antagonists & inhibitors</subject><subject>Receptors, Interleukin-6 - immunology</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>signal transducer and activation of transcription‐3</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>STAT3 Transcription Factor</subject><subject>Suppressor of Cytokine Signaling 3 Protein</subject><subject>Suppressor of Cytokine Signaling Proteins</subject><subject>Time Factors</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9u1DAQxi0EokvhFZCFBLcE24mdBIkDrPirCg7A2Zo4k623jrO1k6W98QgceT6eBKe7ohInfLH1zW8-jecjhHKW83Seb3NeVjwruWxywZjMWSFElV_dIau_hbtkxZgQWcFKcUIexLhljKtS8fvkJJWbWjRqRX69dqO5gA7p2FPrJwwO5wvrf__4qWi0Gw_O-g2FzSbAHiaM1EZzjoM11GDANoCjHQywwdRNk4wv6G6M0bZuUfaj2-OAflrsv0wwFRTMZJOTHf3SMZ0j3YVxQnOjJMrjHEYfH5J7PbiIj473Kfn29s3X9fvs7PO7D-tXZ5mRJasy3nPVCiWlKIUSogMFIGtWcoSq77Cq6iRxybpeFK1sgbWGp7csZMtk3dbFKXl28E1TXM4YJz2kH6Jz4HGco1Y1Y40QKoFP_gG34xzSfqIWTMmy4c3iVh8gE9ISAvZ6F-wA4Vpzppfo9FYvCeklIb1Ep2-i01ep9fHRf24H7G4bj1kl4OkRgGjA9QG8sfGWU3VTVRVL3MsD9906vP7vAfTHT-vlVfwBrJi3YA</recordid><startdate>200507</startdate><enddate>200507</enddate><creator>Yamashita, Toru</creator><creator>Sawamoto, Kazunobu</creator><creator>Suzuki, Shigeaki</creator><creator>Suzuki, Norihiro</creator><creator>Adachi, Kazuhide</creator><creator>Kawase, Takeshi</creator><creator>Mihara, Masahiko</creator><creator>Ohsugi, Yoshiyuki</creator><creator>Abe, Koji</creator><creator>Okano, Hideyuki</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Blackwell Publishing Ltd</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>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>7X8</scope></search><sort><creationdate>200507</creationdate><title>Blockade of interleukin‐6 signaling aggravates ischemic cerebral damage in mice: possible involvement of Stat3 activation in the protection of neurons</title><author>Yamashita, Toru ; Sawamoto, Kazunobu ; Suzuki, Shigeaki ; Suzuki, Norihiro ; Adachi, Kazuhide ; Kawase, Takeshi ; Mihara, Masahiko ; Ohsugi, Yoshiyuki ; Abe, Koji ; Okano, Hideyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5407-1f16b2655242622da6aa58041ea7fde778da6150df23b5ba0bc1df2535b058b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Anatomy & physiology</topic><topic>Animals</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Behavior, Animal</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western - methods</topic><topic>Brain Ischemia - etiology</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Caspase 3</topic><topic>Caspases - metabolism</topic><topic>Cell Count - methods</topic><topic>Cell physiology</topic><topic>Cerebral Cortex - cytology</topic><topic>Cerebral Cortex - pathology</topic><topic>Chi-Square Distribution</topic><topic>Cytokines</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme-Linked Immunosorbent Assay - methods</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>focal cerebral ischemia</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Histocytochemistry - methods</topic><topic>Infarction, Middle Cerebral Artery - complications</topic><topic>Interleukin-6 - antagonists & inhibitors</topic><topic>Interleukin-6 - metabolism</topic><topic>interleukin‐6</topic><topic>interleukin‐6 receptor antibody</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Molecular and cellular biology</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>neuroprotection</topic><topic>Phosphorylation - drug effects</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Receptors, Interleukin-6 - antagonists & inhibitors</topic><topic>Receptors, Interleukin-6 - immunology</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>signal transducer and activation of transcription‐3</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>STAT3 Transcription Factor</topic><topic>Suppressor of Cytokine Signaling 3 Protein</topic><topic>Suppressor of Cytokine Signaling Proteins</topic><topic>Time