Anti-apoA-1 auto-antibodies increase mouse atherosclerotic plaque vulnerability, myocardial necrosis and mortality triggering TLR2 and TLR4
Summary Auto-antibodies to apolipoprotein A-1 (anti-apoA-1 IgG) were shown to promote inflammation and atherogenesis, possibly through innate immune receptors signalling. Here, we aimed at investigating the role of Toll-like receptors (TLR) 2 and 4 on anti-apoA-1 IgG-induced athero-sclerotic plaque...
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| Veröffentlicht in: | Thrombosis and haemostasis 2015-08, Vol.113 (2), p.410-422 |
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| creator | Montecucco, Fabrizio Braunersreuther, Vincent Burger, Fabienne Lenglet, Sébastien Pelli, Graziano Carbone, Federico Fraga-Silva, Rodrigo Stergiopulos, Nikolaos Monaco, Claudia Mueller, Christian Pagano, Sabrina Dallegri, Franco Mach, François Vuilleumier, Nicolas |
| description | Summary
Auto-antibodies to apolipoprotein A-1 (anti-apoA-1 IgG) were shown to promote inflammation and atherogenesis, possibly through innate immune receptors signalling. Here, we aimed at investigating the role of Toll-like receptors (TLR) 2 and 4 on anti-apoA-1 IgG-induced athero-sclerotic plaque vulnerability, myocardial necrosis and mortality in mice. Adult male apolipoprotein E knockout (ApoE)
-/-
(n=72), TLR2
-/-
ApoE
-/-
(n=36) and TLR4
-/-
Apo
-/-
(n=28) mice were intravenously injected with 50 µg/mouse of endotoxin-free polyclonal anti-apoA-1 IgG or control isotype IgG (CTL IgG) every two weeks for 16 weeks. Atherosclerotic plaque size and vulnerability were assessed by histology. Myocardial ischaemia and necrosis, respectively, were determined by electrocardiographic (ECG) changes assessed by telemetry and serum troponin I (cTnI) measurements. Impact on survival was assessed by Kaplan-Meier analyses. In ApoE
-/-
mice, anti-apoA-1 IgG passive immunisation enhanced histological features of athero-sclerotic plaque vulnerability (increase in neutrophil and MMP-9 and reduction in collagen content), induced a substantial cTnI elevation (p=0.001), and increased mortality rate by 23 % (LogRank, p=0.04) when compared to CTL IgG. On a subgroup of ApoE
-/-
mice equipped with telemetry (n=4), a significant ST-segment depression was noted in anti-apoA-1 IgG-treated mice when compared to CTL IgG recipients (p< 0.001), and an acute ST-segment elevation myocardial infarction preceding mouse death was observed in one case. The deleterious effects of anti-apoA-1 IgG on atherosclerotic plaque vulnerability, myocardial necrosis and death were partially reversed in TLR2
-/-
ApoE
-/-
and TLR4
-/-
ApoE
-/-
backgrounds. In conclusion, anti-apoA-1 auto-antibodies seem to be active mediators of atherosclerotic plaque vulnerability, myocardial necrosis, and mortality in mice through TLR2- and TLR4-mediated pathways. |
| doi_str_mv | 10.1160/TH14-12-1039 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1160_TH14_12_1039</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>25879306</sourcerecordid><originalsourceid>FETCH-LOGICAL-c370t-132244c567610553f873b08e05fdad7d308477e3dd2d1a809e40505b8d874cd53</originalsourceid><addsrcrecordid>eNptkE1LAzEQhoMotlZvniV3G5187cexiFqhIEgFb0t2k21T9stsVuhv8E-bterJy8ww8_Ay74vQJYUbSiO4XS-pIJQRCjw9QlMmo5hESfp2jKbABZCICTlBZ32_A6CRSOUpmjCZxCmHaIo-F423RHXtglCsBt8SFRZ5q63psW0KZ1RvcN0OoSq_Na7tiypUbwvcVep9MPhjqBrjVG4r6_dzXO_bQjltVYUbUwTe9lg1Omg4r0YEe2c3G-Nss8Hr1Qv7voZBnKOTUlW9ufjpM_T6cL--W5LV8-PT3WJFCh6DJ5QzJkQRfEYUpORlEvMcEgOy1ErHmkMi4thwrZmmKoHUCJAg80QnsSi05DM0P-iO3_XOlFnnbK3cPqOQjZlmY6YZZdmYacCvDng35LXRf_BviAG4PgB-a01tsl07uCYY-F_uC15rgN0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Anti-apoA-1 