Matrix metalloproteinase induction by EMMPRIN in experimental focal cerebral ischemia
Focal cerebral ischemia leads to the gradual disruption of the extracellular matrix. A key role in the turnover of the extracellular matrix is played by the system of matrix metalloproteinases (MMPs). In this study we describe changes of the MMP inducer protein (EMMPRIN) following experimental cereb...
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| Veröffentlicht in: | The European journal of neuroscience 2005-07, Vol.22 (1), p.273-277 |
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| creator | Burggraf, Dorothe Liebetrau, Martin Martens, Helge K. Wunderlich, Nathalie Jäger, Gabriele Dichgans, Martin Hamann, Gerhard F. |
| description | Focal cerebral ischemia leads to the gradual disruption of the extracellular matrix. A key role in the turnover of the extracellular matrix is played by the system of matrix metalloproteinases (MMPs). In this study we describe changes of the MMP inducer protein (EMMPRIN) following experimental cerebral ischemia (induced for 3 h and followed by 24 h reperfusion, suture model) in rats. Extracellular EMMPRIN was measured by Western blot of the ischemic and nonischemic basal ganglia and cortex separately. Compared with the contralateral nonischemic area, the ischemic hemisphere showed a significant increase in EMMPRIN: basal ganglia, 158% ± 4% (P |
| doi_str_mv | 10.1111/j.1460-9568.2005.04187.x |
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A key role in the turnover of the extracellular matrix is played by the system of matrix metalloproteinases (MMPs). In this study we describe changes of the MMP inducer protein (EMMPRIN) following experimental cerebral ischemia (induced for 3 h and followed by 24 h reperfusion, suture model) in rats. Extracellular EMMPRIN was measured by Western blot of the ischemic and nonischemic basal ganglia and cortex separately. Compared with the contralateral nonischemic area, the ischemic hemisphere showed a significant increase in EMMPRIN: basal ganglia, 158% ± 4% (P < 0.05); cortex, 128% ± 25% (P < 0.05). Immunohistochemistry was used to localize EMMPRIN on cerebral microvessels. EMMPRIN‐positive microvascular structures were quantified by automatic morphometric video‐imaging analysis and a significant increase in the number of cerebral microvessels staining positive for EMMPRIN in the ischemic basal ganglia was shown. The significant loss of microvascular basal lamina antigen collagen type IV in ischemic cortex and basal ganglia was calculated by Western blot. Measured by gelatin zymography, we demonstrated an MMP‐2 and MMP‐9 increase in the ischemic brain regions (P < 0.05). For the first time the MMP activation system EMMPRIN was shown to be relevant in cerebral ischemia. These results raise the possibility that the increased expression of EMMPRIN, the increase in MMPs and the damage of the basal lamina following cerebral ischemia are connected and part of a network of related changes.</description><identifier>ISSN: 0953-816X</identifier><identifier>EISSN: 1460-9568</identifier><identifier>DOI: 10.1111/j.1460-9568.2005.04187.x</identifier><identifier>PMID: 16029217</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; Antigens, CD - metabolism ; basal lamina ; Basement Membrane - metabolism ; Basement Membrane - pathology ; Basigin ; Brain Ischemia - metabolism ; Brain Ischemia - physiopathology ; CD147 ; Cerebral Infarction - metabolism ; Cerebral Infarction - physiopathology ; Collagen Type IV - metabolism ; Disease Models, Animal ; Extracellular Matrix - metabolism ; Immunohistochemistry ; Male ; Matrix Metalloproteinase 2 - metabolism ; Matrix Metalloproteinase 9 - metabolism ; Matrix Metalloproteinases - metabolism ; Microcirculation - metabolism ; Microcirculation - pathology ; Microcirculation - physiopathology ; MMPs ; rat ; Rats ; Rats, Wistar ; Reperfusion Injury - metabolism ; Reperfusion Injury - physiopathology ; Up-Regulation - physiology</subject><ispartof>The European journal of neuroscience, 2005-07, Vol.22 (1), p.273-277</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4057-95a08239588f7913e5a10cc15101df2313b9d17b65ff17109c7e1413fd6363dc3</citedby><cites>FETCH-LOGICAL-c4057-95a08239588f7913e5a10cc15101df2313b9d17b65ff17109c7e1413fd6363dc3</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.1460-9568.2005.04187.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1460-9568.2005.04187.