Poly (I:C) therapy decreases cerebral ischaemia/reperfusion injury via TLR 3‐mediated prevention of Fas/ FADD interaction
Toll‐like receptor ( TLR )‐mediated signalling plays a role in cerebral ischaemia/reperfusion (I/R) injury. Modulation of TLR s has been reported to protect against cerebral I/R injury. This study examined whether modulation of TLR 3 with poly (I:C) will induce protection against cerebral I/R injury...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2015-03, Vol.19 (3), p.555-565 |
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| creator | Zhang, Xia Ha, Tuanzhu Lu, Chen Lam, Fred Liu, Li Schweitzer, John Kalbfleisch, John Kao, Race L. Williams, David L. Li, Chuanfu |
| description | Toll‐like receptor (
TLR
)‐mediated signalling plays a role in cerebral ischaemia/reperfusion (I/R) injury. Modulation of
TLR
s has been reported to protect against cerebral I/R injury. This study examined whether modulation of
TLR
3 with poly (I:C) will induce protection against cerebral I/R injury. Mice were treated with or without Poly (I:C) (
n
= 8/group) 1 hr prior to cerebral ischaemia (60 min.) followed by reperfusion (24 hrs). Poly (I:C) pre‐treatment significantly reduced the infarct volume by 57.2% compared with untreated I/R mice. Therapeutic administration of Poly (I:C), administered 30 min. after cerebral ischaemia, markedly decreased infarct volume by 34.9%. However, Poly (I:C)‐induced protection was lost in
TLR
3 knockout mice. In poly (I:C)‐treated mice, there was less neuronal damage in the hippocampus compared with untreated I/R mice. Poly (I:C) treatment induced
IRF
3 phosphorylation, but it inhibited
NF
‐κB activation in the brain. Poly (I:C) also decreased I/R‐induced apoptosis by attenuation of Fas/FasL‐mediated apoptotic signalling. In addition, Poly (I:C) treatment decreased microglial cell caspase‐3 activity.
In vitro
data showed that Poly (I:C) prevented hypoxia/reoxygenation (H/R)‐induced interaction between Fas and
FADD
as well as caspase‐3 and ‐8 activation in microglial cells. Importantly, Poly (I:C) treatment induced co‐association between
TLR
3 and Fas. Our data suggest that Poly (I:C) decreases in cerebral I/R injury
via
TLR
3 which associates with Fas, thereby preventing the interaction of Fas and
FADD
, as well as microglial cell caspase‐3 and ‐8 activities. We conclude that
TLR
3 modulation by Poly (I:C) could be a potential approach for protection against ischaemic stroke. |
| doi_str_mv | 10.1111/jcmm.12456 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2290479104</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2290479104</sourcerecordid><originalsourceid>FETCH-LOGICAL-c1044-993567fe82e68b2b16d4e7392e50738b882d95475df7f0cd6a4adb3c042a5c7d3</originalsourceid><addsrcrecordid>eNotkM9Kw0AQhxdRsFYvPsGCFxXS7r8ku96ktVooKFLPYbM7oQlNE3eTQvDiI_iMPomJ7VxmYL6ZH3wIXVMyoX1NC1OWE8pEGJ2gEQ0lC4Ti4vQ4U8nlObrwviCER5SrEfp6q7Ydvl0-zO5wswGn6w5bMA60B48NOEid3uLcm42GMtdTBzW4rPV5tcP5rmhdh_e5xuvVO-a_3z8l2Fw3YHHtYA-7ZsCqDC-0n-LF43ze3zR9ihkWl-gs01sPV8c-Rh-Lp_XsJVi9Pi9nj6vAUCJEoBQPozgDySCSKUtpZAXEXDEIScxlKiWzKhRxaLM4I8ZGWmibckME06GJLR-jm8Pf2lWfLfgmKarW7frIhDFFRKz6nJ66P1DGVd47yJLa5aV2XUJJMshNBrnJv1z-B6Bqbb4</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2290479104</pqid></control><display><type>article</type><title>Poly (I:C) therapy decreases cerebral ischaemia/reperfusion injury via TLR 3‐mediated prevention of Fas/ FADD interaction</title><source>Wiley Online Library Open Access</source><source>DOAJ Directory of Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Zhang, Xia ; Ha, Tuanzhu ; Lu, Chen ; Lam, Fred ; Liu, Li ; Schweitzer, John ; Kalbfleisch, John ; Kao, Race L. ; Williams, David L. ; Li, Chuanfu</creator><creatorcontrib>Zhang, Xia ; Ha, Tuanzhu ; Lu, Chen ; Lam, Fred ; Liu, Li ; Schweitzer, John ; Kalbfleisch, John ; Kao, Race L. ; Williams, David L. ; Li, Chuanfu</creatorcontrib><description>Toll‐like receptor (
TLR
)‐mediated signalling plays a role in cerebral ischaemia/reperfusion (I/R) injury. Modulation of
TLR
s has been reported to protect against cerebral I/R injury. This study examined whether modulation of
TLR
3 with poly (I:C) will induce protection against cerebral I/R injury. Mice were treated with or without Poly (I:C) (
