Prolonged Expression of Interferon‐Inducible Protein‐10 in Ischemic Cortex After Permanent Occlusion of the Middle Cerebral Artery in Rat
: Focal cerebral ischemia elicits local inflammatory reaction as demonstrated by the accumulation of inflammatory cells and mediators in the ischemic brain. Interferon‐inducible protein‐10 (IP‐10) is a member of the C‐X‐C chemokine family that possesses potent chemoattractant actions for monocytes,...
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Veröffentlicht in: | Journal of neurochemistry 1998-09, Vol.71 (3), p.1194-1204 |
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description | : Focal cerebral ischemia elicits local inflammatory reaction as demonstrated by the accumulation of inflammatory cells and mediators in the ischemic brain. Interferon‐inducible protein‐10 (IP‐10) is a member of the C‐X‐C chemokine family that possesses potent chemoattractant actions for monocytes, T cells, and smooth muscle cells. To investigate a potential role of IP‐10 in focal stroke, we studied the temporal expression of IP‐10 mRNA after occlusion of the middle cerebral artery in rat by means of northern analysis. IP‐10 mRNA expression after focal stroke demonstrated a unique biphasic profile, with a marked increase early at 3 h (4.9‐fold over control; p < 0.01), a peak level at 6 h (14.5‐fold; p < 0.001) after occlusion of the middle cerebral artery, and a second wave induction 10–15 days after ischemic injury (7.2‐ and 9.3‐fold increase for 10 and 15 days, respectively; p < 0.001). In situ hybridization confirmed the induced expression of IP‐10 mRNA and revealed its spatial distribution after focal stroke. Immunohistochemical studies demonstrated the expression of IP‐10 peptide in neurons (3–12 h) and astroglial cells (6 h to 15 days) of the ischemic zone. To explore further the potential role of IP‐10 in focal stroke, we demonstrated a dose‐dependent chemotactic action of IP‐10 on C6 glial cells and enhanced attachment of rat cerebellar granule neurons. Taken together, the data suggest that ischemia induces IP‐10, which may play a pleiotropic role in prolonged leukocyte recruitment, astrocyte migration/activation, and neuron attachment/sprouting after focal stroke. |
doi_str_mv | 10.1046/j.1471-4159.1998.71031194.x |
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Interferon‐inducible protein‐10 (IP‐10) is a member of the C‐X‐C chemokine family that possesses potent chemoattractant actions for monocytes, T cells, and smooth muscle cells. To investigate a potential role of IP‐10 in focal stroke, we studied the temporal expression of IP‐10 mRNA after occlusion of the middle cerebral artery in rat by means of northern analysis. IP‐10 mRNA expression after focal stroke demonstrated a unique biphasic profile, with a marked increase early at 3 h (4.9‐fold over control; p < 0.01), a peak level at 6 h (14.5‐fold; p < 0.001) after occlusion of the middle cerebral artery, and a second wave induction 10–15 days after ischemic injury (7.2‐ and 9.3‐fold increase for 10 and 15 days, respectively; p < 0.001). In situ hybridization confirmed the induced expression of IP‐10 mRNA and revealed its spatial distribution after focal stroke. Immunohistochemical studies demonstrated the expression of IP‐10 peptide in neurons (3–12 h) and astroglial cells (6 h to 15 days) of the ischemic zone. To explore further the potential role of IP‐10 in focal stroke, we demonstrated a dose‐dependent chemotactic action of IP‐10 on C6 glial cells and enhanced attachment of rat cerebellar granule neurons. Taken together, the data suggest that ischemia induces IP‐10, which may play a pleiotropic role in prolonged leukocyte recruitment, astrocyte migration/activation, and neuron attachment/sprouting after focal stroke.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1046/j.1471-4159.1998.71031194.x</identifier><identifier>PMID: 9721745</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; Arterial Occlusive Diseases - complications ; Astrocyte ; Biological and medical sciences ; Brain ; Brain Ischemia - etiology ; Brain Ischemia - metabolism ; Cell Adhesion - drug effects ; Cell Movement - drug effects ; Cerebellum - cytology ; Cerebellum - drug effects ; Cerebral Arteries ; Cerebral Cortex - metabolism ; Chemokine CXCL10 ; Chemokines ; Chemokines, CXC - genetics ; Chemokines, CXC - metabolism ; Immunohistochemistry ; Inflammation ; Interferon‐inducible protein ‐ 10 ; Interleukin-1 - genetics ; Medical sciences ; Neurology ; Neuron ; Neurons - drug effects ; Neurons - physiology ; Rats ; RNA, Messenger - metabolism ; Tissue Distribution ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha - genetics ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of neurochemistry, 1998-09, Vol.71 (3), p.1194-1204</ispartof><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5034-4d9142cc1870e90f4cab052ee592e9027e200b8c5db8c8d440fb6c39dbde5c253</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1471-4159.1998.71031194.