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16029217$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Burggraf, Dorothe</creatorcontrib><creatorcontrib>Liebetrau, Martin</creatorcontrib><creatorcontrib>Martens, Helge K.</creatorcontrib><creatorcontrib>Wunderlich, Nathalie</creatorcontrib><creatorcontrib>Jäger, Gabriele</creatorcontrib><creatorcontrib>Dichgans, Martin</creatorcontrib><creatorcontrib>Hamann, Gerhard F.</creatorcontrib><title>Matrix metalloproteinase induction by EMMPRIN in experimental focal cerebral ischemia</title><title>The European journal of neuroscience</title><addtitle>Eur J Neurosci</addtitle><description>Focal cerebral ischemia leads to the gradual disruption of the extracellular matrix. A key role in the turnover of the extracellular matrix is played by the system of matrix metalloproteinases (MMPs). In this study we describe changes of the MMP inducer protein (EMMPRIN) following experimental cerebral ischemia (induced for 3 h and followed by 24 h reperfusion, suture model) in rats. Extracellular EMMPRIN was measured by Western blot of the ischemic and nonischemic basal ganglia and cortex separately. Compared with the contralateral nonischemic area, the ischemic hemisphere showed a significant increase in EMMPRIN: basal ganglia, 158% ± 4% (P < 0.05); cortex, 128% ± 25% (P < 0.05). Immunohistochemistry was used to localize EMMPRIN on cerebral microvessels. EMMPRIN‐positive microvascular structures were quantified by automatic morphometric video‐imaging analysis and a significant increase in the number of cerebral microvessels staining positive for EMMPRIN in the ischemic basal ganglia was shown. The significant loss of microvascular basal lamina antigen collagen type IV in ischemic cortex and basal ganglia was calculated by Western blot. Measured by gelatin zymography, we demonstrated an MMP‐2 and MMP‐9 increase in the ischemic brain regions (P < 0.05). For the first time the MMP activation system EMMPRIN was shown to be relevant in cerebral ischemia. These results raise the possibility that the increased expression of EMMPRIN, the increase in MMPs and the damage of the basal lamina following cerebral ischemia are connected and part of a network of related changes.</description><subject>Animals</subject><subject>Antigens, CD - metabolism</subject><subject>basal lamina</subject><subject>Basement Membrane - metabolism</subject><subject>Basement Membrane - pathology</subject><subject>Basigin</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - physiopathology</subject><subject>CD147</subject><subject>Cerebral Infarction - metabolism</subject><subject>Cerebral Infarction - physiopathology</subject><subject>Collagen Type IV - metabolism</subject><subject>Disease Models, Animal</subject><subject>Extracellular Matrix - metabolism</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Matrix Metalloproteinases - metabolism</subject><subject>Microcirculation - metabolism</subject><subject>Microcirculation - pathology</subject><subject>Microcirculation - physiopathology</subject><subject>MMPs</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Up-Regulation - physiology</subject><issn>0953-816X</issn><issn>1460-9568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEtv1DAUhS1ERYfCX0BZsUvwjeNHFixQNbSFzlChKSA2luPcCA95DHZGzfx7HGbUbvHCvrLPd-_xISQBmkFc77YZFIKmJRcqyynlGS1AyWx6RhaPD8_JgpacpQrEj3PyMoQtpVSJgr8g5yBoXuYgF-R-ZUbvpqTD0bTtsPPDiK43ARPX13s7uqFPqkOyXK3uvt6s42WC0w6967CPQNIMNu4WPVY-Fi7YX9g584qcNaYN-Pp0XpD7j8vN5XV6--Xq5vLDbWoLymW0aajKWcmVamQJDLkBai1woFA3OQNWlTXISvCmAQm0tBKhANbUgglWW3ZB3h77Rt9_9hhG3UUL2Lamx2EftFCUc8lYFKqj0PohBI-N3sU_GH_QQPUcqd7qOTk9J6fnSPW_SPUU0TenGfuqw_oJPGUYBe-PggfX4uG_G-vlp_VcRT498i6MOD3yxv_WQjLJ9ff1lf5293m1Wf-kesP-Am2-k94</recordid><startdate>200507</startdate><enddate>200507</enddate><creator>Burggraf, Dorothe</creator><creator>Liebetrau, Martin</creator><creator>Martens, Helge K.</creator><creator>Wunderlich, Nathalie</creator><creator>Jäger, Gabriele</creator><creator>Dichgans, Martin</creator><creator>Hamann, Gerhard F.