Expression of tissue-type transglutaminase (tTG) and the effect of tTG inhibitor on the hippocampal CA1 region after transient ischemia in gerbils
Abstract Chronological changes of tissue-type transglutaminase (tTG) were observed in the hippocampal CA1 region after transient forebrain ischemia in gerbils. In the sham-operated group, tTG immunoreactivity was weakly detected in blood vessels which were immunostained with platelet endothelial cel...
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| Veröffentlicht in: | Brain research 2009-03, Vol.1263, p.134-142 |
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| creator | Hwang, In Koo Yoo, Ki-Yeon Yi, Sun Shin Kim, Il Yong Hwang, Hye Sook Lee, Kyung-Yul Choi, Sun Mi Lee, In Se Yoon, Yeo Sung Kim, Soo Youl Won, Moo Ho Seong, Je Kyung |
| description | Abstract Chronological changes of tissue-type transglutaminase (tTG) were observed in the hippocampal CA1 region after transient forebrain ischemia in gerbils. In the sham-operated group, tTG immunoreactivity was weakly detected in blood vessels which were immunostained with platelet endothelial cell adhesion molecule-1 (PECAM-1), and tTG immunoreactivity in blood vessels was highest 5 days after ischemia/reperfusion. In addition, tTG immunoreaction was expressed in microglia which were immunostained with Iba-1 at 4 days post-ischemia, and tTG immunoreactivity in the microglia was also highest at 5 days post-ischemia. In Western blot analysis, tTG protein levels in the CA1 region after ischemia/reperfusion began to increase 3 days after ischemia/reperfusion and peaked 5 days after ischemia/reperfusion. The expression of tTG in PECAM-1-immunoreactive blood vessels may be associated with integrin regulation or transendothelial migration of leukocytes in the ischemic CA1 region. In this study, we also observed the effect of cystamine, a tTG inhibitor, against ischemic damage. Administration of cystamine protected in certain degree neuronal damage from ischemic damage in the CA1 region. These results suggest that tTG may be associated with neuronal death in the hippocampal CA1 region induced by ischemia/reperfusion. |
| doi_str_mv | 10.1016/j.brainres.2009.01.038 |
| format | Article |
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In the sham-operated group, tTG immunoreactivity was weakly detected in blood vessels which were immunostained with platelet endothelial cell adhesion molecule-1 (PECAM-1), and tTG immunoreactivity in blood vessels was highest 5 days after ischemia/reperfusion. In addition, tTG immunoreaction was expressed in microglia which were immunostained with Iba-1 at 4 days post-ischemia, and tTG immunoreactivity in the microglia was also highest at 5 days post-ischemia. In Western blot analysis, tTG protein levels in the CA1 region after ischemia/reperfusion began to increase 3 days after ischemia/reperfusion and peaked 5 days after ischemia/reperfusion. The expression of tTG in PECAM-1-immunoreactive blood vessels may be associated with integrin regulation or transendothelial migration of leukocytes in the ischemic CA1 region. In this study, we also observed the effect of cystamine, a tTG inhibitor, against ischemic damage. Administration of cystamine protected in certain degree neuronal damage from ischemic damage in the CA1 region. These results suggest that tTG may be associated with neuronal death in the hippocampal CA1 region induced by ischemia/reperfusion.