n
= 8/group) 1 hr prior to cerebral ischaemia (60 min.) followed by reperfusion (24 hrs). Poly (I:C) pre‐treatment significantly reduced the infarct volume by 57.2% compared with untreated I/R mice. Therapeutic administration of Poly (I:C), administered 30 min. after cerebral ischaemia, markedly decreased infarct volume by 34.9%. However, Poly (I:C)‐induced protection was lost in
TLR
3 knockout mice. In poly (I:C)‐treated mice, there was less neuronal damage in the hippocampus compared with untreated I/R mice. Poly (I:C) treatment induced
IRF
3 phosphorylation, but it inhibited
NF
‐κB activation in the brain. Poly (I:C) also decreased I/R‐induced apoptosis by attenuation of Fas/FasL‐mediated apoptotic signalling. In addition, Poly (I:C) treatment decreased microglial cell caspase‐3 activity.
In vitro
data showed that Poly (I:C) prevented hypoxia/reoxygenation (H/R)‐induced interaction between Fas and
FADD
as well as caspase‐3 and ‐8 activation in microglial cells. Importantly, Poly (I:C) treatment induced co‐association between
TLR
3 and Fas. Our data suggest that Poly (I:C) decreases in cerebral I/R injury
via
TLR
3 which associates with Fas, thereby preventing the interaction of Fas and
FADD
, as well as microglial cell caspase‐3 and ‐8 activities. We conclude that
TLR
3 modulation by Poly (I:C) could be a potential approach for protection against ischaemic stroke.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.12456</identifier><language>eng</language><publisher>Chichester: John Wiley & Sons, Inc</publisher><subject>Apoptosis ; Carotid arteries ; Caspase ; Cell activation ; FADD protein ; FasL protein ; Gene expression ; Hypoxia ; Interferon regulatory factor 3 ; Ischemia ; Laboratory animals ; Mice ; Microglial cells ; Phosphorylation ; Polyinosinic:polycytidylic acid ; Reperfusion ; Stroke ; TLR3 protein ; Toll-like receptors ; Veins & arteries</subject><ispartof>Journal of cellular and molecular medicine, 2015-03, Vol.19 (3), p.555-565</ispartof><rights>2015. This work is published under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1044-993567fe82e68b2b16d4e7392e50738b882d95475df7f0cd6a4adb3c042a5c7d3</citedby><cites>FETCH-LOGICAL-c1044-993567fe82e68b2b16d4e7392e50738b882d95475df7f0cd6a4adb3c042a5c7d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27901,27902</link.rule.ids></links><search><creatorcontrib>Zhang, Xia</creatorcontrib><creatorcontrib>Ha, Tuanzhu</creatorcontrib><creatorcontrib>Lu, Chen</creatorcontrib><creatorcontrib>Lam, Fred</creatorcontrib><creatorcontrib>Liu, Li</creatorcontrib><creatorcontrib>Schweitzer, John</creatorcontrib><creatorcontrib>Kalbfleisch, John</creatorcontrib><creatorcontrib>Kao, Race L.</creatorcontrib><creatorcontrib>Williams, David L.</creatorcontrib><creatorcontrib>Li, Chuanfu</creatorcontrib><title>Poly (I:C) therapy decreases cerebral ischaemia/reperfusion injury via TLR 3‐mediated prevention of Fas/ FADD interaction</title><title>Journal of cellular and molecular medicine</title><description>Toll‐like receptor (
TLR
)‐mediated signalling plays a role in cerebral ischaemia/reperfusion (I/R) injury. Modulation of
TLR
s has been reported to protect against cerebral I/R injury. This study examined whether modulation of
TLR
3 with poly (I:C) will induce protection against cerebral I/R injury. Mice were treated with or without Poly (I:C) (
n
= 8/group) 1 hr prior to cerebral ischaemia (60 min.) followed by reperfusion (24 hrs). Poly (I:C) pre‐treatment significantly reduced the infarct volume by 57.2% compared with untreated I/R mice. Therapeutic administration of Poly (I:C), administered 30 min. after cerebral ischaemia, markedly decreased infarct volume by 34.9%. However, Poly (I:C)‐induced protection was lost in
TLR
3 knockout mice. In poly (I:C)‐treated mice, there was less neuronal damage in the hippocampus compared with untreated I/R mice. Poly (I:C) treatment induced
IRF
3 phosphorylation, but it inhibited
NF
‐κB activation in the brain. Poly (I:C) also decreased I/R‐induced apoptosis by attenuation of Fas/FasL‐mediated apoptotic signalling. In addition, Poly (I:C) treatment decreased microglial cell caspase‐3 activity.