auto-antibodies increase mouse atherosclerotic plaque vulnerability, myocardial necrosis and mortality triggering TLR2 and TLR4</title><source>MEDLINE</source><source>Thieme Connect Journals</source><creator>Montecucco, Fabrizio ; Braunersreuther, Vincent ; Burger, Fabienne ; Lenglet, Sébastien ; Pelli, Graziano ; Carbone, Federico ; Fraga-Silva, Rodrigo ; Stergiopulos, Nikolaos ; Monaco, Claudia ; Mueller, Christian ; Pagano, Sabrina ; Dallegri, Franco ; Mach, François ; Vuilleumier, Nicolas</creator><creatorcontrib>Montecucco, Fabrizio ; Braunersreuther, Vincent ; Burger, Fabienne ; Lenglet, Sébastien ; Pelli, Graziano ; Carbone, Federico ; Fraga-Silva, Rodrigo ; Stergiopulos, Nikolaos ; Monaco, Claudia ; Mueller, Christian ; Pagano, Sabrina ; Dallegri, Franco ; Mach, François ; Vuilleumier, Nicolas</creatorcontrib><description>Summary
Auto-antibodies to apolipoprotein A-1 (anti-apoA-1 IgG) were shown to promote inflammation and atherogenesis, possibly through innate immune receptors signalling. Here, we aimed at investigating the role of Toll-like receptors (TLR) 2 and 4 on anti-apoA-1 IgG-induced athero-sclerotic plaque vulnerability, myocardial necrosis and mortality in mice. Adult male apolipoprotein E knockout (ApoE)
-/-
(n=72), TLR2
-/-
ApoE
-/-
(n=36) and TLR4
-/-
Apo
-/-
(n=28) mice were intravenously injected with 50 µg/mouse of endotoxin-free polyclonal anti-apoA-1 IgG or control isotype IgG (CTL IgG) every two weeks for 16 weeks. Atherosclerotic plaque size and vulnerability were assessed by histology. Myocardial ischaemia and necrosis, respectively, were determined by electrocardiographic (ECG) changes assessed by telemetry and serum troponin I (cTnI) measurements. Impact on survival was assessed by Kaplan-Meier analyses. In ApoE
-/-
mice, anti-apoA-1 IgG passive immunisation enhanced histological features of athero-sclerotic plaque vulnerability (increase in neutrophil and MMP-9 and reduction in collagen content), induced a substantial cTnI elevation (p=0.001), and increased mortality rate by 23 % (LogRank, p=0.04) when compared to CTL IgG. On a subgroup of ApoE
-/-
mice equipped with telemetry (n=4), a significant ST-segment depression was noted in anti-apoA-1 IgG-treated mice when compared to CTL IgG recipients (p< 0.001), and an acute ST-segment elevation myocardial infarction preceding mouse death was observed in one case. The deleterious effects of anti-apoA-1 IgG on atherosclerotic plaque vulnerability, myocardial necrosis and death were partially reversed in TLR2
-/-
ApoE
-/-
and TLR4
-/-
ApoE
-/-
backgrounds. In conclusion, anti-apoA-1 auto-antibodies seem to be active mediators of atherosclerotic plaque vulnerability, myocardial necrosis, and mortality in mice through TLR2- and TLR4-mediated pathways.</description><identifier>ISSN: 0340-6245</identifier><identifier>EISSN: 2567-689X</identifier><identifier>DOI: 10.1160/TH14-12-1039</identifier><identifier>PMID: 25879306</identifier><language>eng</language><publisher>Germany: Schattauer GmbH</publisher><subject>Animals ; Aortic Diseases - pathology ; Apolipoprotein A-I - antagonists & inhibitors ; Apolipoprotein A-I - immunology ; Apolipoproteins E - deficiency ; Atherosclerosis and Ischaemic Disease ; Autoantibodies - adverse effects ; Collagen - analysis ; Disease Susceptibility ; Immunization, Passive - adverse effects ; Immunoglobulin G - adverse effects ; Lipids - analysis ; Male ; Mice ; Mice, Knockout ; Myocardial Infarction - etiology ; Myocardial Infarction - immunology ; Myocardial Infarction - pathology ; Myocardial Ischemia - blood ; Myocardial Ischemia - etiology ; Myocardial Ischemia - immunology ; Myocardial Ischemia - pathology ; Myocardium - pathology ; Necrosis ; Plaque, Atherosclerotic - genetics ; Plaque, Atherosclerotic - immunology ; Plaque, Atherosclerotic - metabolism ; Signal Transduction - immunology ; Telemetry ; Toll-Like Receptor 2 - deficiency ; Toll-Like Receptor 2 - genetics ; Toll-Like Receptor 2 - physiology ; Toll-Like Receptor 4 - deficiency ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - physiology ; Troponin I - blood</subject><ispartof>Thrombosis and haemostasis, 2015-08, Vol.113 (2), p.410-422</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-132244c567610553f873b08e05fdad7d308477e3dd2d1a809e40505b8d874cd53</citedby><cites>FETCH-LOGICAL-c370t-132244c567610553f873b08e05fdad7d308477e3dd2d1a809e40505b8d874cd53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.thieme-connect.de/products/ejournals/pdf/10.1160/TH14-12-1039.pdf$$EPDF$$P50$$Gthieme$$H</linktopdf><linktohtml>$$Uhttps://www.thieme-connect.de/products/ejournals/html/10.1160/TH14-12-1039$$EHTML$$P50$$Gthieme$$H</linktohtml><link.rule.ids>314,780,784,3016,27923,27924,54558,54559</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25879306$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Montecucco, Fabrizio</creatorcontrib><creatorcontrib>Braunersreuther, Vincent</creatorcontrib><creatorcontrib>Burger, Fabienne</creatorcontrib><creatorcontrib>Lenglet, Sébastien</creatorcontrib><creatorcontrib>Pelli, Graziano</creatorcontrib><creatorcontrib>Carbone, Federico</creatorcontrib><creatorcontrib>Fraga-Silva, Rodrigo</creatorcontrib><creatorcontrib>Stergiopulos, Nikolaos</creatorcontrib><creatorcontrib>Monaco, Claudia</creatorcontrib><creatorcontrib>Mueller, Christian</creatorcontrib><creatorcontrib>Pagano, Sabrina</creatorcontrib><creatorcontrib>Dallegri, Franco</creatorcontrib><creatorcontrib>Mach, François</creatorcontrib><creatorcontrib>Vuilleumier, Nicolas</creatorcontrib><title>Anti-apoA-1 auto-antibodies increase mouse atherosclerotic plaque vulnerability, myocardial necrosis and mortality triggering TLR2 and TLR4</title><title>Thrombosis and haemostasis</title><addtitle>Thromb Haemost</addtitle><description>Summary
Auto-antibodies to apolipoprotein A-1 (anti-apoA-1 IgG) were shown to promote inflammation and atherogenesis, possibly through innate immune receptors signalling. Here, we aimed at investigating the role of Toll-like receptors (TLR) 2 and 4 on anti-apoA-1 IgG-induced athero-sclerotic plaque vulnerability, myocardial necrosis and mortality in mice. Adult male apolipoprotein E knockout (ApoE)
-/-
(n=72), TLR2
-/-
ApoE
-/-
(n=36) and TLR4
-/-
Apo
-/-
(n=28) mice were intravenously injected with 50 µg/mouse of endotoxin-free polyclonal anti-apoA-1 IgG or control isotype IgG (CTL IgG) every two weeks for 16 weeks. Atherosclerotic plaque size and vulnerability were assessed by histology. Myocardial ischaemia and necrosis, respectively, were determined by electrocardiographic (ECG) changes assessed by telemetry and serum troponin I (cTnI) measurements. Impact on survival was assessed by Kaplan-Meier analyses. In ApoE
-/-
mice, anti-apoA-1 IgG passive immunisation enhanced histological features of athero-sclerotic plaque vulnerability (increase in neutrophil and MMP-9 and reduction in collagen content), induced a substantial cTnI elevation (p=0.001), and increased mortality rate by 23 % (LogRank, p=0.04) when compared to CTL IgG. On a subgroup of ApoE
