Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction—A magnetic resonance study
► Ficolin-2, MBL and MAP-1 are regulatory lectin complement pathway (LP) molecules. ► LP was associated with left ventricular (LV) dilatation after myocardial infarction. ► Interaction of ficolin-2 and CRP was associated with infarct size and LV remodeling. ► LP-pentraxin activation might influence...
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| Veröffentlicht in: | Molecular immunology 2013-07, Vol.54 (3-4), p.408-414 |
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| creator | Schoos, Mikkel Malby Munthe-Fog, Lea Skjoedt, Mikkel-Ole Ripa, Rasmus Sejersten Lønborg, Jacob Kastrup, Jens Kelbæk, Henning Clemmensen, Peter Garred, Peter |
| description | ► Ficolin-2, MBL and MAP-1 are regulatory lectin complement pathway (LP) molecules. ► LP was associated with left ventricular (LV) dilatation after myocardial infarction. ► Interaction of ficolin-2 and CRP was associated with infarct size and LV remodeling. ► LP-pentraxin activation might influence ischemic reperfusion injury and remodeling.
Lectin complement pathway (LP) activation is an important mechanism in myocardial ischemia reperfusion injury (IRI). LP is activated via the recognition molecules mannose-binding lectin (MBL), ficolins-2 and-3 and is regulated by MBL/Ficolin-associated Protein-1 (MAP-1). Also, C-reactive protein (CRP) and ficolin-2 interact in vitro, but the role of the ficolins in IRI is unknown.
In 55 patients with ST segment elevation myocardial infarction, we investigated the association of LP components and CRP in plasma samples with left ventricular (LV) end systolic and diastolic volumes (ESV and EDV) and infarct size, assessed by cardiac magnetic resonance early at 1–3 days after primary percutaneous coronary intervention and at 6 months follow-up. Opposed to MBL, ficolin-3 and MAP-1, ficolin-2 levels were low at baseline. At baseline, ficolin-2>median was associated with ESV and EDV increases by 7.83ml/m2 (p=0.004) and 14.04ml/m2 (pmedian was associated with ESV (11.21ml/m2; p=0.017) and EDV increases (14.72ml/m2; p=0.006). MAP-1median had the greatest LV dilatation (17.61ml/m2). The ficolin-2×CRP interaction variable was positively associated with infarct size and inversely associated with EDV change over 6 months (p=0.006). There was no interaction between CRP and the other LP molecules.
The LP initiator molecule ficolin-2 and combinations of ficolin-2, MBL and MAP-1 are associated with LV dilatation after myocardial infarction. Interaction of ficolin-2 and CRP was associated with infarct size and LV remodeling, indicating a potential role for LP and LP-pentraxin cross-activation in IRI and LV remodeling. |
| doi_str_mv | 10.1016/j.molimm.2013.01.008 |
| format | Article |
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Lectin complement pathway (LP) activation is an important mechanism in myocardial ischemia reperfusion injury (IRI). LP is activated via the recognition molecules mannose-binding lectin (MBL), ficolins-2 and-3 and is regulated by MBL/Ficolin-associated Protein-1 (MAP-1). Also, C-reactive protein (CRP) and ficolin-2 interact in vitro, but the role of the ficolins in IRI is unknown.
In 55 patients with ST segment elevation myocardial infarction, we investigated the association of LP components and CRP in plasma samples with left ventricular (LV) end systolic and diastolic volumes (ESV and EDV) and infarct size, assessed by cardiac magnetic resonance early at 1–3 days after primary percutaneous coronary intervention and at 6 months follow-up. Opposed to MBL, ficolin-3 and MAP-1, ficolin-2 levels were low at baseline. At baseline, ficolin-2>median was associated with ESV and EDV increases by 7.83ml/m2 (p=0.004) and 14.04ml/m2 (p<0.001). MBL and MAP-1 were not associated with LV dilatation, yet ficolin-2 and MBL worked synergistically and the combination of their levels>median was associated with ESV (11.21ml/m2; p=0.017) and EDV increases (14.72ml/m2; p=0.006). MAP-1<median+ficolin-2>median had the greatest LV dilatation (17.61ml/m2). The ficolin-2×CRP interaction variable was positively associated with infarct size and inversely associated with EDV change over 6 months (p=0.006). There was no interaction between CRP and the other LP molecules.