In vitro
data showed that Poly (I:C) prevented hypoxia/reoxygenation (H/R)‐induced interaction between Fas and
FADD
as well as caspase‐3 and ‐8 activation in microglial cells. Importantly, Poly (I:C) treatment induced co‐association between
TLR
3 and Fas. Our data suggest that Poly (I:C) decreases in cerebral I/R injury
via
TLR
3 which associates with Fas, thereby preventing the interaction of Fas and
FADD
, as well as microglial cell caspase‐3 and ‐8 activities. We conclude that
TLR
3 modulation by Poly (I:C) could be a potential approach for protection against ischaemic stroke.</description><subject>Apoptosis</subject><subject>Carotid arteries</subject><subject>Caspase</subject><subject>Cell activation</subject><subject>FADD protein</subject><subject>FasL protein</subject><subject>Gene expression</subject><subject>Hypoxia</subject><subject>Interferon regulatory factor 3</subject><subject>Ischemia</subject><subject>Laboratory animals</subject><subject>Mice</subject><subject>Microglial cells</subject><subject>Phosphorylation</subject><subject>Polyinosinic:polycytidylic acid</subject><subject>Reperfusion</subject><subject>Stroke</subject><subject>TLR3 protein</subject><subject>Toll-like receptors</subject><subject>Veins & arteries</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNotkM9Kw0AQhxdRsFYvPsGCFxXS7r8ku96ktVooKFLPYbM7oQlNE3eTQvDiI_iMPomJ7VxmYL6ZH3wIXVMyoX1NC1OWE8pEGJ2gEQ0lC4Ti4vQ4U8nlObrwviCER5SrEfp6q7Ydvl0-zO5wswGn6w5bMA60B48NOEid3uLcm42GMtdTBzW4rPV5tcP5rmhdh_e5xuvVO-a_3z8l2Fw3YHHtYA-7ZsCqDC-0n-LF43ze3zR9ihkWl-gs01sPV8c-Rh-Lp_XsJVi9Pi9nj6vAUCJEoBQPozgDySCSKUtpZAXEXDEIScxlKiWzKhRxaLM4I8ZGWmibckME06GJLR-jm8Pf2lWfLfgmKarW7frIhDFFRKz6nJ66P1DGVd47yJLa5aV2XUJJMshNBrnJv1z-B6Bqbb4</recordid><startdate>201503</startdate><enddate>201503</enddate><creator>Zhang, Xia</creator><creator>Ha, Tuanzhu</creator><creator>Lu, Chen</creator><creator>Lam, Fred</creator><creator>Liu, Li</creator><creator>Schweitzer, John</creator><creator>Kalbfleisch, John</creator><creator>Kao, Race L.</creator><creator>Williams, David L.</creator><creator>Li, Chuanfu</creator><general>John Wiley & Sons, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</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>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>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>201503</creationdate><title>Poly (I:C) therapy decreases cerebral ischaemia/reperfusion injury via TLR 3‐mediated prevention of Fas/ FADD interaction</title><author>Zhang, Xia ; Ha, Tuanzhu ; Lu, Chen ; Lam, Fred ; Liu, Li ; Schweitzer, John ; Kalbfleisch, John ; Kao, Race L. ; Williams, David L. ; Li, Chuanfu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1044-993567fe82e68b2b16d4e7392e50738b882d95475df7f0cd6a4adb3c042a5c7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Apoptosis</topic><topic>Carotid arteries</topic><topic>Caspase</topic><topic>Cell activation</topic><topic>FADD protein</topic><topic>FasL protein</topic><topic>Gene expression</topic><topic>Hypoxia</topic><topic>Interferon regulatory factor 3</topic><topic>Ischemia</topic><topic>Laboratory animals</topic><topic>Mice</topic><topic>Microglial cells</topic><topic>Phosphorylation</topic><topic>Polyinosinic:polycytidylic acid</topic><topic>Reperfusion</topic><topic>Stroke</topic><topic>TLR3 protein</topic><topic>Toll-like receptors</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Xia</creatorcontrib><creatorcontrib>Ha, Tuanzhu</creatorcontrib><creatorcontrib>Lu, Chen</creatorcontrib><creatorcontrib>Lam, Fred</creatorcontrib><creatorcontrib>Liu, Li</creatorcontrib><creatorcontrib>Schweitzer, John</creatorcontrib><creatorcontrib>Kalbfleisch, John</creatorcontrib><creatorcontrib>Kao, Race L.