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1471-4159.1998.71031194.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2384239$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9721745$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xinkang</creatorcontrib><creatorcontrib>Ellison, Julie A.</creatorcontrib><creatorcontrib>Siren, Anna‐Leena</creatorcontrib><creatorcontrib>Lysko, Paul G.</creatorcontrib><creatorcontrib>Yue, Tian‐Li</creatorcontrib><creatorcontrib>Barone, Frank C.</creatorcontrib><creatorcontrib>Shatzman, Allan</creatorcontrib><creatorcontrib>Feuerstein, Giora Z.</creatorcontrib><title>Prolonged Expression of Interferon‐Inducible Protein‐10 in Ischemic Cortex After Permanent Occlusion of the Middle Cerebral Artery in Rat</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>: Focal cerebral ischemia elicits local inflammatory reaction as demonstrated by the accumulation of inflammatory cells and mediators in the ischemic brain. Interferon‐inducible protein‐10 (IP‐10) is a member of the C‐X‐C chemokine family that possesses potent chemoattractant actions for monocytes, T cells, and smooth muscle cells. To investigate a potential role of IP‐10 in focal stroke, we studied the temporal expression of IP‐10 mRNA after occlusion of the middle cerebral artery in rat by means of northern analysis. IP‐10 mRNA expression after focal stroke demonstrated a unique biphasic profile, with a marked increase early at 3 h (4.9‐fold over control; p < 0.01), a peak level at 6 h (14.5‐fold; p < 0.001) after occlusion of the middle cerebral artery, and a second wave induction 10–15 days after ischemic injury (7.2‐ and 9.3‐fold increase for 10 and 15 days, respectively; p < 0.001). In situ hybridization confirmed the induced expression of IP‐10 mRNA and revealed its spatial distribution after focal stroke. Immunohistochemical studies demonstrated the expression of IP‐10 peptide in neurons (3–12 h) and astroglial cells (6 h to 15 days) of the ischemic zone. To explore further the potential role of IP‐10 in focal stroke, we demonstrated a dose‐dependent chemotactic action of IP‐10 on C6 glial cells and enhanced attachment of rat cerebellar granule neurons. Taken together, the data suggest that ischemia induces IP‐10, which may play a pleiotropic role in prolonged leukocyte recruitment, astrocyte migration/activation, and neuron attachment/sprouting after focal stroke.</description><subject>Animals</subject><subject>Arterial Occlusive Diseases - complications</subject><subject>Astrocyte</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain Ischemia - etiology</subject><subject>Brain Ischemia - metabolism</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Movement - drug effects</subject><subject>Cerebellum - cytology</subject><subject>Cerebellum - drug effects</subject><subject>Cerebral Arteries</subject><subject>Cerebral Cortex - metabolism</subject><subject>Chemokine CXCL10</subject><subject>Chemokines</subject><subject>Chemokines, CXC - genetics</subject><subject>Chemokines, CXC - metabolism</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Interferon‐inducible protein ‐ 10</subject><subject>Interleukin-1 - genetics</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Neuron</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Rats</subject><subject>RNA, Messenger - metabolism</subject><subject>Tissue Distribution</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Necrosis Factor-alpha - genetics</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>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkc2KFDEUhYMoYzv6CEJAcVdlbipVqeCqKUdtGZ1BdB2qkltOmvrpSaqxe-cLCD6jT2KK_tmKm4Sb852TC4eQF8BSYKJ4vU5BSEgE5CoFpcpUAssAlEh3D8jirD0kC8Y4TzIm-GPyJIQ1Y1CIAi7IhZIcpMgX5NetH7tx-I6WXu02HkNw40DHlq6GCX2Lfhz-_Py9GuzWuKZDGvEJ3fwGjLqBroK5w94ZWo1-wh1dttFGb9H39YDDRG-M6banzOkO6Sdnbcyp0GPj644uo83v56gv9fSUPGrrLuCz431Jvr27-lp9SK5v3q-q5XVicpaJRFgFghsDpWSoWCtM3bCcI-aKx5lL5Iw1pcltPEorBGubwmTKNhZzw_Pskrw65G78eL_FMOneBYNdF5cet0HLrCwKyfg_QZAArJAz-OYAGj-G4LHVG-_62u81MD23ptd6bkbPzei5NX1qTe-i-_nxm23Toz17jzVF_eVRr4Opu9bXg3HhjPGsFDxTEXt7wH64Dvf_s4H--Lk6Tdlf4663bw</recordid><startdate>199809</startdate><enddate>199809</enddate><creator>Wang, Xinkang</creator><creator>Ellison, Julie A.</creator><creator>Siren, Anna‐Leena</creator><creator>Lysko, Paul G.</creator><creator>Yue, Tian‐Li</creator><creator>Barone, Frank C.</creator><creator>Shatzman, Allan</creator><creator>Feuerstein, Giora Z.</creator><general>Blackwell Science Ltd</general><general>Blackwell</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>199809</creationdate><title>Prolonged Expression of Interferon‐Inducible Protein‐10 in Ischemic Cortex After Permanent Occlusion of the Middle Cerebral Artery in Rat</title><author>Wang, Xinkang ; Ellison, Julie A. ; Siren, Anna‐Leena ; Lysko, Paul G. ; Yue, Tian‐Li ; Barone, Frank C. ; Shatzman, Allan ; Feuerstein, Giora Z.