AntimiR-132 Attenuates Myocardial Hypertrophy in an Animal Model of Percutaneous Aortic Constriction
Pathological cardiac hypertrophy is a result of afterload-increasing pathologies including untreated hypertension and aortic stenosis. It features progressive adverse cardiac remodeling, myocardial dysfunction, capillary rarefaction, and interstitial fibrosis often leading to heart failure. This stu...
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| Veröffentlicht in: | Journal of the American College of Cardiology 2021-06, Vol.77 (23), p.2923-2935 |
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| creator | Hinkel, Rabea Batkai, Sandor Bähr, Andrea Bozoglu, Tarik Straub, Sarah Borchert, Tobias Viereck, Janika Howe, Andrea Hornaschewitz, Nadja Oberberger, Lisa Jurisch, Victoria Kozlik-Feldmann, Rainer Freudenthal, Franz Ziegler, Tilman Weber, Christian Sperandio, Markus Engelhardt, Stefan Laugwitz, Karl Ludwig Moretti, Alessandra Klymiuk, Nik Thum, Thomas Kupatt, Christian |
| description | Pathological cardiac hypertrophy is a result of afterload-increasing pathologies including untreated hypertension and aortic stenosis. It features progressive adverse cardiac remodeling, myocardial dysfunction, capillary rarefaction, and interstitial fibrosis often leading to heart failure.
This study aimed to establish a novel porcine model of pressure-overload-induced heart failure and to determine the effect of inhibition of microribonucleic acid 132 (miR-132) on heart failure development in this model.
This study developed a novel porcine model of percutaneous aortic constriction by implantation of a percutaneous reduction stent in the thoracic aorta, inducing progressive remodeling at day 56 (d56) after pressure-overload induction. In this study, an antisense oligonucleotide specifically inhibiting miR-132 (antimiR-132), was regionally applied via intracoronary injection at d0 (percutaneous transverse aortic constriction induction) and d28.
At d56, antimiR-132 treatment diminished cardiomyocyte cross-sectional area (188.9 ± 2.8 vs. 258.4 ± 9.0 μm
in untreated hypertrophic hearts) and improved global cardiac function (ejection fraction 48.9 ± 1.0% vs. 36.1 ± 1.7% in control hearts). Moreover, at d56 antimiR-132-treated hearts displayed less increase of interstitial fibrosis compared with sham-operated hearts (Δsham 1.8 ± 0.5%) than control hearts (Δsham 10.8 ± 0.6%). Of note, cardiac platelet and endothelial cell adhesion molecule 1
capillary density was higher in the antimiR-132-treated hearts (647 ± 20 cells/mm
) compared with in the control group (485 ± 23 cells/mm
).
The inhibition of miR-132 is a valid strategy in prevention of heart failure progression in hypertrophic heart disease and may be developed as a treatment for heart failure of nonischemic origin. |
| doi_str_mv | 10.1016/j.jacc.2021.04.028 |
| format | Article |
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This study aimed to establish a novel porcine model of pressure-overload-induced heart failure and to determine the effect of inhibition of microribonucleic acid 132 (miR-132) on heart failure development in this model.
This study developed a novel porcine model of percutaneous aortic constriction by implantation of a percutaneous reduction stent in the thoracic aorta, inducing progressive remodeling at day 56 (d56) after pressure-overload induction. In this study, an antisense oligonucleotide specifically inhibiting miR-132 (antimiR-132), was regionally applied via intracoronary injection at d0 (percutaneous transverse aortic constriction induction) and d28.
At d56, antimiR-132 treatment diminished cardiomyocyte cross-sectional area (188.9 ± 2.8 vs. 258.4 ± 9.0 μm
in untreated hypertrophic hearts) and improved global cardiac function (ejection fraction 48.9 ± 1.0% vs. 36.1 ± 1.7% in control hearts). Moreover, at d56 antimiR-132-treated hearts displayed less increase of interstitial fibrosis compared with sham-operated hearts (Δsham 1.8 ± 0.5%) than control hearts (Δsham 10.8 ± 0.6%). Of note, cardiac platelet and endothelial cell adhesion molecule 1
capillary density was higher in the antimiR-132-treated hearts (647 ± 20 cells/mm
) compared with in the control group (485 ± 23 cells/mm
).