-/-
mice equipped with telemetry (n=4), a significant ST-segment depression was noted in anti-apoA-1 IgG-treated mice when compared to CTL IgG recipients (p< 0.001), and an acute ST-segment elevation myocardial infarction preceding mouse death was observed in one case. The deleterious effects of anti-apoA-1 IgG on atherosclerotic plaque vulnerability, myocardial necrosis and death were partially reversed in TLR2
-/-
ApoE
-/-
and TLR4
-/-
ApoE
-/-
backgrounds. In conclusion, anti-apoA-1 auto-antibodies seem to be active mediators of atherosclerotic plaque vulnerability, myocardial necrosis, and mortality in mice through TLR2- and TLR4-mediated pathways.</description><subject>Animals</subject><subject>Aortic Diseases - pathology</subject><subject>Apolipoprotein A-I - antagonists & inhibitors</subject><subject>Apolipoprotein A-I - immunology</subject><subject>Apolipoproteins E - deficiency</subject><subject>Atherosclerosis and Ischaemic Disease</subject><subject>Autoantibodies - adverse effects</subject><subject>Collagen - analysis</subject><subject>Disease Susceptibility</subject><subject>Immunization, Passive - adverse effects</subject><subject>Immunoglobulin G - adverse effects</subject><subject>Lipids - analysis</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Myocardial Infarction - etiology</subject><subject>Myocardial Infarction - immunology</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Ischemia - blood</subject><subject>Myocardial Ischemia - etiology</subject><subject>Myocardial Ischemia - immunology</subject><subject>Myocardial Ischemia - pathology</subject><subject>Myocardium - pathology</subject><subject>Necrosis</subject><subject>Plaque, Atherosclerotic - genetics</subject><subject>Plaque, Atherosclerotic - immunology</subject><subject>Plaque, Atherosclerotic - metabolism</subject><subject>Signal Transduction - immunology</subject><subject>Telemetry</subject><subject>Toll-Like Receptor 2 - deficiency</subject><subject>Toll-Like Receptor 2 - genetics</subject><subject>Toll-Like Receptor 2 - physiology</subject><subject>Toll-Like Receptor 4 - deficiency</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - physiology</subject><subject>Troponin I - blood</subject><issn>0340-6245</issn><issn>2567-689X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkE1LAzEQhoMotlZvniV3G5187cexiFqhIEgFb0t2k21T9stsVuhv8E-bterJy8ww8_Ay74vQJYUbSiO4XS-pIJQRCjw9QlMmo5hESfp2jKbABZCICTlBZ32_A6CRSOUpmjCZxCmHaIo-F423RHXtglCsBt8SFRZ5q63psW0KZ1RvcN0OoSq_Na7tiypUbwvcVep9MPhjqBrjVG4r6_dzXO_bQjltVYUbUwTe9lg1Omg4r0YEe2c3G-Nss8Hr1Qv7voZBnKOTUlW9ufjpM_T6cL--W5LV8-PT3WJFCh6DJ5QzJkQRfEYUpORlEvMcEgOy1ErHmkMi4thwrZmmKoHUCJAg80QnsSi05DM0P-iO3_XOlFnnbK3cPqOQjZlmY6YZZdmYacCvDng35LXRf_BviAG4PgB-a01tsl07uCYY-F_uC15rgN0</recordid><startdate>20150801</startdate><enddate>20150801</enddate><creator>Montecucco, Fabrizio</creator><creator>Braunersreuther, Vincent</creator><creator>Burger, Fabienne</creator><creator>Lenglet, Sébastien</creator><creator>Pelli, Graziano</creator><creator>Carbone, Federico</creator><creator>Fraga-Silva, Rodrigo</creator><creator>Stergiopulos, Nikolaos</creator><creator>Monaco, Claudia</creator><creator>Mueller, Christian</creator><creator>Pagano, Sabrina</creator><creator>Dallegri, Franco</creator><creator>Mach, François</creator><creator>Vuilleumier, Nicolas</creator><general>Schattauer GmbH</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20150801</creationdate><title>Anti-apoA-1 auto-antibodies increase mouse atherosclerotic plaque