Hypercholesterolemia affects cardiac function, infarct size and inflammation in APOE3-Leiden mice following myocardial ischemia-reperfusion injury
Hypercholesterolemia is a major risk factor for ischemic heart disease including acute myocardial infarction. However, long-term effects of hypercholesterolemia in a rodent myocardial ischemia-reperfusion injury model are unknown. Therefore, the effects of diet-induced hypercholesterolemia on cardia...
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| Veröffentlicht in: | PloS one 2019-06, Vol.14 (6), p.e0217582-e0217582 |
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| creator | Pluijmert, Niek J den Haan, Melina C van Zuylen, Vanessa L Steendijk, Paul de Boer, Hetty C van Zonneveld, Anton J Fibbe, Willem E Schalij, Martin J Quax, Paul H A Atsma, Douwe E |
| description | Hypercholesterolemia is a major risk factor for ischemic heart disease including acute myocardial infarction. However, long-term effects of hypercholesterolemia in a rodent myocardial ischemia-reperfusion injury model are unknown. Therefore, the effects of diet-induced hypercholesterolemia on cardiac function and remodeling were investigated up to eight weeks after myocardial ischemia-reperfusion (MI-R) injury which was induced in either normocholesterolemic (NC-MI) or hypercholesterolemic (HC-MI) APOE*3-Leiden mice.
Left ventricular (LV) dimensions were serially assessed using parasternal long-axis echocardiography followed by LV pressure-volume measurements. Subsequently, infarct size and the inflammatory response were analyzed by histology and fluorescence-activated cell sorting (FACS) analysis.
Intrinsic LV function eight weeks after MI-R was significantly impaired in HC-MI compared to NC-MI mice as assessed by end-systolic pressure, dP/dtMAX, and -dP/dtMIN. Paradoxically, infarct size was significantly decreased in HC-MI compared to NC-MI mice, accompanied by an increased wall thickness. Hypercholesterolemia caused a pre-ischemic peripheral monocytosis, in particular of Ly-6Chi monocytes whereas accumulation of macrophages in the ischemic-reperfused myocardium of HC-MI mice was decreased.
Diet-induced hypercholesterolemia caused impaired LV function eight weeks after MI-R injury despite a reduced post-ischemic infarct size. This was preceded by a pre-ischemic peripheral monocytosis, while there was a suppressed accumulation of inflammatory cells in the ischemic-reperfused myocardium after eight weeks. This experimental model using hypercholesterolemic APOE*3-Leiden mice exposed to MI-R seems suitable to study novel cardioprotective therapies in a more clinically relevant animal model. |
| doi_str_mv | 10.1371/journal.pone.0217582 |
| format | Article |
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Left ventricular (LV) dimensions were serially assessed using parasternal long-axis echocardiography followed by LV pressure-volume measurements. Subsequently, infarct size and the inflammatory response were analyzed by histology and fluorescence-activated cell sorting (FACS) analysis.
Intrinsic LV function eight weeks after MI-R was significantly impaired in HC-MI compared to NC-MI mice as assessed by end-systolic pressure, dP/dtMAX, and -dP/dtMIN. Paradoxically, infarct size was significantly decreased in HC-MI compared to NC-MI mice, accompanied by an increased wall thickness. Hypercholesterolemia caused a pre-ischemic peripheral monocytosis, in particular of Ly-6Chi monocytes whereas accumulation of macrophages in the ischemic-reperfused myocardium of HC-MI mice was decreased.
