Hepatocyte growth factor attenuates cerebral ischemia-induced increase in permeability of the blood–brain barrier and decreases in expression of tight junctional proteins in cerebral vessels
Hepatocyte growth factor (HGF) exerts its physiological activities as that of an organotropic factor for regeneration and can prevent ischemia-induced injuries; however, its effect and mechanism of action under in vivo pathophysiological conditions remains to be determined. Recently, we demonstrated...
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| Veröffentlicht in: | Neuroscience letters 2006-10, Vol.407 (2), p.141-145 |
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| creator | Date, Ichiro Takagi, Norio Takagi, Keiko Tanonaka, Kouichi Funakoshi, Hiroshi Matsumoto, Kunio Nakamura, Toshikazu Takeo, Satoshi |
| description | Hepatocyte growth factor (HGF) exerts its physiological activities as that of an organotropic factor for regeneration and can prevent ischemia-induced injuries; however, its effect and mechanism of action under
in vivo pathophysiological conditions remains to be determined. Recently, we demonstrated that treatment with human recombinant HGF (hrHGF) attenuated the disruption of the blood–brain barrier (BBB) observed after microsphere embolism-induced sustained cerebral ischemia. To see if tight junctional proteins were involved in this attenuation, in the present study, we investigated the effects of HGF on the levels of occludin and zonula occludens (ZO)-1 in cerebrovascular endothelial cells after microsphere embolism. Sustained cerebral ischemia was induced by the injection of 700 microspheres (48
μm diameter) into the right internal carotid artery of rats. hrHGF was injected into the right ventricle of the brain by using an osmotic pump at a dose of 30
μg/7 days per animal. The levels of tight junctional proteins in the endothelial cells were examined by immunohistochemical analysis. Treatment with hrHGF attenuated the decrease in the expression of occludin and ZO-1 proteins in the endothelial cells that occurred after sustained cerebral ischemia. Furthermore, treatment with hrHGF resulted in retention of these tight junctional proteins in fluorescein isothiocyanate (FITC)-albumin-perfused cerebral vessels, which did not leak FITC–albumin in the ipsilateral cortex. These results suggest that HGF-mediated maintenance of the tight junctional proteins in the endothelial cells may be a possible mechanism for the protective effect of HGF against the disruption of the BBB after cerebral ischemia. |
| doi_str_mv | 10.1016/j.neulet.2006.08.050 |
| format | Article |
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in vivo pathophysiological conditions remains to be determined. Recently, we demonstrated that treatment with human recombinant HGF (hrHGF) attenuated the disruption of the blood–brain barrier (BBB) observed after microsphere embolism-induced sustained cerebral ischemia. To see if tight junctional proteins were involved in this attenuation, in the present study, we investigated the effects of HGF on the levels of occludin and zonula occludens (ZO)-1 in cerebrovascular endothelial cells after microsphere embolism. Sustained cerebral ischemia was induced by the injection of 700 microspheres (48
μm diameter) into the right internal carotid artery of rats. hrHGF was injected into the right ventricle of the brain by using an osmotic pump at a dose of 30
μg/7 days per animal. The levels of tight junctional proteins in the endothelial cells were examined by immunohistochemical analysis. Treatment with hrHGF attenuated the decrease in the expression of occludin and ZO-1 proteins in the endothelial cells that occurred after sustained cerebral ischemia. Furthermore, treatment with hrHGF resulted in retention of these tight junctional proteins in fluorescein isothiocyanate (FITC)-albumin-perfused cerebral vessels, which did not leak FITC–albumin in the ipsilateral cortex. These results suggest that HGF-mediated maintenance of the tight junctional proteins in the endothelial cells may be a possible mechanism for the protective effect of HGF against the disruption of the BBB after cerebral ischemia.