</creatorcontrib><creatorcontrib>Williams, David L.</creatorcontrib><creatorcontrib>Li, Chuanfu</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Xia</au><au>Ha, Tuanzhu</au><au>Lu, Chen</au><au>Lam, Fred</au><au>Liu, Li</au><au>Schweitzer, John</au><au>Kalbfleisch, John</au><au>Kao, Race L.</au><au>Williams, David L.</au><au>Li, Chuanfu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Poly (I:C) therapy decreases cerebral ischaemia/reperfusion injury via TLR 3‐mediated prevention of Fas/ FADD interaction</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><date>2015-03</date><risdate>2015</risdate><volume>19</volume><issue>3</issue><spage>555</spage><epage>565</epage><pages>555-565</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Toll‐like receptor (
TLR
)‐mediated signalling plays a role in cerebral ischaemia/reperfusion (I/R) injury. Modulation of
TLR
s has been reported to protect against cerebral I/R injury. This study examined whether modulation of
TLR
3 with poly (I:C) will induce protection against cerebral I/R injury. Mice were treated with or without Poly (I:C) (
n
= 8/group) 1 hr prior to cerebral ischaemia (60 min.) followed by reperfusion (24 hrs). Poly (I:C) pre‐treatment significantly reduced the infarct volume by 57.2% compared with untreated I/R mice. Therapeutic administration of Poly (I:C), administered 30 min. after cerebral ischaemia, markedly decreased infarct volume by 34.9%. However, Poly (I:C)‐induced protection was lost in
TLR
3 knockout mice. In poly (I:C)‐treated mice, there was less neuronal damage in the hippocampus compared with untreated I/R mice. Poly (I:C) treatment induced
IRF
3 phosphorylation, but it inhibited
NF
‐κB activation in the brain. Poly (I:C) also decreased I/R‐induced apoptosis by attenuation of Fas/FasL‐mediated apoptotic signalling. In addition, Poly (I:C) treatment decreased microglial cell caspase‐3 activity.
In vitro
data showed that Poly (I:C) prevented hypoxia/reoxygenation (H/R)‐induced interaction between Fas and
FADD
as well as caspase‐3 and ‐8 activation in microglial cells. Importantly, Poly (I:C) treatment induced co‐association between
TLR
3 and Fas. Our data suggest that Poly (I:C) decreases in cerebral I/R injury
via
TLR
3 which associates with Fas, thereby preventing the interaction of Fas and
FADD
, as well as microglial cell caspase‐3 and ‐8 activities. We conclude that
TLR
3 modulation by Poly (I:C) could be a potential approach for protection against ischaemic stroke.</abstract><cop>Chichester</cop><pub>John Wiley & Sons, Inc</pub><doi>10.1111/jcmm.12456</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular and molecular medicine, 2015-03, Vol.19 (3), p.555-565 |
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| language | eng |
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| source | Wiley Online Library Open Access; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Apoptosis Carotid arteries Caspase Cell activation FADD protein FasL protein Gene expression Hypoxia Interferon regulatory factor 3 Ischemia Laboratory animals Mice Microglial cells Phosphorylation Polyinosinic:polycytidylic acid Reperfusion Stroke TLR3 protein Toll-like receptors Veins & arteries |
| title | Poly (I:C) therapy decreases cerebral ischaemia/reperfusion injury via TLR 3‐mediated prevention of Fas/ FADD interaction |
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