The inhibition of miR-132 is a valid strategy in prevention of heart failure progression in hypertrophic heart disease and may be developed as a treatment for heart failure of nonischemic origin.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2021.04.028</identifier><identifier>PMID: 34112319</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Antagomirs - administration & dosage ; Aorta, Thoracic - surgery ; Aortic Diseases - complications ; Cardiomegaly - complications ; Cardiomegaly - diagnosis ; Cardiomegaly - drug therapy ; Constriction ; Constriction, Pathologic - complications ; Coronary Vessels ; Disease Models, Animal ; Heart Failure - etiology ; Heart Failure - physiopathology ; Heart Failure - prevention & control ; Injections, Intra-Arterial ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Stents - adverse effects ; Swine ; Treatment Outcome ; Ventricular Remodeling - drug effects</subject><ispartof>Journal of the American College of Cardiology, 2021-06, Vol.77 (23), p.2923-2935</ispartof><rights>Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-940cbb488692b3f3699f1e27b7014604e675f9a1e40e8a06ed773111e7241ae43</citedby><cites>FETCH-LOGICAL-c413t-940cbb488692b3f3699f1e27b7014604e675f9a1e40e8a06ed773111e7241ae43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34112319$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hinkel, Rabea</creatorcontrib><creatorcontrib>Batkai, Sandor</creatorcontrib><creatorcontrib>Bähr, Andrea</creatorcontrib><creatorcontrib>Bozoglu, Tarik</creatorcontrib><creatorcontrib>Straub, Sarah</creatorcontrib><creatorcontrib>Borchert, Tobias</creatorcontrib><creatorcontrib>Viereck, Janika</creatorcontrib><creatorcontrib>Howe, Andrea</creatorcontrib><creatorcontrib>Hornaschewitz, Nadja</creatorcontrib><creatorcontrib>Oberberger, Lisa</creatorcontrib><creatorcontrib>Jurisch, Victoria</creatorcontrib><creatorcontrib>Kozlik-Feldmann, Rainer</creatorcontrib><creatorcontrib>Freudenthal, Franz</creatorcontrib><creatorcontrib>Ziegler, Tilman</creatorcontrib><creatorcontrib>Weber, Christian</creatorcontrib><creatorcontrib>Sperandio, Markus</creatorcontrib><creatorcontrib>Engelhardt, Stefan</creatorcontrib><creatorcontrib>Laugwitz, Karl Ludwig</creatorcontrib><creatorcontrib>Moretti, Alessandra</creatorcontrib><creatorcontrib>Klymiuk, Nik</creatorcontrib><creatorcontrib>Thum, Thomas</creatorcontrib><creatorcontrib>Kupatt, Christian</creatorcontrib><title>AntimiR-132 Attenuates Myocardial Hypertrophy in an Animal Model of Percutaneous Aortic Constriction</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>Pathological cardiac hypertrophy is a result of afterload-increasing pathologies including untreated hypertension and aortic stenosis. It features progressive adverse cardiac remodeling, myocardial dysfunction, capillary rarefaction, and interstitial fibrosis often leading to heart failure.
This study aimed to establish a novel porcine model of pressure-overload-induced heart failure and to determine the effect of inhibition of microribonucleic acid 132 (miR-132) on heart failure development in this model.
This study developed a novel porcine model of percutaneous aortic constriction by implantation of a percutaneous reduction stent in the thoracic aorta, inducing progressive remodeling at day 56 (d56) after pressure-overload induction. In this study, an antisense oligonucleotide specifically inhibiting miR-132 (antimiR-132), was regionally applied via intracoronary injection at d0 (percutaneous transverse aortic constriction induction) and d28.
At d56, antimiR-132 treatment diminished cardiomyocyte cross-sectional area (188.9 ± 2.8 vs. 258.4 ± 9.0 μm
in untreated hypertrophic hearts) and improved global cardiac function (ejection fraction 48.9 ± 1.0% vs. 36.1 ± 1.7% in control hearts). Moreover, at d56 antimiR-132-treated hearts displayed less increase of interstitial fibrosis compared with sham-operated hearts (Δsham 1.8 ± 0.5%) than control hearts (Δsham 10.8 ± 0.6%). Of note, cardiac platelet and endothelial cell adhesion molecule 1
capillary density was higher in the antimiR-132-treated hearts (647 ± 20 cells/mm
) compared with in the control group (485 ± 23 cells/mm
).