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2009.01.038</identifier><identifier>PMID: 19368835</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Analysis of Variance ; Animals ; Benzoxazines ; Biological and medical sciences ; Blood vessel ; Blood Vessels - enzymology ; Blotting, Western ; Brain Ischemia - drug therapy ; Brain Ischemia - enzymology ; Cystamine ; Cystamine - therapeutic use ; Enzyme Inhibitors - therapeutic use ; Fluorescent Antibody Technique ; Gerbillinae ; GTP-Binding Proteins - antagonists & inhibitors ; GTP-Binding Proteins - metabolism ; Hippocampus - blood supply ; Hippocampus - drug effects ; Hippocampus - enzymology ; Iba-1 ; Immunohistochemistry ; Ischemia ; Male ; Medical sciences ; Microglia ; Microglia - metabolism ; Motor Activity - drug effects ; Neurology ; Neurons - drug effects ; Neurons - physiology ; Neuroprotective Agents - therapeutic use ; Oxazines ; PECAM-1 ; Platelet Endothelial Cell Adhesion Molecule-1 - metabolism ; Reperfusion Injury - drug therapy ; Reperfusion Injury - physiopathology ; Transglutaminase 2 ; Transglutaminases - antagonists & inhibitors ; Transglutaminases - metabolism ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Brain research, 2009-03, Vol.1263, p.134-142</ispartof><rights>Elsevier B.V.</rights><rights>2008 Elsevier B.V.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c548t-51918e6f33859742c76d248008bf741405ebd98c8086b54cbb914e348dc6fbbf3</citedby><cites>FETCH-LOGICAL-c548t-51918e6f33859742c76d248008bf741405ebd98c8086b54cbb914e348dc6fbbf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainres.2009.01.038$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21336250$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19368835$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hwang, In Koo</creatorcontrib><creatorcontrib>Yoo, Ki-Yeon</creatorcontrib><creatorcontrib>Yi, Sun Shin</creatorcontrib><creatorcontrib>Kim, Il Yong</creatorcontrib><creatorcontrib>Hwang, Hye Sook</creatorcontrib><creatorcontrib>Lee, Kyung-Yul</creatorcontrib><creatorcontrib>Choi, Sun Mi</creatorcontrib><creatorcontrib>Lee, In Se</creatorcontrib><creatorcontrib>Yoon, Yeo Sung</creatorcontrib><creatorcontrib>Kim, Soo Youl</creatorcontrib><creatorcontrib>Won, Moo Ho</creatorcontrib><creatorcontrib>Seong, Je Kyung</creatorcontrib><title>Expression of tissue-type transglutaminase (tTG) and the effect of tTG inhibitor on the hippocampal CA1 region after transient ischemia in gerbils</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract Chronological changes of tissue-type transglutaminase (tTG) were observed in the hippocampal CA1 region after transient forebrain ischemia in gerbils. In the sham-operated group, tTG immunoreactivity was weakly detected in blood vessels which were immunostained with platelet endothelial cell adhesion molecule-1 (PECAM-1), and tTG immunoreactivity in blood vessels was highest 5 days after ischemia/reperfusion. In addition, tTG immunoreaction was expressed in microglia which were immunostained with Iba-1 at 4 days post-ischemia, and tTG immunoreactivity in the microglia was also highest at 5 days post-ischemia. In Western blot analysis, tTG protein levels in the CA1 region after ischemia/reperfusion began to increase 3 days after ischemia/reperfusion and peaked 5 days after ischemia/reperfusion. The expression of tTG in PECAM-1-immunoreactive blood vessels may be associated with integrin regulation or transendothelial migration of leukocytes in the ischemic CA1 region. In this study, we also observed the effect of cystamine, a tTG inhibitor, against ischemic damage. Administration of cystamine protected in certain degree neuronal damage from ischemic damage in the CA1 region. These results suggest that tTG may be associated with neuronal death in the hippocampal CA1 region induced by ischemia/reperfusion.