Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3)
Our aim was to examine the role of mitogen-activated protein kinase kinase 3 (MKK3) in the development of left ventricular (LV) remodeling following myocardial infarction (MI). MKK3-null mice were subjected to permanent coronary artery ligation. Twenty-eight days after MI, haemodynamics in male mkk3...
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| Veröffentlicht in: | Cardiovascular research 2007-06, Vol.74 (3), p.466-470 |
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| creator | CLARK, James E FLAVELL, Richard A FAIRCLOTH, Matthew E DAVIS, Roger J HEADS, Richard J MARBER, Michael S |
| description | Our aim was to examine the role of mitogen-activated protein kinase kinase 3 (MKK3) in the development of left ventricular (LV) remodeling following myocardial infarction (MI).
MKK3-null mice were subjected to permanent coronary artery ligation. Twenty-eight days after MI, haemodynamics in male mkk3+/+(WT) and mkk3-/-(KO) littermates were assessed using a pressure-conductance catheter. MI groups were compared to un-operated time-matched WT and KO controls.
MI caused significant LV contractile dysfunction and dilatation which did not differ by genotype. Detailed morphometric analysis of excised hearts confirmed these similar global indices of remodeling and also demonstrated that pathological changes within remote myocardium and scar did not differ between KO and WT hearts.
Despite numerous lines of evidence suggesting MKK3 is the relevant kinase upstream of p38 mitogen-activated protein kinase in LV remodeling these processes can continue in its absence. |
| doi_str_mv | 10.1016/j.cardiores.2007.02.027 |
| format | Article |
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MKK3-null mice were subjected to permanent coronary artery ligation. Twenty-eight days after MI, haemodynamics in male mkk3+/+(WT) and mkk3-/-(KO) littermates were assessed using a pressure-conductance catheter. MI groups were compared to un-operated time-matched WT and KO controls.
MI caused significant LV contractile dysfunction and dilatation which did not differ by genotype. Detailed morphometric analysis of excised hearts confirmed these similar global indices of remodeling and also demonstrated that pathological changes within remote myocardium and scar did not differ between KO and WT hearts.
Despite numerous lines of evidence suggesting MKK3 is the relevant kinase upstream of p38 mitogen-activated protein kinase in LV remodeling these processes can continue in its absence.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1016/j.cardiores.2007.02.027</identifier><identifier>PMID: 17399693</identifier><identifier>CODEN: CVREAU</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Coronary heart disease ; Dilatation, Pathologic ; Heart ; Immunoblotting ; Male ; MAP Kinase Kinase 3 - genetics ; MAP Kinase Kinase 3 - physiology ; Medical sciences ; Mice ; Mice, Knockout ; Myocardial Contraction ; Myocardial Infarction - enzymology ; Myocardium - enzymology ; Ventricular Function, Left ; Ventricular Remodeling - physiology</subject><ispartof>Cardiovascular research, 2007-06, Vol.74 (3), p.466-470</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-8e1383727b6fdca599cfeb87dc00d6ab01f59250f92383606f6a3801d52395b33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18777090$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17399693$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CLARK, James E</creatorcontrib><creatorcontrib>FLAVELL, Richard A</creatorcontrib><creatorcontrib>FAIRCLOTH, Matthew E</creatorcontrib><creatorcontrib>DAVIS, Roger J</creatorcontrib><creatorcontrib>HEADS, Richard J</creatorcontrib><creatorcontrib>MARBER, Michael S</creatorcontrib><title>Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3)</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>Our aim was to examine the role of mitogen-activated protein kinase kinase 3 (MKK3) in the development of left ventricular (LV) remodeling following myocardial infarction (MI).
MKK3-null mice were subjected to permanent coronary artery ligation. Twenty-eight days after MI, haemodynamics in male mkk3+/+(WT) and mkk3-/-(KO) littermates were assessed using a pressure-conductance catheter. MI groups were compared to un-operated time-matched WT and KO controls.
MI caused significant LV contractile dysfunction and dilatation which did not differ by genotype. Detailed morphometric analysis of excised hearts confirmed these similar global indices of remodeling and also demonstrated that pathological changes within remote myocardium and scar did not differ between KO and WT hearts.