The inhibition of miR-132 is a valid strategy in prevention of heart failure progression in hypertrophic heart disease and may be developed as a treatment for heart failure of nonischemic origin.</description><subject>Animals</subject><subject>Antagomirs - administration & dosage</subject><subject>Aorta, Thoracic - surgery</subject><subject>Aortic Diseases - complications</subject><subject>Cardiomegaly - complications</subject><subject>Cardiomegaly - diagnosis</subject><subject>Cardiomegaly - drug therapy</subject><subject>Constriction</subject><subject>Constriction, Pathologic - complications</subject><subject>Coronary Vessels</subject><subject>Disease Models, Animal</subject><subject>Heart Failure - etiology</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Failure - prevention & control</subject><subject>Injections, Intra-Arterial</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Stents - adverse effects</subject><subject>Swine</subject><subject>Treatment Outcome</subject><subject>Ventricular Remodeling - drug effects</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kEFv1DAQhS0EotvCH-CAfOSSdMZ24vgYrWiL1AqEytlynInwKhsvtnPYf99dbcvpHea9p3kfY18QagRsb3f1znlfCxBYg6pBdO_YBpumq2Rj9Hu2AS2bCsHoK3ad8w4A2g7NR3YlFaKQaDZs7JcS9uF3hVLwvhRaVlco86dj9C6Nwc384XigVFI8_D3ysHC38H4J-9PhKY408zjxX5T8WtxCcc28j6kEz7dxySUFX0JcPrEPk5szfX7VG_bn7vvz9qF6_Hn_Y9s_Vl6hLJVR4IdBdV1rxCAn2RozIQk9aEDVgqJWN5NxSAqoc9DSqLVERNJCoSMlb9i3S-8hxX8r5WL3IXua58trVjQKGtQdnq3iYvUp5pxosod0GpWOFsGe6dqdPdO1Z7oWlD3RPYW-vvavw57G_5E3nPIFT8p2Cw</recordid><startdate>20210615</startdate><enddate>20210615</enddate><creator>Hinkel, Rabea</creator><creator>Batkai, Sandor</creator><creator>Bähr, Andrea</creator><creator>Bozoglu, Tarik</creator><creator>Straub, Sarah</creator><creator>Borchert, Tobias</creator><creator>Viereck, Janika</creator><creator>Howe, Andrea</creator><creator>Hornaschewitz, Nadja</creator><creator>Oberberger, Lisa</creator><creator>Jurisch, Victoria</creator><creator>Kozlik-Feldmann, Rainer</creator><creator>Freudenthal, Franz</creator><creator>Ziegler, Tilman</creator><creator>Weber, Christian</creator><creator>Sperandio, Markus</creator><creator>Engelhardt, Stefan</creator><creator>Laugwitz, Karl Ludwig</creator><creator>Moretti, Alessandra</creator><creator>Klymiuk, Nik</creator><creator>Thum, Thomas</creator><creator>Kupatt, Christian</creator><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>20210615</creationdate><title>AntimiR-132 Attenuates Myocardial Hypertrophy in an Animal Model of Percutaneous Aortic Constriction</title><author>Hinkel, Rabea ; Batkai, Sandor ; Bähr, Andrea ; Bozoglu, Tarik ; Straub, Sarah ; Borchert, Tobias ; Viereck, Janika ; Howe, Andrea ; Hornaschewitz, Nadja ; Oberberger, Lisa ; Jurisch, Victoria ; Kozlik-Feldmann, Rainer ; Freudenthal, Franz ; Ziegler, Tilman ; Weber, Christian ; Sperandio, Markus ; Engelhardt, Stefan ; Laugwitz, Karl Ludwig ; Moretti, Alessandra ; Klymiuk, Nik ; Thum, Thomas ; Kupatt, Christian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-940cbb488692b3f3699f1e27b7014604e675f9a1e40e8a06ed773111e7241ae43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Antagomirs - administration & dosage</topic><topic>Aorta, Thoracic - surgery</topic><topic>Aortic Diseases - complications</topic><topic>Cardiomegaly - complications</topic><topic>Cardiomegaly - diagnosis</topic><topic>Cardiomegaly - drug therapy</topic><topic>Constriction</topic><topic>Constriction, Pathologic - complications</topic><topic>Coronary Vessels</topic><topic>Disease Models, Animal</topic><topic>Heart Failure - etiology</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Failure - prevention & control</topic><topic>Injections, Intra-Arterial</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Stents - adverse effects</topic><topic>Swine</topic><topic>Treatment Outcome</topic><topic>Ventricular Remodeling - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hinkel, Rabea</creatorcontrib><creatorcontrib>Batkai, Sandor</creatorcontrib><creatorcontrib>Bähr, Andrea</creatorcontrib><creatorcontrib>Bozoglu, Tarik</creatorcontrib><creatorcontrib>Straub, Sarah</creatorcontrib><creatorcontrib>Borchert, Tobias</creatorcontrib><creatorcontrib>Viereck, Janika</creatorcontrib><creatorcontrib>Howe, Andrea</creatorcontrib><creatorcontrib>Hornaschewitz, Nadja</creatorcontrib><creatorcontrib>Oberberger, Lisa</creatorcontrib><creatorcontrib>Jurisch, Victoria</creatorcontrib><creatorcontrib>Kozlik-Feldmann, Rainer</creatorcontrib><creatorcontrib>Freudenthal, Franz</creatorcontrib><creatorcontrib>Ziegler, Tilman</creatorcontrib><creatorcontrib>Weber, Christian</creatorcontrib><creatorcontrib>Sperandio, Markus</creatorcontrib><creatorcontrib>Engelhardt, Stefan</creatorcontrib><creatorcontrib>Laugwitz, Karl