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Benzoxazines</subject><subject>Biological and medical sciences</subject><subject>Blood vessel</subject><subject>Blood Vessels - enzymology</subject><subject>Blotting, Western</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - enzymology</subject><subject>Cystamine</subject><subject>Cystamine - therapeutic use</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Fluorescent Antibody Technique</subject><subject>Gerbillinae</subject><subject>GTP-Binding Proteins - antagonists & inhibitors</subject><subject>GTP-Binding Proteins - metabolism</subject><subject>Hippocampus - blood supply</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - enzymology</subject><subject>Iba-1</subject><subject>Immunohistochemistry</subject><subject>Ischemia</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microglia</subject><subject>Microglia - metabolism</subject><subject>Motor Activity - drug effects</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Oxazines</subject><subject>PECAM-1</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Transglutaminase 2</subject><subject>Transglutaminases - antagonists & inhibitors</subject><subject>Transglutaminases - metabolism</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks-O0zAQxiMEYpeFV1j5AoJDyjh2EueCdlUtBWklDpSzZTvj1iX_sB1EX4MnxqEFJC4rHyzLv_m-0XyTZdcUVhRo9faw0l65wWNYFQDNCugKmHiUXVJRF3lVcHicXQJAlYumYRfZsxAO6clYA0-zC9qwSghWXmY_735MSSS4cSCjJdGFMGMejxOS6NUQdt0cVe8GFZC8jtvNG6KGlsQ9ErQWTfxdtN0QN-yddnH0JAkt33s3TaNR_aQ6sr6lxONu8VA2oj9JOxwiccHssXcqCZAdeu268Dx7YlUX8MX5vsq-vL_brj_k9582H9e397kpuYh5SRsqsLKMibKpeWHqqi24ABDa1pxyKFG3jTACRKVLbrRuKEfGRWsqq7VlV9mrk-7kx28zhij71A12nRpwnIOs6iTCS_4gWABn6dAEVifQ-DEEj1ZO3vXKHyUFucQmD_JPbHKJTQKVKbZUeH12mHWP7b-yc04JeHkGVDCqs2l-xoW_XEEZq4oSEndz4jAN7rtDL4NJczbYOp_Sku3oHu7l3X8SpnODS65f8YjhMM5-SLFIKkMhQX5elmzZMWgAaJ16_QUqq890</recordid><startdate>20090331</startdate><enddate>20090331</enddate><creator>Hwang, In Koo</creator><creator>Yoo, Ki-Yeon</creator><creator>Yi, Sun Shin</creator><creator>Kim, Il Yong</creator><creator>Hwang, Hye Sook</creator><creator>Lee, Kyung-Yul</creator><creator>Choi, Sun Mi</creator><creator>Lee, In Se</creator><creator>Yoon, Yeo Sung</creator><creator>Kim, Soo Youl</creator><creator>Won, Moo Ho</creator><creator>Seong, Je Kyung</creator><general>Elsevier B.V</general><general>Elsevier</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>20090331</creationdate><title>Expression of tissue-type transglutaminase (tTG) and the effect of tTG inhibitor on the hippocampal CA1 region after transient ischemia in gerbils</title><author>Hwang, In Koo ; Yoo, Ki-Yeon ; Yi, Sun Shin ; Kim, Il Yong ; Hwang, Hye Sook ; Lee, Kyung-Yul ; Choi, Sun Mi ; Lee, In Se ; Yoon, Yeo Sung ; Kim, Soo Youl ; Won, Moo Ho ; Seong, Je Kyung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c548t-51918e6f33859742c76d248008bf741405ebd98c8086b54cbb914e348dc6fbbf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Benzoxazines</topic><topic>Biological and medical sciences</topic><topic>Blood vessel</topic><topic>Blood Vessels - enzymology</topic><topic>Blotting, Western</topic><topic>Brain Ischemia - drug therapy</topic><topic>Brain Ischemia - enzymology</topic><topic>Cystamine</topic><topic>Cystamine - therapeutic use</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Fluorescent Antibody Technique</topic><topic>Gerbillinae</topic><topic>GTP-Binding Proteins - antagonists & inhibitors</topic><topic>GTP-Binding Proteins - metabolism</topic><topic>Hippocampus - blood supply</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - enzymology</topic><topic>Iba-1</topic><topic>Immunohistochemistry</topic><topic>Ischemia</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microglia</topic><topic>Microglia - metabolism</topic><topic>Motor Activity - drug effects</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Oxazines</topic><topic>PECAM-1</topic><topic>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Transglutaminase 2</topic><topic>Transglutaminases - antagonists & inhibitors</topic><topic>Transglutaminases - metabolism</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hwang, In Koo</creatorcontrib><creatorcontrib>Yoo, Ki-Yeon</creatorcontrib><creatorcontrib>Yi, Sun Shin</creatorcontrib><creatorcontrib>Kim, Il