Relaxin remodels fibrotic healing following myocardial infarction
In the setting of myocardial infarction (MI), implanted stem cell viability is low and scar formation limits stem cell homing, viability, and integration. Thus, interventions that favorably remodel fibrotic healing may benefit stem cell therapies. However, it remains unclear whether it is feasible a...
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| Veröffentlicht in: | Laboratory investigation 2011-05, Vol.91 (5), p.675-690 |
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| creator | Samuel, Chrishan S Cendrawan, Sofia Gao, Xiao-Ming Ming, Ziqiu Zhao, Chongxin Kiriazis, Helen Xu, Qi Tregear, Geoffrey W Bathgate, Ross A D Du, Xiao-Jun |
| description | In the setting of myocardial infarction (MI), implanted stem cell viability is low and scar formation limits stem cell homing, viability, and integration. Thus, interventions that favorably remodel fibrotic healing may benefit stem cell therapies. However, it remains unclear whether it is feasible and safe to remodel fibrotic healing post-MI without compromising ventricular remodeling and dysfunction. This study, therefore, determined the anti-fibrotic and other effects of the hormone, relaxin in a mouse model of MI. Adult male mice underwent left coronary artery ligation-induced MI and were immediately treated with recombinant human relaxin (MI+RLX) or vehicle (MI+VEH) over 7 or 30 days, representing time points of early and mature fibrotic healing. Cardiac function was assessed by echocardiography and catheterization, while comprehensive immunohistochemistry, morphometry, and western blotting were performed to explore the relaxin-induced mechanisms of action post-MI. RLX significantly inhibited the MI-induced progression of cardiac fibrosis over 7 and 30 days, which was associated with a reduction in TGF-β1 expression, myofibroblast differentiation, and cardiomyocyte apoptosis in addition to a promotion of matrix metalloproteinase-13 levels and de novo blood vessel growth (all P |
| doi_str_mv | 10.1038/labinvest.2010.198 |
| format | Article |
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Thus, interventions that favorably remodel fibrotic healing may benefit stem cell therapies. However, it remains unclear whether it is feasible and safe to remodel fibrotic healing post-MI without compromising ventricular remodeling and dysfunction. This study, therefore, determined the anti-fibrotic and other effects of the hormone, relaxin in a mouse model of MI. Adult male mice underwent left coronary artery ligation-induced MI and were immediately treated with recombinant human relaxin (MI+RLX) or vehicle (MI+VEH) over 7 or 30 days, representing time points of early and mature fibrotic healing. Cardiac function was assessed by echocardiography and catheterization, while comprehensive immunohistochemistry, morphometry, and western blotting were performed to explore the relaxin-induced mechanisms of action post-MI. RLX significantly inhibited the MI-induced progression of cardiac fibrosis over 7 and 30 days, which was associated with a reduction in TGF-β1 expression, myofibroblast differentiation, and cardiomyocyte apoptosis in addition to a promotion of matrix metalloproteinase-13 levels and de novo blood vessel growth (all P<0.05 vs respective measurements from MI+VEH mice). Despite the evident fibrotic healing post-MI, relaxin did not adversely affect the incidence of ventricular free-wall rupture or the extent of LV remodeling and dysfunction. These combined findings demonstrate that RLX favorably remodels the process of fibrotic healing post-infarction by lowering the density of mature scar tissue in the infarcted myocardium, border zone, and non-infarcted myocardium, and may, therefore, facilitate cell-based therapies in the setting of ischemic heart disease.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/labinvest.2010.198</identifier><identifier>PMID: 21221074</identifier><identifier>CODEN: LAINAW</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>631/136/16 ; 692/699/75/2/1674 ; 692/700/565/1331/238 ; angiogenesis ; Animals ; apoptosis ; Biological and medical sciences ; Biotechnology ; Blotting, Western ; cardiac fibrosis ; Cardiology. Vascular system ; Coronary heart disease ; Fibrosis ; Fundamental and applied biological sciences. Psychology ; Heart ; Investigative techniques, diagnostic techniques (general aspects) ; Laboratory Medicine ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred C57BL ; Myocardial Infarction - drug therapy ; Myocardial Infarction - physiopathology ; Organ Size ; Pathology ; relaxin ; Relaxin - therapeutic use ; remodeling ; research-article ; TGF-β1 ; Treatment