Ludwig</creatorcontrib><creatorcontrib>Moretti, Alessandra</creatorcontrib><creatorcontrib>Klymiuk, Nik</creatorcontrib><creatorcontrib>Thum, Thomas</creatorcontrib><creatorcontrib>Kupatt, Christian</creatorcontrib><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>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hinkel, Rabea</au><au>Batkai, Sandor</au><au>Bähr, Andrea</au><au>Bozoglu, Tarik</au><au>Straub, Sarah</au><au>Borchert, Tobias</au><au>Viereck, Janika</au><au>Howe, Andrea</au><au>Hornaschewitz, Nadja</au><au>Oberberger, Lisa</au><au>Jurisch, Victoria</au><au>Kozlik-Feldmann, Rainer</au><au>Freudenthal, Franz</au><au>Ziegler, Tilman</au><au>Weber, Christian</au><au>Sperandio, Markus</au><au>Engelhardt, Stefan</au><au>Laugwitz, Karl Ludwig</au><au>Moretti, Alessandra</au><au>Klymiuk, Nik</au><au>Thum, Thomas</au><au>Kupatt, Christian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AntimiR-132 Attenuates Myocardial Hypertrophy in an Animal Model of Percutaneous Aortic Constriction</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2021-06-15</date><risdate>2021</risdate><volume>77</volume><issue>23</issue><spage>2923</spage><epage>2935</epage><pages>2923-2935</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><abstract>Pathological cardiac hypertrophy is a result of afterload-increasing pathologies including untreated hypertension and aortic stenosis. It features progressive adverse cardiac remodeling, myocardial dysfunction, capillary rarefaction, and interstitial fibrosis often leading to heart failure.
This study aimed to establish a novel porcine model of pressure-overload-induced heart failure and to determine the effect of inhibition of microribonucleic acid 132 (miR-132) on heart failure development in this model.
This study developed a novel porcine model of percutaneous aortic constriction by implantation of a percutaneous reduction stent in the thoracic aorta, inducing progressive remodeling at day 56 (d56) after pressure-overload induction. In this study, an antisense oligonucleotide specifically inhibiting miR-132 (antimiR-132), was regionally applied via intracoronary injection at d0 (percutaneous transverse aortic constriction induction) and d28.
At d56, antimiR-132 treatment diminished cardiomyocyte cross-sectional area (188.9 ± 2.8 vs. 258.4 ± 9.0 μm
in untreated hypertrophic hearts) and improved global cardiac function (ejection fraction 48.9 ± 1.0% vs. 36.1 ± 1.7% in control hearts). Moreover, at d56 antimiR-132-treated hearts displayed less increase of interstitial fibrosis compared with sham-operated hearts (Δsham 1.8 ± 0.5%) than control hearts (Δsham 10.8 ± 0.6%). Of note, cardiac platelet and endothelial cell adhesion molecule 1
capillary density was higher in the antimiR-132-treated hearts (647 ± 20 cells/mm
) compared with in the control group (485 ± 23 cells/mm
).
The inhibition of miR-132 is a valid strategy in prevention of heart failure progression in hypertrophic heart disease and may be developed as a treatment for heart failure of nonischemic origin.</abstract><cop>United States</cop><pmid>34112319</pmid><doi>10.1016/j.jacc.2021.04.028</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Access via ScienceDirect (Elsevier); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Antagomirs - administration & dosage Aorta, Thoracic - surgery Aortic Diseases - complications Cardiomegaly - complications Cardiomegaly - diagnosis Cardiomegaly - drug therapy Constriction Constriction, Pathologic - complications Coronary Vessels Disease Models, Animal Heart Failure - etiology Heart Failure - physiopathology Heart Failure - prevention & control Injections, Intra-Arterial MicroRNAs - antagonists & inhibitors MicroRNAs - genetics MicroRNAs - metabolism Stents - adverse effects Swine Treatment Outcome Ventricular Remodeling - drug effects |
| title | AntimiR-132 Attenuates Myocardial Hypertrophy in an Animal Model of Percutaneous Aortic Constriction |
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