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2006.08.050</identifier><identifier>PMID: 16973272</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Biological and medical sciences ; Blood Vessels - drug effects ; Blood-Brain Barrier - drug effects ; Blood–brain barrier ; Brain Ischemia - drug therapy ; Brain Ischemia - physiopathology ; Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges ; Cerebral ischemia ; Cerebrovascular Circulation - drug effects ; CHO Cells ; Cricetinae ; Fluorescein-5-isothiocyanate ; Fluorescent Dyes ; Fundamental and applied biological sciences. Psychology ; Hepatocyte growth factor ; Hepatocyte Growth Factor - pharmacology ; Immunohistochemistry ; Intracranial Embolism - pathology ; Male ; Medical sciences ; Microsphere embolism ; Microspheres ; Nerve Tissue Proteins - biosynthesis ; Neurology ; Occludin ; Osmosis ; Permeability ; Rats ; Rats, Wistar ; Recombinant Proteins - pharmacology ; Tight junctions ; Tight Junctions - drug effects ; Tight Junctions - metabolism ; Vascular diseases and vascular malformations of the nervous system ; Vertebrates: nervous system and sense organs ; ZO-1</subject><ispartof>Neuroscience letters, 2006-10, Vol.407 (2), p.141-145</ispartof><rights>2006 Elsevier Ireland Ltd</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-7debd9a702cc659200cacdbd7ec9d2453179a52be01ff2cd3ce9267c16ab29173</citedby><cites>FETCH-LOGICAL-c456t-7debd9a702cc659200cacdbd7ec9d2453179a52be01ff2cd3ce9267c16ab29173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neulet.2006.08.050$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18207273$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16973272$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Date, Ichiro</creatorcontrib><creatorcontrib>Takagi, Norio</creatorcontrib><creatorcontrib>Takagi, Keiko</creatorcontrib><creatorcontrib>Tanonaka, Kouichi</creatorcontrib><creatorcontrib>Funakoshi, Hiroshi</creatorcontrib><creatorcontrib>Matsumoto, Kunio</creatorcontrib><creatorcontrib>Nakamura, Toshikazu</creatorcontrib><creatorcontrib>Takeo, Satoshi</creatorcontrib><title>Hepatocyte growth factor attenuates cerebral ischemia-induced increase in permeability of the blood–brain barrier and decreases in expression of tight junctional proteins in cerebral vessels</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Hepatocyte growth factor (HGF) exerts its physiological activities as that of an organotropic factor for regeneration and can prevent ischemia-induced injuries; however, its effect and mechanism of action under
in vivo pathophysiological conditions remains to be determined. Recently, we demonstrated that treatment with human recombinant HGF (hrHGF) attenuated the disruption of the blood–brain barrier (BBB) observed after microsphere embolism-induced sustained cerebral ischemia. To see if tight junctional proteins were involved in this attenuation, in the present study, we investigated the effects of HGF on the levels of occludin and zonula occludens (ZO)-1 in cerebrovascular endothelial cells after microsphere embolism. Sustained cerebral ischemia was induced by the injection of 700 microspheres (48
μm diameter) into the right internal carotid artery of rats. hrHGF was injected into the right ventricle of the brain by using an osmotic pump at a dose of 30
μg/7 days per animal. The levels of tight junctional proteins in the endothelial cells were examined by immunohistochemical analysis. Treatment with hrHGF attenuated the decrease in the expression of occludin and ZO-1 proteins in the endothelial cells that occurred after sustained cerebral ischemia. Furthermore, treatment with hrHGF resulted in retention of these tight junctional proteins in fluorescein isothiocyanate (FITC)-albumin-perfused cerebral vessels, which did not leak FITC–albumin in the ipsilateral cortex. These results suggest that HGF-mediated maintenance of the tight junctional proteins in the endothelial cells may be a possible mechanism for the protective effect of HGF against the disruption of the BBB after cerebral ischemia.