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5034-4d9142cc1870e90f4cab052ee592e9027e200b8c5db8c8d440fb6c39dbde5c253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Arterial Occlusive Diseases - complications</topic><topic>Astrocyte</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Brain Ischemia - etiology</topic><topic>Brain Ischemia - metabolism</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Movement - drug effects</topic><topic>Cerebellum - cytology</topic><topic>Cerebellum - drug effects</topic><topic>Cerebral Arteries</topic><topic>Cerebral Cortex - metabolism</topic><topic>Chemokine CXCL10</topic><topic>Chemokines</topic><topic>Chemokines, CXC - genetics</topic><topic>Chemokines, CXC - metabolism</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Interferon‐inducible protein ‐ 10</topic><topic>Interleukin-1 - genetics</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Neuron</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Rats</topic><topic>RNA, Messenger - metabolism</topic><topic>Tissue Distribution</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xinkang</creatorcontrib><creatorcontrib>Ellison, Julie A.</creatorcontrib><creatorcontrib>Siren, Anna‐Leena</creatorcontrib><creatorcontrib>Lysko, Paul G.</creatorcontrib><creatorcontrib>Yue, Tian‐Li</creatorcontrib><creatorcontrib>Barone, Frank C.</creatorcontrib><creatorcontrib>Shatzman, Allan</creatorcontrib><creatorcontrib>Feuerstein, Giora Z.</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>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xinkang</au><au>Ellison, Julie A.</au><au>Siren, Anna‐Leena</au><au>Lysko, Paul G.</au><au>Yue, Tian‐Li</au><au>Barone, Frank C.</au><au>Shatzman, Allan</au><au>Feuerstein, Giora Z.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prolonged Expression of Interferon‐Inducible Protein‐10 in Ischemic Cortex After Permanent Occlusion of the Middle Cerebral Artery in Rat</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>1998-09</date><risdate>1998</risdate><volume>71</volume><issue>3</issue><spage>1194</spage><epage>1204</epage><pages>1194-1204</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>: Focal cerebral ischemia elicits local inflammatory reaction as demonstrated by the accumulation of inflammatory cells and mediators in the ischemic brain. Interferon‐inducible protein‐10 (IP‐10) is a member of the C‐X‐C chemokine family that possesses potent chemoattractant actions for monocytes, T cells, and smooth muscle cells. To investigate a potential role of IP‐10 in focal stroke, we studied the temporal expression of IP‐10 mRNA after occlusion of the middle cerebral artery in rat by means of northern analysis. IP‐10 mRNA expression after focal stroke demonstrated a unique biphasic profile, with a marked increase early at 3 h (4.9‐fold over control; p < 0.01), a peak level at 6 h (14.5‐fold; p < 0.001) after occlusion of the middle cerebral artery, and a second wave induction 10–15 days after ischemic injury (7.2‐ and 9.3‐fold increase for 10 and 15 days, respectively; p < 0.001). In situ hybridization confirmed the induced expression of IP‐10 mRNA and revealed its spatial distribution after focal stroke. Immunohistochemical studies demonstrated the expression of IP‐10 peptide in neurons (3–12 h) and astroglial cells (6 h to 15 days) of the ischemic zone. To explore further the potential role of IP‐10 in focal stroke, we demonstrated a dose‐dependent chemotactic action of IP‐10 on C6 glial cells and enhanced attachment of rat cerebellar granule neurons. Taken together, the data suggest that ischemia induces IP‐10, which may play a pleiotropic role in prolonged leukocyte recruitment, astrocyte migration/activation, and neuron attachment/sprouting after focal stroke.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>9721745</pmid><doi>10.1046/j.1471-4159.1998.71031194.x</doi><tpages>11</tpages></addata></record> |
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subjects | Animals Arterial Occlusive Diseases - complications Astrocyte Biological and medical sciences Brain Brain Ischemia - etiology Brain Ischemia - metabolism Cell Adhesion - drug effects Cell Movement - drug effects Cerebellum - cytology Cerebellum - drug effects Cerebral Arteries Cerebral Cortex - metabolism Chemokine CXCL10 Chemokines Chemokines, CXC - genetics Chemokines, CXC - metabolism Immunohistochemistry Inflammation Interferon‐inducible protein ‐ 10 Interleukin-1 - genetics Medical sciences Neurology Neuron Neurons - drug effects Neurons - physiology Rats RNA, Messenger - metabolism Tissue Distribution Tumor Cells, Cultured Tumor Necrosis Factor-alpha - genetics Vascular diseases and vascular malformations of the nervous system |
title | Prolonged Expression of Interferon‐Inducible Protein‐10 in Ischemic Cortex After Permanent Occlusion of the Middle Cerebral Artery in Rat |
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