Diet-induced hypercholesterolemia caused impaired LV function eight weeks after MI-R injury despite a reduced post-ischemic infarct size. This was preceded by a pre-ischemic peripheral monocytosis, while there was a suppressed accumulation of inflammatory cells in the ischemic-reperfused myocardium after eight weeks. This experimental model using hypercholesterolemic APOE*3-Leiden mice exposed to MI-R seems suitable to study novel cardioprotective therapies in a more clinically relevant animal model.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0217582</identifier><identifier>PMID: 31199833</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Accumulation ; Animal models ; Animals ; Apolipoprotein E ; Apolipoprotein E3 - genetics ; Apolipoprotein E3 - metabolism ; Apolipoproteins ; Atherosclerosis ; Biology and Life Sciences ; Blood pressure ; Cardiac function ; Cardiology ; Cardiovascular disease ; Cardiovascular diseases ; Cholesterol ; Complications and side effects ; Coronary artery disease ; Diet ; Echocardiography ; Female ; Flow cytometry ; Fluorescence ; Health risks ; Heart ; Heart attack ; Heart attacks ; Heart diseases ; Heart Ventricles - metabolism ; Heart Ventricles - pathology ; Heart Ventricles - physiopathology ; Histology ; Hypercholesterolemia ; Hypercholesterolemia - genetics ; Hypercholesterolemia - metabolism ; Hypercholesterolemia - pathology ; Hypercholesterolemia - physiopathology ; Inflammation ; Inflammation - genetics ; Inflammation - metabolism ; Inflammation - pathology ; Inflammation - physiopathology ; Inflammatory response ; Injury prevention ; Ischemia ; Laboratory animals ; Lipids ; Lipoproteins ; Long-term effects ; Ly-6 antigen ; Macrophages ; Medical research ; Medicine and Health Sciences ; Mice ; Mice, Transgenic ; Monocytes ; Monocytosis ; Myocardial infarction ; Myocardial ischemia ; Myocardial Reperfusion Injury - genetics ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - physiopathology ; Myocardium ; Nephrology ; Neutrophils ; Pulmonary arteries ; Reperfusion ; Reperfusion injury ; Research and Analysis Methods ; Risk analysis ; Risk factors ; Rodents ; Studies ; Surgery ; Systolic pressure ; Time Factors ; Transgenic animals ; Ventricle ; Ventricular Function, Left ; Wall thickness</subject><ispartof>PloS one, 2019-06, Vol.14 (6), p.e0217582-e0217582</ispartof><rights>COPYRIGHT 2019 Public Library of Science</rights><rights>2019 Pluijmert et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 Pluijmert et al 2019 Pluijmert et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-bb173c622d256ec0ce6eff8ddb7007a1d34e5e31185bc9f568aeda0e72a936683</citedby><cites>FETCH-LOGICAL-c692t-bb173c622d256ec0ce6eff8ddb7007a1d34e5e31185bc9f568aeda0e72a936683</cites><orcidid>0000-0002-7251-5244</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6570022/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6570022/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31199833$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pluijmert, Niek J</creatorcontrib><creatorcontrib>den Haan, Melina C</creatorcontrib><creatorcontrib>van Zuylen, Vanessa L</creatorcontrib><creatorcontrib>Steendijk, Paul</creatorcontrib><creatorcontrib>de Boer, Hetty C</creatorcontrib><creatorcontrib>van Zonneveld, Anton J</creatorcontrib><creatorcontrib>Fibbe, Willem E</creatorcontrib><creatorcontrib>Schalij, Martin J</creatorcontrib><creatorcontrib>Quax, Paul H A</creatorcontrib><creatorcontrib>Atsma, Douwe E</creatorcontrib><title>Hypercholesterolemia affects cardiac function, infarct size and inflammation in APOE3-Leiden mice following myocardial ischemia-reperfusion injury</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Hypercholesterolemia is a major risk factor for ischemic heart disease including acute myocardial infarction. However, long-term effects of hypercholesterolemia in a rodent myocardial ischemia-reperfusion injury model are unknown. Therefore, the effects of diet-induced hypercholesterolemia on cardiac function and remodeling were investigated up to eight weeks after myocardial ischemia-reperfusion (MI-R) injury which was induced in either normocholesterolemic (NC-MI) or hypercholesterolemic (HC-MI) APOE*3-Leiden mice.
Left ventricular (LV) dimensions were serially assessed using parasternal long-axis echocardiography followed by LV pressure-volume measurements. Subsequently, infarct size and the inflammatory response were analyzed by histology and fluorescence-activated cell sorting (FACS) analysis.
Intrinsic LV function eight weeks after MI-R was significantly impaired in HC-MI compared to NC-MI mice as assessed by end-systolic pressure, dP/dtMAX, and -dP/dtMIN. Paradoxically, infarct size was significantly decreased in HC-MI compared to NC-MI mice, accompanied by an increased wall thickness. Hypercholesterolemia caused a pre-ischemic peripheral monocytosis, in particular of Ly-6Chi monocytes whereas accumulation of macrophages in the ischemic-reperfused myocardium of HC-MI mice was decreased.