vulnerability, myocardial necrosis and mortality triggering TLR2 and TLR4</title><author>Montecucco, Fabrizio ; Braunersreuther, Vincent ; Burger, Fabienne ; Lenglet, Sébastien ; Pelli, Graziano ; Carbone, Federico ; Fraga-Silva, Rodrigo ; Stergiopulos, Nikolaos ; Monaco, Claudia ; Mueller, Christian ; Pagano, Sabrina ; Dallegri, Franco ; Mach, François ; Vuilleumier, Nicolas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-132244c567610553f873b08e05fdad7d308477e3dd2d1a809e40505b8d874cd53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Aortic Diseases - pathology</topic><topic>Apolipoprotein A-I - antagonists & inhibitors</topic><topic>Apolipoprotein A-I - immunology</topic><topic>Apolipoproteins E - deficiency</topic><topic>Atherosclerosis and Ischaemic Disease</topic><topic>Autoantibodies - adverse effects</topic><topic>Collagen - analysis</topic><topic>Disease Susceptibility</topic><topic>Immunization, Passive - adverse effects</topic><topic>Immunoglobulin G - adverse effects</topic><topic>Lipids - analysis</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Myocardial Infarction - etiology</topic><topic>Myocardial Infarction - immunology</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Ischemia - blood</topic><topic>Myocardial Ischemia - etiology</topic><topic>Myocardial Ischemia - immunology</topic><topic>Myocardial Ischemia - pathology</topic><topic>Myocardium - pathology</topic><topic>Necrosis</topic><topic>Plaque, Atherosclerotic - genetics</topic><topic>Plaque, Atherosclerotic - immunology</topic><topic>Plaque, Atherosclerotic - metabolism</topic><topic>Signal Transduction - immunology</topic><topic>Telemetry</topic><topic>Toll-Like Receptor 2 - deficiency</topic><topic>Toll-Like Receptor 2 - genetics</topic><topic>Toll-Like Receptor 2 - physiology</topic><topic>Toll-Like Receptor 4 - deficiency</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - physiology</topic><topic>Troponin I - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Montecucco, Fabrizio</creatorcontrib><creatorcontrib>Braunersreuther, Vincent</creatorcontrib><creatorcontrib>Burger, Fabienne</creatorcontrib><creatorcontrib>Lenglet, Sébastien</creatorcontrib><creatorcontrib>Pelli, Graziano</creatorcontrib><creatorcontrib>Carbone, Federico</creatorcontrib><creatorcontrib>Fraga-Silva, Rodrigo</creatorcontrib><creatorcontrib>Stergiopulos, Nikolaos</creatorcontrib><creatorcontrib>Monaco, Claudia</creatorcontrib><creatorcontrib>Mueller, Christian</creatorcontrib><creatorcontrib>Pagano, Sabrina</creatorcontrib><creatorcontrib>Dallegri, Franco</creatorcontrib><creatorcontrib>Mach, François</creatorcontrib><creatorcontrib>Vuilleumier, Nicolas</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Montecucco, Fabrizio</au><au>Braunersreuther, Vincent</au><au>Burger, Fabienne</au><au>Lenglet, Sébastien</au><au>Pelli, Graziano</au><au>Carbone, Federico</au><au>Fraga-Silva, Rodrigo</au><au>Stergiopulos, Nikolaos</au><au>Monaco, Claudia</au><au>Mueller, Christian</au><au>Pagano, Sabrina</au><au>Dallegri, Franco</au><au>Mach, François</au><au>Vuilleumier, Nicolas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-apoA-1 auto-antibodies increase mouse atherosclerotic plaque vulnerability, myocardial necrosis and mortality triggering TLR2 and TLR4</atitle><jtitle>Thrombosis and haemostasis</jtitle><addtitle>Thromb Haemost</addtitle><date>2015-08-01</date><risdate>2015</risdate><volume>113</volume><issue>2</issue><spage>410</spage><epage>422</epage><pages>410-422</pages><issn>0340-6245</issn><eissn>2567-689X</eissn><abstract>Summary
