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Activation of STAT1 in Neurons Following Spinal Cord Injury in Mice
The signal transducer and activator of transcription 1 (STAT1) has been reported to be associated with neuronal cell death after cerebral ischemia. On the contrary, STAT3 has been revealed to regulate cell survival. We examined the chronological alteration and cellular localization of phosphorylated...
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| Published in: | Neurochemical research 2011-12, Vol.36 (12), p.2236-2243 |
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| Main Authors: | , , , , , , , |
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| cited_by | cdi_FETCH-LOGICAL-c468t-441088c32f97c6295023ffe0d57338ce9a4bf6852002145fbef0fb21ee0990163 |
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| cites | cdi_FETCH-LOGICAL-c468t-441088c32f97c6295023ffe0d57338ce9a4bf6852002145fbef0fb21ee0990163 |
| container_end_page | 2243 |
| container_issue | 12 |
| container_start_page | 2236 |
| container_title | Neurochemical research |
| container_volume | 36 |
| creator | Osuka, Koji Watanabe, Yasuo Usuda, Nobuteru Atsuzawa, Kimie Yasuda, Muneyoshi Aoshima, Chihiro Wakabayashi, Toshihiko Takayasu, Masakazu |
| description | The signal transducer and activator of transcription 1 (STAT1) has been reported to be associated with neuronal cell death after cerebral ischemia. On the contrary, STAT3 has been revealed to regulate cell survival. We examined the chronological alteration and cellular localization of phosphorylated (
p
)-JAK1,
p
-STAT1 and
p
-STAT3 following mild spinal cord injury (SCI) in mice. Western blot analysis indicated that JAK1 is significantly phosphorylated, accompanied by the phosphorylation of STAT1 at Tyr
701
within a similar timeframe. Immunofluorescence staining indicated that signal transduction of STAT3 is introduced into the nucleus of the neurons within the anterior horns; however, in mirror sections, that of STAT1 is limited to the cytoplasm. These findings suggest that STAT3 signal is predominantly transduced into the nucleus and plays a stronger role in neuronal survival than STAT1. Modulation of the functional balance between STAT1 and STAT3 might determine the survival or death of neurons after SCI. |
| doi_str_mv | 10.1007/s11064-011-0547-6 |
| format | article |
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p
)-JAK1,
p
-STAT1 and
p
-STAT3 following mild spinal cord injury (SCI) in mice. Western blot analysis indicated that JAK1 is significantly phosphorylated, accompanied by the phosphorylation of STAT1 at Tyr
701
within a similar timeframe. Immunofluorescence staining indicated that signal transduction of STAT3 is introduced into the nucleus of the neurons within the anterior horns; however, in mirror sections, that of STAT1 is limited to the cytoplasm. These findings suggest that STAT3 signal is predominantly transduced into the nucleus and plays a stronger role in neuronal survival than STAT1. Modulation of the functional balance between STAT1 and STAT3 might determine the survival or death of neurons after SCI.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-011-0547-6</identifier><identifier>PMID: 21833847</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Enzyme Activation ; Female ; Janus Kinase 1 - metabolism ; Mice ; Neurochemistry ; Neurology ; Neurons - metabolism ; Neurosciences ; Original Paper ; Phosphorylation ; Signal Transduction - physiology ; Spinal Cord Injuries - metabolism ; STAT1 Transcription Factor - metabolism ; STAT3 Transcription Factor - metabolism ; Tyrosine - metabolism</subject><ispartof>Neurochemical research, 2011-12, Vol.36 (12), p.2236-2243</ispartof><rights>Springer Science+Business Media, LLC 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-441088c32f97c6295023ffe0d57338ce9a4bf6852002145fbef0fb21ee0990163</citedby><cites>FETCH-LOGICAL-c468t-441088c32f97c6295023ffe0d57338ce9a4bf6852002145fbef0fb21ee0990163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21833847$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Osuka, Koji</creatorcontrib><creatorcontrib>Watanabe, Yasuo</creatorcontrib><creatorcontrib>Usuda, Nobuteru</creatorcontrib><creatorcontrib>Atsuzawa, Kimie</creatorcontrib><creatorcontrib>Yasuda, Muneyoshi</creatorcontrib><creatorcontrib>Aoshima, Chihiro</creatorcontrib><creatorcontrib>Wakabayashi, Toshihiko</creatorcontrib><creatorcontrib>Takayasu, Masakazu</creatorcontrib><title>Activation of STAT1 in Neurons Following Spinal Cord Injury in Mice</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>The signal transducer and activator of transcription 1 (STAT1) has been reported to be associated with neuronal cell death after cerebral ischemia. On the contrary, STAT3 has been revealed to regulate cell survival. We examined the chronological alteration and cellular localization of phosphorylated (
p
)-JAK1,
p
-STAT1 and
p
-STAT3 following mild spinal cord injury (SCI) in mice. Western blot analysis indicated that JAK1 is significantly phosphorylated, accompanied by the phosphorylation of STAT1 at Tyr
701