The LP initiator molecule ficolin-2 and combinations of ficolin-2, MBL and MAP-1 are associated with LV dilatation after myocardial infarction. Interaction of ficolin-2 and CRP was associated with infarct size and LV remodeling, indicating a potential role for LP and LP-pentraxin cross-activation in IRI and LV remodeling.</description><identifier>ISSN: 0161-5890</identifier><identifier>EISSN: 1872-9142</identifier><identifier>DOI: 10.1016/j.molimm.2013.01.008</identifier><identifier>PMID: 23399387</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Adaptor Proteins, Signal Transducing - metabolism ; Apoptosis Regulatory Proteins - metabolism ; C-reactive protein ; C-Reactive Protein - metabolism ; Complement Pathway, Mannose-Binding Lectin - physiology ; Double-Blind Method ; Female ; Ficolins ; Follow-Up Studies ; Glycoproteins - metabolism ; Humans ; Lectin complement pathway ; Lectins - metabolism ; Left ventricular remodeling ; Magnetic Resonance Imaging - methods ; Male ; Mannose-Binding Lectins - metabolism ; Middle Aged ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardial ischemia reperfusion injury ; Prospective Studies ; Randomized Controlled Trials as Topic ; Retrospective Studies ; Ventricular Remodeling - physiology</subject><ispartof>Molecular immunology, 2013-07, Vol.54 (3-4), p.408-414</ispartof><rights>2013 Elsevier Ltd</rights><rights>Copyright © 2013 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-3a7f7769ce24179d9dc302ab70d61c5dd4f6c7a2845d0bbef3732fbd5bd7eb383</citedby><cites>FETCH-LOGICAL-c362t-3a7f7769ce24179d9dc302ab70d61c5dd4f6c7a2845d0bbef3732fbd5bd7eb383</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.molimm.2013.01.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23399387$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schoos, Mikkel Malby</creatorcontrib><creatorcontrib>Munthe-Fog, Lea</creatorcontrib><creatorcontrib>Skjoedt, Mikkel-Ole</creatorcontrib><creatorcontrib>Ripa, Rasmus Sejersten</creatorcontrib><creatorcontrib>Lønborg, Jacob</creatorcontrib><creatorcontrib>Kastrup, Jens</creatorcontrib><creatorcontrib>Kelbæk, Henning</creatorcontrib><creatorcontrib>Clemmensen, Peter</creatorcontrib><creatorcontrib>Garred, Peter</creatorcontrib><title>Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction—A magnetic resonance study</title><title>Molecular immunology</title><addtitle>Mol Immunol</addtitle><description>► Ficolin-2, MBL and MAP-1 are regulatory lectin complement pathway (LP) molecules. ► LP was associated with left ventricular (LV) dilatation after myocardial infarction. ► Interaction of ficolin-2 and CRP was associated with infarct size and LV remodeling. ► LP-pentraxin activation might influence ischemic reperfusion injury and remodeling.
Lectin complement pathway (LP) activation is an important mechanism in myocardial ischemia reperfusion injury (IRI). LP is activated via the recognition molecules mannose-binding lectin (MBL), ficolins-2 and-3 and is regulated by MBL/Ficolin-associated Protein-1 (MAP-1). Also, C-reactive protein (CRP) and ficolin-2 interact in vitro, but the role of the ficolins in IRI is unknown.
In 55 patients with ST segment elevation myocardial infarction, we investigated the association of LP components and CRP in plasma samples with left ventricular (LV) end systolic and diastolic volumes (ESV and EDV) and infarct size, assessed by cardiac magnetic resonance early at 1–3 days after primary percutaneous coronary intervention and at 6 months follow-up. Opposed to MBL, ficolin-3 and MAP-1, ficolin-2 levels were low at baseline. At baseline, ficolin-2>median was associated with ESV and EDV increases by 7.83ml/m2 (p=0.004) and 14.04ml/m2 (p<0.001). MBL and MAP-1 were not associated with LV dilatation, yet ficolin-2 and MBL worked synergistically and the combination of their levels>median was associated with ESV (11.21ml/m2; p=0.017) and EDV increases (14.72ml/m2; p=0.006). MAP-1<median+ficolin-2>median had the greatest LV dilatation (17.61ml/m2). The ficolin-2×CRP interaction variable was positively associated with infarct size and inversely associated with EDV change over 6 months (p=0.006). There was no interaction between CRP and the other LP molecules.