Factors</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamashita, Toru</creatorcontrib><creatorcontrib>Sawamoto, Kazunobu</creatorcontrib><creatorcontrib>Suzuki, Shigeaki</creatorcontrib><creatorcontrib>Suzuki, Norihiro</creatorcontrib><creatorcontrib>Adachi, Kazuhide</creatorcontrib><creatorcontrib>Kawase, Takeshi</creatorcontrib><creatorcontrib>Mihara, Masahiko</creatorcontrib><creatorcontrib>Ohsugi, Yoshiyuki</creatorcontrib><creatorcontrib>Abe, Koji</creatorcontrib><creatorcontrib>Okano, Hideyuki</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamashita, Toru</au><au>Sawamoto, Kazunobu</au><au>Suzuki, Shigeaki</au><au>Suzuki, Norihiro</au><au>Adachi, Kazuhide</au><au>Kawase, Takeshi</au><au>Mihara, Masahiko</au><au>Ohsugi, Yoshiyuki</au><au>Abe, Koji</au><au>Okano, Hideyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Blockade of interleukin‐6 signaling aggravates ischemic cerebral damage in mice: possible involvement of Stat3 activation in the protection of neurons</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2005-07</date><risdate>2005</risdate><volume>94</volume><issue>2</issue><spage>459</spage><epage>468</epage><pages>459-468</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>Interleukin (IL)‐6 expression transiently increases in the acute phase of cerebral ischemia. To investigate the physiological significance of endogenous IL‐6 expression and to identify the main signal pathway for the action of IL‐6, we administered anti‐mouse IL‐6 receptor monoclonal antibody (IL‐6RA), which blocks IL‐6 signaling, to mice immediately after a 45‐min period of middle cerebral artery occlusion (MCAO). At 6 h after MCAO, IL‐6RA administration had resulted in a significant reduction in the amount of phosphorylated signal transducer and activator of transcription‐3 (Stat3) protein in the peri‐infarct area of the cortex. At 24 h after MCAO, blockade of IL‐6 signaling had led to an increase in number of apoptotic cells in the peri‐infarct area and enlargement of the size of the infarct, and it had adversely affected neurological function. These results suggest that endogenous IL‐6 plays a critical role in preventing damaged neurons from undergoing apoptosis in the acute phase of cerebral ischemia and that its role may be mediated by Stat3 activation.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>15998296</pmid><doi>10.1111/j.1471-4159.2005.03227.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anatomy & physiology Animals Antibodies, Monoclonal - pharmacology Apoptosis - drug effects Behavior, Animal Biological and medical sciences Blotting, Western - methods Brain Ischemia - etiology Brain Ischemia - metabolism Brain Ischemia - pathology Caspase 3 Caspases - metabolism Cell Count - methods Cell physiology Cerebral Cortex - cytology Cerebral Cortex - pathology Chi-Square Distribution Cytokines DNA-Binding Proteins - metabolism Enzyme Activation - drug effects Enzyme-Linked Immunosorbent Assay - methods Extracellular Signal-Regulated MAP Kinases - metabolism focal cerebral ischemia Fundamental and applied biological sciences. Psychology Histocytochemistry - methods Infarction, Middle Cerebral Artery - complications Interleukin-6 - antagonists & inhibitors Interleukin-6 - metabolism interleukin‐6 interleukin‐6 receptor antibody Male Medical sciences Mice Mice, Inbred C57BL Molecular and cellular biology Neurology Neurons Neurons - drug effects neuroprotection Phosphorylation - drug effects Protein-Serine-Threonine Kinases - metabolism Proteins Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-akt Receptors, Interleukin-6 - antagonists & inhibitors Receptors, Interleukin-6 - immunology Repressor Proteins - genetics Repressor Proteins - metabolism Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - metabolism Rodents signal transducer and activation of transcription‐3 Signal transduction Signal Transduction - drug effects STAT3 Transcription Factor Suppressor of Cytokine Signaling 3 Protein Suppressor of Cytokine Signaling Proteins Time Factors Trans-Activators - metabolism Transcription Factors - genetics Transcription Factors - metabolism Vascular diseases and vascular malformations of the nervous system |
| title | Blockade of interleukin‐6 signaling aggravates ischemic cerebral damage in mice: possible involvement of Stat3 activation in the protection of neurons |
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