Despite numerous lines of evidence suggesting MKK3 is the relevant kinase upstream of p38 mitogen-activated protein kinase in LV remodeling these processes can continue in its absence.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Dilatation, Pathologic</subject><subject>Heart</subject><subject>Immunoblotting</subject><subject>Male</subject><subject>MAP Kinase Kinase 3 - genetics</subject><subject>MAP Kinase Kinase 3 - physiology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Myocardial Contraction</subject><subject>Myocardial Infarction - enzymology</subject><subject>Myocardium - enzymology</subject><subject>Ventricular Function, Left</subject><subject>Ventricular Remodeling - physiology</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkN9LHDEQx4O01PPsv6D70tI-7DnZXJLNo0hrixb7YB9LyCYTybmbnMme0P_eiGdlhvky8JkffAk5pbCiQMXZZmVNdiFlLKsOQK6gqykPyIJKzlvWrfk7sgCAvhVMsENyVMqmtpzL9QdySCVTSii2IH9_pzK3IXqT7RxSbDJOyeEY4l0TShOiwy3WEucm-WYKc7rD2JrKPpoZXbPNacYQm_sQTcFXYc2XX1dX7Osxee_NWPDjXpfkz_dvtxc_2uuby58X59etZQrmtkfKeiY7OQjvrOFKWY9DL50FcMIMQD1XHQevusoJEF4Y1gN1vGOKD4wtyeeXvfWdhx2WWU-hWBxHEzHtipawVozXWBL5AtqcSsno9TaHyeR_moJ-dlZv9H9n9bOzGrqask6e7E_shgnd29zeygp82gOmWDP6bKIN5Y3rpZSggD0B8IGEhg</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>CLARK, James E</creator><creator>FLAVELL, Richard A</creator><creator>FAIRCLOTH, Matthew E</creator><creator>DAVIS, Roger J</creator><creator>HEADS, Richard J</creator><creator>MARBER, Michael S</creator><general>Oxford University Press</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>20070601</creationdate><title>Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3)</title><author>CLARK, James E ; FLAVELL, Richard A ; FAIRCLOTH, Matthew E ; DAVIS, Roger J ; HEADS, Richard J ; MARBER, Michael S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-8e1383727b6fdca599cfeb87dc00d6ab01f59250f92383606f6a3801d52395b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Dilatation, Pathologic</topic><topic>Heart</topic><topic>Immunoblotting</topic><topic>Male</topic><topic>MAP Kinase Kinase 3 - genetics</topic><topic>MAP Kinase Kinase 3 - physiology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Myocardial Contraction</topic><topic>Myocardial Infarction - enzymology</topic><topic>Myocardium - enzymology</topic><topic>Ventricular Function, Left</topic><topic>Ventricular Remodeling - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CLARK, James E</creatorcontrib><creatorcontrib>FLAVELL, Richard A</creatorcontrib><creatorcontrib>FAIRCLOTH, Matthew E</creatorcontrib><creatorcontrib>DAVIS, Roger J</creatorcontrib><creatorcontrib>HEADS, Richard J</creatorcontrib><creatorcontrib>MARBER, Michael S</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>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CLARK, James E</au><au>FLAVELL, Richard A</au><au>FAIRCLOTH, Matthew E</au><au>DAVIS, Roger J</au><au>HEADS, Richard J</au><au>MARBER, Michael S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3)</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>74</volume><issue>3</issue><spage>466</spage><epage>470</epage><pages>466-470</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><coden>CVREAU</coden><abstract>Our aim was to examine the role of mitogen-activated protein kinase kinase 3 (MKK3) in the development of left ventricular (LV) remodeling following myocardial infarction (MI).
MKK3-null mice were subjected to permanent coronary artery ligation. Twenty-eight days after MI, haemodynamics in male mkk3+/+(WT) and mkk3-/-(KO) littermates were assessed using a pressure-conductance catheter. MI groups were compared to un-operated time-matched WT and KO controls.
MI caused significant LV contractile dysfunction and dilatation which did not differ by genotype. Detailed morphometric analysis of excised hearts confirmed these similar global indices of remodeling and also demonstrated that pathological changes within remote myocardium and scar did not differ between KO and WT hearts.
Despite numerous lines of evidence suggesting MKK3 is the relevant kinase upstream of p38 mitogen-activated protein kinase in LV remodeling these processes can continue in its absence.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>17399693</pmid><doi>10.1016/j.cardiores.2007.02.027</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cardiovascular research, 2007-06, Vol.74 (3), p.466-470 |
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| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Freely accessible e-journals; Alma/SFX Local Collection; Oxford Journals |
| subjects | Animals Biological and medical sciences Cardiology. Vascular system Coronary heart disease Dilatation, Pathologic Heart Immunoblotting Male MAP Kinase Kinase 3 - genetics MAP Kinase Kinase 3 - physiology Medical sciences Mice Mice, Knockout Myocardial Contraction Myocardial Infarction - enzymology Myocardium - enzymology Ventricular Function, Left Ventricular Remodeling - physiology |
| title | Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3) |
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