within a similar timeframe. Immunofluorescence staining indicated that signal transduction of STAT3 is introduced into the nucleus of the neurons within the anterior horns; however, in mirror sections, that of STAT1 is limited to the cytoplasm. These findings suggest that STAT3 signal is predominantly transduced into the nucleus and plays a stronger role in neuronal survival than STAT1. Modulation of the functional balance between STAT1 and STAT3 might determine the survival or death of neurons after SCI.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Enzyme Activation</subject><subject>Female</subject><subject>Janus Kinase 1 - metabolism</subject><subject>Mice</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurons - metabolism</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Phosphorylation</subject><subject>Signal Transduction - physiology</subject><subject>Spinal Cord Injuries - metabolism</subject><subject>STAT1 Transcription Factor - metabolism</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Tyrosine - metabolism</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqFkTFPwzAQhS0EoqXwA1hQxMIUuLMdxxmrikKlAkPLbKWpXaVK42I3oP57HKWAhISYbrjv3r27R8glwi0CpHceEQSPATGGhKexOCJ9TFIWiwzYMekDC12GGfTImfdrgDBF8ZT0KErGJE_7ZDQsduV7vittHVkTzebDOUZlHT3rxtnaR2NbVfajrFfRbFvWeRWNrFtGk3rduH3LPZWFPicnJq-8vjjUAXkd389Hj_H05WEyGk7jggu5izlHkLJg1GRpIWiWAGXGaFgGx0wWOsv5wgiZ0NYkT8xCGzALilpDlgEKNiA3ne7W2bdG-53alL7QVZXX2jZeZVRIyRNM_yfDakZZ-MKAXP8i17Zx4dAWwlRQGcgBwQ4qnPXeaaO2rtzkbq8QVJuE6pJQIQnVJqFas1cH4Wax0cvvia_XB4B2gA-teqXdz-a_VT8Bx5OPmA</recordid><startdate>20111201</startdate><enddate>20111201</enddate><creator>Osuka, Koji</creator><creator>Watanabe, Yasuo</creator><creator>Usuda, Nobuteru</creator><creator>Atsuzawa, Kimie</creator><creator>Yasuda, Muneyoshi</creator><creator>Aoshima, Chihiro</creator><creator>Wakabayashi, Toshihiko</creator><creator>Takayasu, Masakazu</creator><general>Springer US</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20111201</creationdate><title>Activation of STAT1 in Neurons Following Spinal Cord Injury in Mice</title><author>Osuka, Koji ; Watanabe, Yasuo ; Usuda, Nobuteru ; Atsuzawa, Kimie ; Yasuda, Muneyoshi ; Aoshima, Chihiro ; Wakabayashi, Toshihiko ; Takayasu, Masakazu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-441088c32f97c6295023ffe0d57338ce9a4bf6852002145fbef0fb21ee0990163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Enzyme Activation</topic><topic>Female</topic><topic>Janus Kinase 1 - metabolism</topic><topic>Mice</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurons - metabolism</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Phosphorylation</topic><topic>Signal Transduction - physiology</topic><topic>Spinal Cord Injuries - metabolism</topic><topic>STAT1 Transcription Factor - metabolism</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Tyrosine - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Osuka, Koji</creatorcontrib><creatorcontrib>Watanabe, Yasuo</creatorcontrib><creatorcontrib>Usuda, Nobuteru</creatorcontrib><creatorcontrib>Atsuzawa, Kimie</creatorcontrib><creatorcontrib>Yasuda, Muneyoshi</creatorcontrib><creatorcontrib>Aoshima, Chihiro</creatorcontrib><creatorcontrib>Wakabayashi, Toshihiko</creatorcontrib><creatorcontrib>Takayasu, Masakazu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Complete (ProQuest Database)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Biological Science Journals</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Osuka, Koji</au><au>Watanabe, Yasuo</au><au>Usuda, Nobuteru</au><au>Atsuzawa, Kimie</au><au>Yasuda, Muneyoshi</au><au>Aoshima, Chihiro</au><au>Wakabayashi, Toshihiko</au><au>Takayasu, Masakazu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of STAT1 in Neurons Following Spinal Cord Injury in Mice</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2011-12-01</date><risdate>2011</risdate><volume>36</volume><issue>12</issue><spage>2236</spage><epage>2243</epage><pages>2236-2243</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>The signal transducer and activator of transcription 1 (STAT1) has been reported to be associated with neuronal cell death after cerebral ischemia. On the contrary, STAT3 has been revealed to regulate cell survival. We examined the chronological alteration and cellular localization of phosphorylated (
p
)-JAK1,
p
-STAT1 and
p
-STAT3 following mild spinal cord injury (SCI) in mice. Western blot analysis indicated that JAK1 is significantly phosphorylated, accompanied by the phosphorylation of STAT1 at Tyr
701
within a similar timeframe. Immunofluorescence staining indicated that signal transduction of STAT3 is introduced into the nucleus of the neurons within the anterior horns; however, in mirror sections, that of STAT1 is limited to the cytoplasm. These findings suggest that STAT3 signal is predominantly transduced into the nucleus and plays a stronger role in neuronal survival than STAT1. Modulation of the functional balance between STAT1 and STAT3 might determine the survival or death of neurons after SCI.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21833847</pmid><doi>10.1007/s11064-011-0547-6</doi><tpages>8</tpages></addata></record> |
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| ispartof | Neurochemical research, 2011-12, Vol.36 (12), p.2236-2243 |
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| language | eng |
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| subjects | Animals Biochemistry Biomedical and Life Sciences Biomedicine Cell Biology Enzyme Activation Female Janus Kinase 1 - metabolism Mice Neurochemistry Neurology Neurons - metabolism Neurosciences Original Paper Phosphorylation Signal Transduction - physiology Spinal Cord Injuries - metabolism STAT1 Transcription Factor - metabolism STAT3 Transcription Factor - metabolism Tyrosine - metabolism |
| title | Activation of STAT1 in Neurons Following Spinal Cord Injury in Mice |
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