Yong</creatorcontrib><creatorcontrib>Hwang, Hye Sook</creatorcontrib><creatorcontrib>Lee, Kyung-Yul</creatorcontrib><creatorcontrib>Choi, Sun Mi</creatorcontrib><creatorcontrib>Lee, In Se</creatorcontrib><creatorcontrib>Yoon, Yeo Sung</creatorcontrib><creatorcontrib>Kim, Soo Youl</creatorcontrib><creatorcontrib>Won, Moo Ho</creatorcontrib><creatorcontrib>Seong, Je Kyung</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>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hwang, In Koo</au><au>Yoo, Ki-Yeon</au><au>Yi, Sun Shin</au><au>Kim, Il Yong</au><au>Hwang, Hye Sook</au><au>Lee, Kyung-Yul</au><au>Choi, Sun Mi</au><au>Lee, In Se</au><au>Yoon, Yeo Sung</au><au>Kim, Soo Youl</au><au>Won, Moo Ho</au><au>Seong, Je Kyung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of tissue-type transglutaminase (tTG) and the effect of tTG inhibitor on the hippocampal CA1 region after transient ischemia in gerbils</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2009-03-31</date><risdate>2009</risdate><volume>1263</volume><spage>134</spage><epage>142</epage><pages>134-142</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Abstract Chronological changes of tissue-type transglutaminase (tTG) were observed in the hippocampal CA1 region after transient forebrain ischemia in gerbils. In the sham-operated group, tTG immunoreactivity was weakly detected in blood vessels which were immunostained with platelet endothelial cell adhesion molecule-1 (PECAM-1), and tTG immunoreactivity in blood vessels was highest 5 days after ischemia/reperfusion. In addition, tTG immunoreaction was expressed in microglia which were immunostained with Iba-1 at 4 days post-ischemia, and tTG immunoreactivity in the microglia was also highest at 5 days post-ischemia. In Western blot analysis, tTG protein levels in the CA1 region after ischemia/reperfusion began to increase 3 days after ischemia/reperfusion and peaked 5 days after ischemia/reperfusion. The expression of tTG in PECAM-1-immunoreactive blood vessels may be associated with integrin regulation or transendothelial migration of leukocytes in the ischemic CA1 region. In this study, we also observed the effect of cystamine, a tTG inhibitor, against ischemic damage. Administration of cystamine protected in certain degree neuronal damage from ischemic damage in the CA1 region. These results suggest that tTG may be associated with neuronal death in the hippocampal CA1 region induced by ischemia/reperfusion.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>19368835</pmid><doi>10.1016/j.brainres.2009.01.038</doi><tpages>9</tpages></addata></record> |
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| subjects | Analysis of Variance Animals Benzoxazines Biological and medical sciences Blood vessel Blood Vessels - enzymology Blotting, Western Brain Ischemia - drug therapy Brain Ischemia - enzymology Cystamine Cystamine - therapeutic use Enzyme Inhibitors - therapeutic use Fluorescent Antibody Technique Gerbillinae GTP-Binding Proteins - antagonists & inhibitors GTP-Binding Proteins - metabolism Hippocampus - blood supply Hippocampus - drug effects Hippocampus - enzymology Iba-1 Immunohistochemistry Ischemia Male Medical sciences Microglia Microglia - metabolism Motor Activity - drug effects Neurology Neurons - drug effects Neurons - physiology Neuroprotective Agents - therapeutic use Oxazines PECAM-1 Platelet Endothelial Cell Adhesion Molecule-1 - metabolism Reperfusion Injury - drug therapy Reperfusion Injury - physiopathology Transglutaminase 2 Transglutaminases - antagonists & inhibitors Transglutaminases - metabolism Vascular diseases and vascular malformations of the nervous system |
| title | Expression of tissue-type transglutaminase (tTG) and the effect of tTG inhibitor on the hippocampal CA1 region after transient ischemia in gerbils |
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