Auto-antibodies to apolipoprotein A-1 (anti-apoA-1 IgG) were shown to promote inflammation and atherogenesis, possibly through innate immune receptors signalling. Here, we aimed at investigating the role of Toll-like receptors (TLR) 2 and 4 on anti-apoA-1 IgG-induced athero-sclerotic plaque vulnerability, myocardial necrosis and mortality in mice. Adult male apolipoprotein E knockout (ApoE)
-/-
(n=72), TLR2
-/-
ApoE
-/-
(n=36) and TLR4
-/-
Apo
-/-
(n=28) mice were intravenously injected with 50 µg/mouse of endotoxin-free polyclonal anti-apoA-1 IgG or control isotype IgG (CTL IgG) every two weeks for 16 weeks. Atherosclerotic plaque size and vulnerability were assessed by histology. Myocardial ischaemia and necrosis, respectively, were determined by electrocardiographic (ECG) changes assessed by telemetry and serum troponin I (cTnI) measurements. Impact on survival was assessed by Kaplan-Meier analyses. In ApoE
-/-
mice, anti-apoA-1 IgG passive immunisation enhanced histological features of athero-sclerotic plaque vulnerability (increase in neutrophil and MMP-9 and reduction in collagen content), induced a substantial cTnI elevation (p=0.001), and increased mortality rate by 23 % (LogRank, p=0.04) when compared to CTL IgG. On a subgroup of ApoE
-/-
mice equipped with telemetry (n=4), a significant ST-segment depression was noted in anti-apoA-1 IgG-treated mice when compared to CTL IgG recipients (p< 0.001), and an acute ST-segment elevation myocardial infarction preceding mouse death was observed in one case. The deleterious effects of anti-apoA-1 IgG on atherosclerotic plaque vulnerability, myocardial necrosis and death were partially reversed in TLR2
-/-
ApoE
-/-
and TLR4
-/-
ApoE
-/-
backgrounds. In conclusion, anti-apoA-1 auto-antibodies seem to be active mediators of atherosclerotic plaque vulnerability, myocardial necrosis, and mortality in mice through TLR2- and TLR4-mediated pathways.</abstract><cop>Germany</cop><pub>Schattauer GmbH</pub><pmid>25879306</pmid><doi>10.1160/TH14-12-1039</doi><tpages>13</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0340-6245 |
| ispartof | Thrombosis and haemostasis, 2015-08, Vol.113 (2), p.410-422 |
| issn | 0340-6245 2567-689X |
| language | eng |
| recordid | cdi_crossref_primary_10_1160_TH14_12_1039 |
| source | MEDLINE; Thieme Connect Journals |
| subjects | Animals Aortic Diseases - pathology Apolipoprotein A-I - antagonists & inhibitors Apolipoprotein A-I - immunology Apolipoproteins E - deficiency Atherosclerosis and Ischaemic Disease Autoantibodies - adverse effects Collagen - analysis Disease Susceptibility Immunization, Passive - adverse effects Immunoglobulin G - adverse effects Lipids - analysis Male Mice Mice, Knockout Myocardial Infarction - etiology Myocardial Infarction - immunology Myocardial Infarction - pathology Myocardial Ischemia - blood Myocardial Ischemia - etiology Myocardial Ischemia - immunology Myocardial Ischemia - pathology Myocardium - pathology Necrosis Plaque, Atherosclerotic - genetics Plaque, Atherosclerotic - immunology Plaque, Atherosclerotic - metabolism Signal Transduction - immunology Telemetry Toll-Like Receptor 2 - deficiency Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - physiology Toll-Like Receptor 4 - deficiency Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - physiology Troponin I - blood |
| title | Anti-apoA-1 auto-antibodies increase mouse atherosclerotic plaque vulnerability, myocardial necrosis and mortality triggering TLR2 and TLR4 |
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