Outcome ; Ventricular Remodeling</subject><ispartof>Laboratory investigation, 2011-05, Vol.91 (5), p.675-690</ispartof><rights>2011 United States & Canadian Academy of Pathology</rights><rights>United States and Canadian Academy of Pathology, Inc. 2011</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group May 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c500t-fa4598c733b59213ef9335896cb3b0a8077776ad1b2d045d817e38deca5f73223</citedby><cites>FETCH-LOGICAL-c500t-fa4598c733b59213ef9335896cb3b0a8077776ad1b2d045d817e38deca5f73223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24181324$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21221074$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Samuel, Chrishan S</creatorcontrib><creatorcontrib>Cendrawan, Sofia</creatorcontrib><creatorcontrib>Gao, Xiao-Ming</creatorcontrib><creatorcontrib>Ming, Ziqiu</creatorcontrib><creatorcontrib>Zhao, Chongxin</creatorcontrib><creatorcontrib>Kiriazis, Helen</creatorcontrib><creatorcontrib>Xu, Qi</creatorcontrib><creatorcontrib>Tregear, Geoffrey W</creatorcontrib><creatorcontrib>Bathgate, Ross A D</creatorcontrib><creatorcontrib>Du, Xiao-Jun</creatorcontrib><title>Relaxin remodels fibrotic healing following myocardial infarction</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>In the setting of myocardial infarction (MI), implanted stem cell viability is low and scar formation limits stem cell homing, viability, and integration. Thus, interventions that favorably remodel fibrotic healing may benefit stem cell therapies. However, it remains unclear whether it is feasible and safe to remodel fibrotic healing post-MI without compromising ventricular remodeling and dysfunction. This study, therefore, determined the anti-fibrotic and other effects of the hormone, relaxin in a mouse model of MI. Adult male mice underwent left coronary artery ligation-induced MI and were immediately treated with recombinant human relaxin (MI+RLX) or vehicle (MI+VEH) over 7 or 30 days, representing time points of early and mature fibrotic healing. Cardiac function was assessed by echocardiography and catheterization, while comprehensive immunohistochemistry, morphometry, and western blotting were performed to explore the relaxin-induced mechanisms of action post-MI. RLX significantly inhibited the MI-induced progression of cardiac fibrosis over 7 and 30 days, which was associated with a reduction in TGF-β1 expression, myofibroblast differentiation, and cardiomyocyte apoptosis in addition to a promotion of matrix metalloproteinase-13 levels and de novo blood vessel growth (all P<0.05 vs respective measurements from MI+VEH mice). Despite the evident fibrotic healing post-MI, relaxin did not adversely affect the incidence of ventricular free-wall rupture or the extent of LV remodeling and dysfunction. These combined findings demonstrate that RLX favorably remodels the process of fibrotic healing post-infarction by lowering the density of mature scar tissue in the infarcted myocardium, border zone, and non-infarcted myocardium, and may, therefore, facilitate cell-based therapies in the setting of ischemic heart disease.</description><subject>631/136/16</subject><subject>692/699/75/2/1674</subject><subject>692/700/565/1331/238</subject><subject>angiogenesis</subject><subject>Animals</subject><subject>apoptosis</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Blotting, Western</subject><subject>cardiac fibrosis</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Fibrosis</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heart</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Laboratory Medicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Organ Size</subject><subject>Pathology</subject><subject>relaxin</subject><subject>Relaxin - therapeutic use</subject><subject>remodeling</subject><subject>research-article</subject><subject>TGF-β1</subject><subject>Treatment Outcome</subject><subject>Ventricular Remodeling</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kVtrHSEUhaW0NKdp_0AfwlAIfZrE6-hAXkLoDQKFkj6Lo9vE4Giic3L59_X0nCbQh_iiuL-1XXuJ0EeCjwhm6jiaKaQ7qMsRxZu7Ub1CKyIY7jHD8jVaYUxZPygm99C7Wq8xJpwP4i3ao4RSgiVfodNfEM1DSF2BOTuItfNhKnkJtrsCE0O67HyOMd9vTvNjtqa4YGIXkjfFLiGn9-iNN7HCh92-j35__XJx9r0___ntx9npeW8FxkvvDRejspKxSYyUMPAjY0KNg53YhI3Csq3BODJRh7lwikhgyoE1wktGKdtHn7d9b0q-Xbep9RyqhRhNgryuWg2cjGSkvJGf_iOv87qkZq5BTErFBWkQ3UK25FoLeH1TwmzKoyZYb-LVT_HqTby6xdtEB7vO62kG9yT5l2cDDneAqdZEX0yyoT5znCjC_lpkW662UrqE8mzxxedPtqr2T3AXmqraAMmCCwXsol0OL8n_ALQBqto</recordid><startdate>20110501</startdate><enddate>20110501</enddate><creator>Samuel, Chrishan