</creator><general>Blackwell Science Ltd</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>200507</creationdate><title>Matrix metalloproteinase induction by EMMPRIN in experimental focal cerebral ischemia</title><author>Burggraf, Dorothe ; Liebetrau, Martin ; Martens, Helge K. ; Wunderlich, Nathalie ; Jäger, Gabriele ; Dichgans, Martin ; Hamann, Gerhard F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4057-95a08239588f7913e5a10cc15101df2313b9d17b65ff17109c7e1413fd6363dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Antigens, CD - metabolism</topic><topic>basal lamina</topic><topic>Basement Membrane - metabolism</topic><topic>Basement Membrane - pathology</topic><topic>Basigin</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - physiopathology</topic><topic>CD147</topic><topic>Cerebral Infarction - metabolism</topic><topic>Cerebral Infarction - physiopathology</topic><topic>Collagen Type IV - metabolism</topic><topic>Disease Models, Animal</topic><topic>Extracellular Matrix - metabolism</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Matrix Metalloproteinases - metabolism</topic><topic>Microcirculation - metabolism</topic><topic>Microcirculation - pathology</topic><topic>Microcirculation - physiopathology</topic><topic>MMPs</topic><topic>rat</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Up-Regulation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Burggraf, Dorothe</creatorcontrib><creatorcontrib>Liebetrau, Martin</creatorcontrib><creatorcontrib>Martens, Helge K.</creatorcontrib><creatorcontrib>Wunderlich, Nathalie</creatorcontrib><creatorcontrib>Jäger, Gabriele</creatorcontrib><creatorcontrib>Dichgans, Martin</creatorcontrib><creatorcontrib>Hamann, Gerhard F.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The European journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Burggraf, Dorothe</au><au>Liebetrau, Martin</au><au>Martens, Helge K.</au><au>Wunderlich, Nathalie</au><au>Jäger, Gabriele</au><au>Dichgans, Martin</au><au>Hamann, Gerhard F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Matrix metalloproteinase induction by EMMPRIN in experimental focal cerebral ischemia</atitle><jtitle>The European journal of neuroscience</jtitle><addtitle>Eur J Neurosci</addtitle><date>2005-07</date><risdate>2005</risdate><volume>22</volume><issue>1</issue><spage>273</spage><epage>277</epage><pages>273-277</pages><issn>0953-816X</issn><eissn>1460-9568</eissn><abstract>Focal cerebral ischemia leads to the gradual disruption of the extracellular matrix. A key role in the turnover of the extracellular matrix is played by the system of matrix metalloproteinases (MMPs). In this study we describe changes of the MMP inducer protein (EMMPRIN) following experimental cerebral ischemia (induced for 3 h and followed by 24 h reperfusion, suture model) in rats. Extracellular EMMPRIN was measured by Western blot of the ischemic and nonischemic basal ganglia and cortex separately. Compared with the contralateral nonischemic area, the ischemic hemisphere showed a significant increase in EMMPRIN: basal ganglia, 158% ± 4% (P < 0.05); cortex, 128% ± 25% (P < 0.05). Immunohistochemistry was used to localize EMMPRIN on cerebral microvessels. EMMPRIN‐positive microvascular structures were quantified by automatic morphometric video‐imaging analysis and a significant increase in the number of cerebral microvessels staining positive for EMMPRIN in the ischemic basal ganglia was shown. The significant loss of microvascular basal lamina antigen collagen type IV in ischemic cortex and basal ganglia was calculated by Western blot. Measured by gelatin zymography, we demonstrated an MMP‐2 and MMP‐9 increase in the ischemic brain regions (P < 0.05). For the first time the MMP activation system EMMPRIN was shown to be relevant in cerebral ischemia. These results raise the possibility that the increased expression of EMMPRIN, the increase in MMPs and the damage of the basal lamina following cerebral ischemia are connected and part of a network of related changes.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>16029217</pmid><doi>10.1111/j.1460-9568.2005.04187.x</doi><tpages>5</tpages></addata></record> |
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| subjects | Animals Antigens, CD - metabolism basal lamina Basement Membrane - metabolism Basement Membrane - pathology Basigin Brain Ischemia - metabolism Brain Ischemia - physiopathology CD147 Cerebral Infarction - metabolism Cerebral Infarction - physiopathology Collagen Type IV - metabolism Disease Models, Animal Extracellular Matrix - metabolism Immunohistochemistry Male Matrix Metalloproteinase 2 - metabolism Matrix Metalloproteinase 9 - metabolism Matrix Metalloproteinases - metabolism Microcirculation - metabolism Microcirculation - pathology Microcirculation - physiopathology MMPs rat Rats Rats, Wistar Reperfusion Injury - metabolism Reperfusion Injury - physiopathology Up-Regulation - physiology |
| title | Matrix metalloproteinase induction by EMMPRIN in experimental focal cerebral ischemia |
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