Diet-induced hypercholesterolemia caused impaired LV function eight weeks after MI-R injury despite a reduced post-ischemic infarct size. This was preceded by a pre-ischemic peripheral monocytosis, while there was a suppressed accumulation of inflammatory cells in the ischemic-reperfused myocardium after eight weeks. This experimental model using hypercholesterolemic APOE*3-Leiden mice exposed to MI-R seems suitable to study novel cardioprotective therapies in a more clinically relevant animal model.</description><subject>Accumulation</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apolipoprotein E</subject><subject>Apolipoprotein E3 - genetics</subject><subject>Apolipoprotein E3 - metabolism</subject><subject>Apolipoproteins</subject><subject>Atherosclerosis</subject><subject>Biology and Life Sciences</subject><subject>Blood pressure</subject><subject>Cardiac function</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cholesterol</subject><subject>Complications and side effects</subject><subject>Coronary artery disease</subject><subject>Diet</subject><subject>Echocardiography</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Fluorescence</subject><subject>Health risks</subject><subject>Heart</subject><subject>Heart attack</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Heart Ventricles - metabolism</subject><subject>Heart Ventricles - pathology</subject><subject>Heart Ventricles - physiopathology</subject><subject>Histology</subject><subject>Hypercholesterolemia</subject><subject>Hypercholesterolemia - genetics</subject><subject>Hypercholesterolemia - metabolism</subject><subject>Hypercholesterolemia - pathology</subject><subject>Hypercholesterolemia - physiopathology</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammation - physiopathology</subject><subject>Inflammatory response</subject><subject>Injury prevention</subject><subject>Ischemia</subject><subject>Laboratory animals</subject><subject>Lipids</subject><subject>Lipoproteins</subject><subject>Long-term effects</subject><subject>Ly-6 antigen</subject><subject>Macrophages</subject><subject>Medical research</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Monocytes</subject><subject>Monocytosis</subject><subject>Myocardial infarction</subject><subject>Myocardial ischemia</subject><subject>Myocardial Reperfusion Injury - genetics</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Myocardium</subject><subject>Nephrology</subject><subject>Neutrophils</subject><subject>Pulmonary arteries</subject><subject>Reperfusion</subject><subject>Reperfusion injury</subject><subject>Research and Analysis Methods</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Studies</subject><subject>Surgery</subject><subject>Systolic pressure</subject><subject>Time Factors</subject><subject>Transgenic animals</subject><subject>Ventricle</subject><subject>Ventricular Function, Left</subject><subject>Wall thickness</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk92K1DAUx4so7jr6BqIFQRTsmCZN2t4Iw7K6AwMjft2GND2ZyZA2Y9Kq42P4xKY73WUqeyG9SHvyO__T8xVFT1M0T0mevt3Z3rXCzPe2hTnCaU4LfC86T0uCE4YRuX_yfhY98n6HECUFYw-jM5KmZVkQch79uTrswcmtNeA7cOFotIiFUiA7H0vhai1krPpWdtq2b2LdKuFkF3v9G2LR1oPBiKYRw3X4iBcf15ckWYGuoY0bLSFW1hj7U7ebuDnYo6KJtZfbIVTiIMRXvT-673p3eBw9UMJ4eDKes-jr-8svF1fJav1hebFYJZKVuEuqKs2JZBjXmDKQSAIDpYq6rnKEcpHWJAMKIdOCVrJUlBUCaoEgx6IkjBVkFj0_6u6N9Xwsp-cYZ4gEBcQCsTwStRU7vne6Ee7ArdD82mDdhgvXaWmA0ypLgYVATNIsA1HQvKqLjGWsIhIyGrTejdH6qoFaQts5YSai05tWb_nG_uCMhnwwDgKvRgFnv_ehW7wJRQRjRAu2v_5vyrIyR3lAX_yD3p3dSG1ESCD00Ya4chDlC1qUKMfDjMyi-R1UeOrQPhlmT-lgnzi8njgEpoNf3Ub03vPl50__z66_TdmXJ-wWhOm23pp-GDw_BbMjKJ313oG6LXKK-LA6N9Xgw-rwcXWC27PTBt063ewK-QsT8Bcn</recordid><startdate>20190614</startdate><enddate>20190614</enddate><creator>Pluijmert, 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Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pluijmert, Niek J</au><au>den Haan, Melina C</au><au>van Zuylen, Vanessa L</au><au>Steendijk, Paul</au><au>de Boer, Hetty C</au><au>van Zonneveld, Anton J</au><au>Fibbe, Willem E</au><au>Schalij, Martin J</au><au>Quax, Paul H A</au><au>Atsma, Douwe E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypercholesterolemia affects cardiac function, infarct size and inflammation in APOE3-Leiden mice following myocardial ischemia-reperfusion injury</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2019-06-14</date><risdate>2019</risdate><volume>14</volume><issue>6</issue><spage>e0217582</spage><epage>e0217582</epage><pages>e0217582-e0217582</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Hypercholesterolemia is a major risk factor for ischemic heart disease including acute myocardial infarction. However, long-term effects of hypercholesterolemia in a rodent myocardial ischemia-reperfusion injury model are unknown. Therefore, the effects of diet-induced hypercholesterolemia on cardiac function and remodeling were investigated up to eight weeks after myocardial ischemia-reperfusion (MI-R) injury which was induced in either normocholesterolemic (NC-MI) or hypercholesterolemic (HC-MI) APOE*3-Leiden mice.