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Vessels - drug effects</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Blood–brain barrier</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - physiopathology</subject><subject>Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</subject><subject>Cerebral ischemia</subject><subject>Cerebrovascular Circulation - drug effects</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>Fluorescein-5-isothiocyanate</subject><subject>Fluorescent Dyes</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hepatocyte growth factor</subject><subject>Hepatocyte Growth Factor - pharmacology</subject><subject>Immunohistochemistry</subject><subject>Intracranial Embolism - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microsphere embolism</subject><subject>Microspheres</subject><subject>Nerve Tissue Proteins - biosynthesis</subject><subject>Neurology</subject><subject>Occludin</subject><subject>Osmosis</subject><subject>Permeability</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Tight junctions</subject><subject>Tight Junctions - drug effects</subject><subject>Tight Junctions - metabolism</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>ZO-1</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1DAURiMEokPhDRDyBnYJtvPjeIOEKqBIldjA2nKubzoeJfZgOy2z4x36Qn0WngRPM6I7Vrasc66vvq8oXjNaMcq697vK4TJhqjilXUX7irb0SbFhveClkII_LTa0pk1Zy4aeFS9i3FFKW9Y2z4sz1klRc8E3xf0l7nXycEhIroO_TVsyakg-EJ0SukUnjAQw4BD0RGyELc5Wl9aZBdAQ6yCgjpgvZI9hRj3YyaYD8SNJWyTD5L358_su25kYdAgW82hniMHVjEcVf-0Dxmi9exDt9TaR3eIg5Zf87T74hNY9oP92uckCTvFl8WzUU8RXp_O8-PH50_eLy_Lq25evFx-vSmjaLpXC4GCkFpQDdK3MmYEGMxiBIA1v2poJqVs-IGXjyMHUgJJ3AlinBy6ZqM-Ld-vcvMzPBWNSc04Dp0k79EtUXd9LWguZwWYFIfgYA45qH-ysw0Exqo7NqZ1am1PH5hTtVW4ua29O85dhRvMonarKwNsToCPoaQzagY2PXM-p4KLO3IeVy-HgTY5bRbDocls2ICRlvP3_Jn8BEjXAwg</recordid><startdate>20061023</startdate><enddate>20061023</enddate><creator>Date, Ichiro</creator><creator>Takagi, Norio</creator><creator>Takagi, Keiko</creator><creator>Tanonaka, Kouichi</creator><creator>Funakoshi, Hiroshi</creator><creator>Matsumoto, Kunio</creator><creator>Nakamura, Toshikazu</creator><creator>Takeo, Satoshi</creator><general>Elsevier Ireland Ltd</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>7X8</scope></search><sort><creationdate>20061023</creationdate><title>Hepatocyte growth factor attenuates cerebral ischemia-induced increase in permeability of the blood–brain barrier and decreases in expression of tight junctional proteins in cerebral vessels</title><author>Date, Ichiro ; Takagi, Norio ; Takagi, Keiko ; Tanonaka, Kouichi ; Funakoshi, Hiroshi ; Matsumoto, Kunio ; Nakamura, Toshikazu ; Takeo, Satoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-7debd9a702cc659200cacdbd7ec9d2453179a52be01ff2cd3ce9267c16ab29173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Vessels - drug effects</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Blood–brain barrier</topic><topic>Brain Ischemia - drug therapy</topic><topic>Brain Ischemia - physiopathology</topic><topic>Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges</topic><topic>Cerebral ischemia</topic><topic>Cerebrovascular Circulation - drug effects</topic><topic>CHO Cells</topic><topic>Cricetinae</topic><topic>Fluorescein-5-isothiocyanate</topic><topic>Fluorescent Dyes</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hepatocyte growth factor</topic><topic>Hepatocyte Growth Factor - pharmacology</topic><topic>Immunohistochemistry</topic><topic>Intracranial Embolism - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microsphere embolism</topic><topic>Microspheres</topic><topic>Nerve Tissue Proteins - biosynthesis</topic><topic>Neurology</topic><topic>Occludin</topic><topic>Osmosis</topic><topic>Permeability</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Tight junctions</topic><topic>Tight Junctions - drug effects</topic><topic>Tight Junctions - metabolism</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>ZO-1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Date, Ichiro</creatorcontrib><creatorcontrib>Takagi, Norio</creatorcontrib><creatorcontrib>Takagi, Keiko</creatorcontrib><creatorcontrib>Tanonaka, Kouichi</creatorcontrib><creatorcontrib>Funakoshi, Hiroshi</creatorcontrib><creatorcontrib>Matsumoto, Kunio</creatorcontrib><creatorcontrib>Nakamura, Toshikazu</creatorcontrib><creatorcontrib>Takeo, Satoshi</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>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Date, Ichiro</au><au>Takagi, Norio</au><au>Takagi, Keiko</au><au>Tanonaka, Kouichi</au><au>Funakoshi, Hiroshi</au><au>Matsumoto, Kunio</au><au>Nakamura, Toshikazu</au><au>Takeo, Satoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatocyte growth factor attenuates cerebral ischemia-induced increase in permeability of the blood–brain barrier and decreases in expression of tight junctional proteins in cerebral vessels</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2006-10-23</date><risdate>2006</risdate><volume>407</volume><issue>2</issue><spage>141</spage><epage>145</epage><pages>141-145</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>Hepatocyte growth factor (HGF) exerts its physiological activities as that of an organotropic factor for regeneration and can prevent ischemia-induced injuries; however, its effect and mechanism of action under
in vivo pathophysiological conditions remains to be determined. Recently, we demonstrated that treatment with human recombinant HGF (hrHGF) attenuated the disruption of the blood–brain barrier (BBB) observed after microsphere embolism-induced sustained cerebral ischemia. To see if tight junctional proteins were involved in this attenuation, in the present study, we investigated the effects of HGF on the levels of occludin and zonula occludens (ZO)-1 in cerebrovascular endothelial cells after microsphere embolism. Sustained cerebral ischemia was induced by the injection of 700 microspheres (48
μm diameter) into the right internal carotid artery of rats. hrHGF was injected into the right ventricle of the brain by using an osmotic pump at a dose of 30
μg/7 days per animal. The levels of tight junctional proteins in the endothelial cells were examined by immunohistochemical analysis. Treatment with hrHGF attenuated the decrease in the expression of occludin and ZO-1 proteins in the endothelial cells that occurred after sustained cerebral ischemia. Furthermore, treatment with hrHGF resulted in retention of these tight junctional proteins in fluorescein isothiocyanate (FITC)-albumin-perfused cerebral vessels, which did not leak FITC–albumin in the ipsilateral cortex. These results suggest that HGF-mediated maintenance of the tight junctional proteins in the endothelial cells may be a possible mechanism for the protective effect of HGF against the disruption of the BBB after cerebral ischemia.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>16973272</pmid><doi>10.1016/j.neulet.2006.08.050</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3940 |
| ispartof | Neuroscience letters, 2006-10, Vol.407 (2), p.141-145 |
| issn | 0304-3940 1872-7972 |
| language | eng |
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| subjects | Animals Biological and medical sciences Blood Vessels - drug effects Blood-Brain Barrier - drug effects Blood–brain barrier Brain Ischemia - drug therapy Brain Ischemia - physiopathology Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges Cerebral ischemia Cerebrovascular Circulation - drug effects CHO Cells Cricetinae Fluorescein-5-isothiocyanate Fluorescent Dyes Fundamental and applied biological sciences. Psychology Hepatocyte growth factor Hepatocyte Growth Factor - pharmacology Immunohistochemistry Intracranial Embolism - pathology Male Medical sciences Microsphere embolism Microspheres Nerve Tissue Proteins - biosynthesis Neurology Occludin Osmosis Permeability Rats Rats, Wistar Recombinant Proteins - pharmacology Tight junctions Tight Junctions - drug effects Tight Junctions - metabolism Vascular diseases and vascular malformations of the nervous system Vertebrates: nervous system and sense organs ZO-1 |
| title | Hepatocyte growth factor attenuates cerebral ischemia-induced increase in permeability of the blood–brain barrier and decreases in expression of tight junctional proteins in cerebral vessels |
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