The LP initiator molecule ficolin-2 and combinations of ficolin-2, MBL and MAP-1 are associated with LV dilatation after myocardial infarction. Interaction of ficolin-2 and CRP was associated with infarct size and LV remodeling, indicating a potential role for LP and LP-pentraxin cross-activation in IRI and LV remodeling.</description><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>C-reactive protein</subject><subject>C-Reactive Protein - metabolism</subject><subject>Complement Pathway, Mannose-Binding Lectin - physiology</subject><subject>Double-Blind Method</subject><subject>Female</subject><subject>Ficolins</subject><subject>Follow-Up Studies</subject><subject>Glycoproteins - metabolism</subject><subject>Humans</subject><subject>Lectin complement pathway</subject><subject>Lectins - metabolism</subject><subject>Left ventricular remodeling</subject><subject>Magnetic Resonance Imaging - methods</subject><subject>Male</subject><subject>Mannose-Binding Lectins - metabolism</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial ischemia reperfusion injury</subject><subject>Prospective Studies</subject><subject>Randomized Controlled Trials as Topic</subject><subject>Retrospective Studies</subject><subject>Ventricular Remodeling - physiology</subject><issn>0161-5890</issn><issn>1872-9142</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcuKFDEUQIMoTjv6ByJZurDKPKoqVRuhacYHDLjRdUglt8Y0ebRJqofe-RF-gZ_ml5imR5euQuCcXG4OQi8paSmhw9t966Oz3reMUN4S2hIyPkIbOgrWTLRjj9GmYrTpx4lcoWc57wkhAxn6p-iKcT5NfBQb9Gubc9RWFRsDnqHcAwTsQBcbsI7-4MBDKPigyrd7dcI22FLhmPIbvGsSqAoeAR9SLFANFUyVl4KPVUpWr04lnMBHA86Gu6pjf4paJWOVq7dFJX2e_PvHzy326i5AsboKOQYVNOBcVnN6jp4symV48XBeo6_vb77sPja3nz982m1vG80HVhquxCLEMGlgHRWTmYzmhKlZEDNQ3RvTLYMWio1db8g8w8IFZ8ts-tkImPnIr9Hry7t1m-8r5CK9zRqcUwHimiXlVIw9E4RVtLugOsWcEyzykKxX6SQpkec6ci8vdeS5jiRU1jpVe_UwYZ09mH_S3xwVeHcBoO55tJBk1hbqTxibahNpov3_hD8Fv6kz</recordid><startdate>201307</startdate><enddate>201307</enddate><creator>Schoos, Mikkel Malby</creator><creator>Munthe-Fog, Lea</creator><creator>Skjoedt, Mikkel-Ole</creator><creator>Ripa, Rasmus Sejersten</creator><creator>Lønborg, Jacob</creator><creator>Kastrup, Jens</creator><creator>Kelbæk, Henning</creator><creator>Clemmensen, Peter</creator><creator>Garred, Peter</creator><general>Elsevier Ltd</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><scope>7X8</scope></search><sort><creationdate>201307</creationdate><title>Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction—A magnetic resonance study</title><author>Schoos, Mikkel Malby ; 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Lectin complement pathway (LP) activation is an important mechanism in myocardial ischemia reperfusion injury (IRI). LP is activated via the recognition molecules mannose-binding lectin (MBL), ficolins-2 and-3 and is regulated by MBL/Ficolin-associated Protein-1 (MAP-1). Also, C-reactive protein (CRP) and ficolin-2 interact in vitro, but the role of the ficolins in IRI is unknown.
In 55 patients with ST segment elevation myocardial infarction, we investigated the association of LP components and CRP in plasma samples with left ventricular (LV) end systolic and diastolic volumes (ESV and EDV) and infarct size, assessed by cardiac magnetic resonance early at 1–3 days after primary percutaneous coronary intervention and at 6 months follow-up. Opposed to MBL, ficolin-3 and MAP-1, ficolin-2 levels were low at baseline. At baseline, ficolin-2>median was associated with ESV and EDV increases by 7.83ml/m2 (p=0.004) and 14.04ml/m2 (p<0.001). MBL and MAP-1 were not associated with LV dilatation, yet ficolin-2 and MBL worked synergistically and the combination of their levels>median was associated with ESV (11.21ml/m2; p=0.017) and EDV increases (14.72ml/m2; p=0.006). MAP-1<median+ficolin-2>median had the greatest LV dilatation (17.61ml/m2). The ficolin-2×CRP interaction variable was positively associated with infarct size and inversely associated with EDV change over 6 months (p=0.006). There was no interaction between CRP and the other LP molecules.
The LP initiator molecule ficolin-2 and combinations of ficolin-2, MBL and MAP-1 are associated with LV dilatation after myocardial infarction. Interaction of ficolin-2 and CRP was associated with infarct size and LV remodeling, indicating a potential role for LP and LP-pentraxin cross-activation in IRI and LV remodeling.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>23399387</pmid><doi>10.1016/j.molimm.2013.01.008</doi><tpages>7</tpages></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - metabolism Apoptosis Regulatory Proteins - metabolism C-reactive protein C-Reactive Protein - metabolism Complement Pathway, Mannose-Binding Lectin - physiology Double-Blind Method Female Ficolins Follow-Up Studies Glycoproteins - metabolism Humans Lectin complement pathway Lectins - metabolism Left ventricular remodeling Magnetic Resonance Imaging - methods Male Mannose-Binding Lectins - metabolism Middle Aged Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardial ischemia reperfusion injury Prospective Studies Randomized Controlled Trials as Topic Retrospective Studies Ventricular Remodeling - physiology |
| title | Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction—A magnetic resonance study |
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