S</creator><creator>Cendrawan, Sofia</creator><creator>Gao, Xiao-Ming</creator><creator>Ming, Ziqiu</creator><creator>Zhao, Chongxin</creator><creator>Kiriazis, Helen</creator><creator>Xu, Qi</creator><creator>Tregear, Geoffrey W</creator><creator>Bathgate, Ross A D</creator><creator>Du, Xiao-Jun</creator><general>Elsevier Inc</general><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</scope><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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20110501</creationdate><title>Relaxin remodels fibrotic healing following myocardial infarction</title><author>Samuel, Chrishan S ; Cendrawan, Sofia ; Gao, Xiao-Ming ; Ming, Ziqiu ; Zhao, Chongxin ; Kiriazis, Helen ; Xu, Qi ; Tregear, Geoffrey W ; Bathgate, Ross A D ; Du, Xiao-Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c500t-fa4598c733b59213ef9335896cb3b0a8077776ad1b2d045d817e38deca5f73223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>631/136/16</topic><topic>692/699/75/2/1674</topic><topic>692/700/565/1331/238</topic><topic>angiogenesis</topic><topic>Animals</topic><topic>apoptosis</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Blotting, Western</topic><topic>cardiac fibrosis</topic><topic>Cardiology. 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Academic</collection><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Samuel, Chrishan S</au><au>Cendrawan, Sofia</au><au>Gao, Xiao-Ming</au><au>Ming, Ziqiu</au><au>Zhao, Chongxin</au><au>Kiriazis, Helen</au><au>Xu, Qi</au><au>Tregear, Geoffrey W</au><au>Bathgate, Ross A D</au><au>Du, Xiao-Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relaxin remodels fibrotic healing following myocardial infarction</atitle><jtitle>Laboratory investigation</jtitle><stitle>Lab Invest</stitle><addtitle>Lab Invest</addtitle><date>2011-05-01</date><risdate>2011</risdate><volume>91</volume><issue>5</issue><spage>675</spage><epage>690</epage><pages>675-690</pages><issn>0023-6837</issn><eissn>1530-0307</eissn><coden>LAINAW</coden><abstract>In the setting of myocardial infarction (MI), implanted stem cell viability is low and scar formation limits stem cell homing, viability, and integration. Thus, interventions that favorably remodel fibrotic healing may benefit stem cell therapies. However, it remains unclear whether it is feasible and safe to remodel fibrotic healing post-MI without compromising ventricular remodeling and dysfunction. This study, therefore, determined the anti-fibrotic and other effects of the hormone, relaxin in a mouse model of MI. Adult male mice underwent left coronary artery ligation-induced MI and were immediately treated with recombinant human relaxin (MI+RLX) or vehicle (MI+VEH) over 7 or 30 days, representing time points of early and mature fibrotic healing. Cardiac function was assessed by echocardiography and catheterization, while comprehensive immunohistochemistry, morphometry, and western blotting were performed to explore the relaxin-induced mechanisms of action post-MI. RLX significantly inhibited the MI-induced progression of cardiac fibrosis over 7 and 30 days, which was associated with a reduction in TGF-β1 expression, myofibroblast differentiation, and cardiomyocyte apoptosis in addition to a promotion of matrix metalloproteinase-13 levels and de novo blood vessel growth (all P<0.05 vs respective measurements from MI+VEH mice). Despite the evident fibrotic healing post-MI, relaxin did not adversely affect the incidence of ventricular free-wall rupture or the extent of LV remodeling and dysfunction. These combined findings demonstrate that RLX favorably remodels the process of fibrotic healing post-infarction by lowering the density of mature scar tissue in the infarcted myocardium, border zone, and non-infarcted myocardium, and may, therefore, facilitate cell-based therapies in the setting of ischemic heart disease.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>21221074</pmid><doi>10.1038/labinvest.2010.198</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/136/16 692/699/75/2/1674 692/700/565/1331/238 angiogenesis Animals apoptosis Biological and medical sciences Biotechnology Blotting, Western cardiac fibrosis Cardiology. Vascular system Coronary heart disease Fibrosis Fundamental and applied biological sciences. Psychology Heart Investigative techniques, diagnostic techniques (general aspects) Laboratory Medicine Male Medical sciences Medicine Medicine & Public Health Mice Mice, Inbred C57BL Myocardial Infarction - drug therapy Myocardial Infarction - physiopathology Organ Size Pathology relaxin Relaxin - therapeutic use remodeling research-article TGF-β1 Treatment Outcome Ventricular Remodeling |
| title | Relaxin remodels fibrotic healing following myocardial infarction |
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