Left ventricular (LV) dimensions were serially assessed using parasternal long-axis echocardiography followed by LV pressure-volume measurements. Subsequently, infarct size and the inflammatory response were analyzed by histology and fluorescence-activated cell sorting (FACS) analysis.
Intrinsic LV function eight weeks after MI-R was significantly impaired in HC-MI compared to NC-MI mice as assessed by end-systolic pressure, dP/dtMAX, and -dP/dtMIN. Paradoxically, infarct size was significantly decreased in HC-MI compared to NC-MI mice, accompanied by an increased wall thickness. Hypercholesterolemia caused a pre-ischemic peripheral monocytosis, in particular of Ly-6Chi monocytes whereas accumulation of macrophages in the ischemic-reperfused myocardium of HC-MI mice was decreased.
Diet-induced hypercholesterolemia caused impaired LV function eight weeks after MI-R injury despite a reduced post-ischemic infarct size. This was preceded by a pre-ischemic peripheral monocytosis, while there was a suppressed accumulation of inflammatory cells in the ischemic-reperfused myocardium after eight weeks. This experimental model using hypercholesterolemic APOE*3-Leiden mice exposed to MI-R seems suitable to study novel cardioprotective therapies in a more clinically relevant animal model.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>31199833</pmid><doi>10.1371/journal.pone.0217582</doi><tpages>e0217582</tpages><orcidid>https://orcid.org/0000-0002-7251-5244</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2019-06, Vol.14 (6), p.e0217582-e0217582 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2240300706 |
| source | Electronic Journals Library; Public Library of Science (PLoS) Journals Open Access; MEDLINE; PubMed Central; Directory of Open Access Journals; Free Full-Text Journals in Chemistry |
| subjects | Accumulation Animal models Animals Apolipoprotein E Apolipoprotein E3 - genetics Apolipoprotein E3 - metabolism Apolipoproteins Atherosclerosis Biology and Life Sciences Blood pressure Cardiac function Cardiology Cardiovascular disease Cardiovascular diseases Cholesterol Complications and side effects Coronary artery disease Diet Echocardiography Female Flow cytometry Fluorescence Health risks Heart Heart attack Heart attacks Heart diseases Heart Ventricles - metabolism Heart Ventricles - pathology Heart Ventricles - physiopathology Histology Hypercholesterolemia Hypercholesterolemia - genetics Hypercholesterolemia - metabolism Hypercholesterolemia - pathology Hypercholesterolemia - physiopathology Inflammation Inflammation - genetics Inflammation - metabolism Inflammation - pathology Inflammation - physiopathology Inflammatory response Injury prevention Ischemia Laboratory animals Lipids Lipoproteins Long-term effects Ly-6 antigen Macrophages Medical research Medicine and Health Sciences Mice Mice, Transgenic Monocytes Monocytosis Myocardial infarction Myocardial ischemia Myocardial Reperfusion Injury - genetics Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - physiopathology Myocardium Nephrology Neutrophils Pulmonary arteries Reperfusion Reperfusion injury Research and Analysis Methods Risk analysis Risk factors Rodents Studies Surgery Systolic pressure Time Factors Transgenic animals Ventricle Ventricular Function, Left Wall thickness |
| title | Hypercholesterolemia affects cardiac function, infarct size and inflammation in APOE3-Leiden mice following myocardial ischemia-reperfusion injury |
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