Angiotensinase C mRNA and Protein Downregulations Are Involved in Ethanol-Deteriorated Left Ventricular Systolic Dysfunction in Spontaneously Hypertensive Rats
The influences of angiotensinase C on ethanol-induced left ventricular (LV) systolic function were assessed in spontaneously hypertensive rats (SHRs). SHRs were fed by a liquid diet with or without ethanol for 49 days. The normotensive Wistar Kyoto rats (WKY) were fed by the liquid diet without etha...
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| description | The influences of angiotensinase C on ethanol-induced left ventricular (LV) systolic function were assessed in spontaneously hypertensive rats (SHRs). SHRs were fed by a liquid diet with or without ethanol for 49 days. The normotensive Wistar Kyoto rats (WKY) were fed by the liquid diet without ethanol and used as control. We evaluated LV systolic function, angiotensinase C mRNA and protein expressions, activation of the renin-angiotensin system (RAS), and the gene expressions of LV collagen (Col) III a1 and matrix metalloproteinases- (MMP-) 9. Compared to the WKY, LV systolic dysfunction (expressed by decreased fractional shortening and ejection fraction) was observed in the SHRs before ethanol treatment and further deteriorated by ethanol treatment. In the ethanol-treated SHRs, the following were observed: downregulations of angiotensinase C mRNA and protein, increased RAS activity with low collagen production as evidenced by angiotensin II and angiotensin type 1 receptor (AT1R) protein upregulation, A T 1 a R mRNA downregulation, and an MMP-9 mRNA expression upregulation trend with the downregulation of Col III a1 mRNA expression in LV. We conclude that chronic ethanol regimen is sufficient to promote the enhanced RAS activity-induced decrease in the production of cardiac collagen via downregulated angiotensinase C, leading to the further deterioration of LV systolic dysfunction in SHRs. |
| doi_str_mv | 10.1155/2015/409350 |
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SHRs were fed by a liquid diet with or without ethanol for 49 days. The normotensive Wistar Kyoto rats (WKY) were fed by the liquid diet without ethanol and used as control. We evaluated LV systolic function, angiotensinase C mRNA and protein expressions, activation of the renin-angiotensin system (RAS), and the gene expressions of LV collagen (Col) III a1 and matrix metalloproteinases- (MMP-) 9. Compared to the WKY, LV systolic dysfunction (expressed by decreased fractional shortening and ejection fraction) was observed in the SHRs before ethanol treatment and further deteriorated by ethanol treatment. In the ethanol-treated SHRs, the following were observed: downregulations of angiotensinase C mRNA and protein, increased RAS activity with low collagen production as evidenced by angiotensin II and angiotensin type 1 receptor (AT1R) protein upregulation, A T 1 a R mRNA downregulation, and an MMP-9 mRNA expression upregulation trend with the downregulation of Col III a1 mRNA expression in LV. We conclude that chronic ethanol regimen is sufficient to promote the enhanced RAS activity-induced decrease in the production of cardiac collagen via downregulated angiotensinase C, leading to the further deterioration of LV systolic dysfunction in SHRs.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2015/409350</identifier><identifier>PMID: 26509155</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Angiotensin ; Animals ; Arterial Pressure ; Biomedical research ; Blood Pressure ; Carboxypeptidases - metabolism ; Collagen Type III - metabolism ; Disease Models, Animal ; Ethanol ; Ethanol - chemistry ; Gene Expression Regulation ; Genetic aspects ; Health aspects ; Heart attacks ; Heart Rate ; Heart Ventricles ; Hypertension ; Male ; Matrix Metalloproteinase 9 - metabolism ; Messenger RNA ; Methods ; Myocardium - pathology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Real-Time Polymerase Chain Reaction ; Receptor, Angiotensin, Type 1 - metabolism ; Renin-Angiotensin System ; RNA sequencing ; RNA, Messenger - metabolism ; Rodents ; Studies ; Systole - drug effects ; Ventricular Dysfunction, Left - chemically induced ; Ventricular Dysfunction, Left - metabolism</subject><ispartof>BioMed research international, 2015-01, Vol.2015 (2015), p.1-10</ispartof><rights>Copyright © 2015 Jinyao Liu et al.</rights><rights>COPYRIGHT 2015 John Wiley & Sons, Inc.</rights><rights>Copyright © 2015 Jinyao Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2015 Jinyao Liu et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-8e9b314a66be7de324c728e64fe3053b39df6bba76dd20586c437dfac8f0bc113</citedby><cites>FETCH-LOGICAL-c528t-8e9b314a66be7de324c728e64fe3053b39df6bba76dd20586c437dfac8f0bc113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609779/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609779/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26509155$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Jugdutt, Bodh I.</contributor><creatorcontrib>Liu, Jinyao</creatorcontrib><creatorcontrib>Fujimiya, Tatsuya</creatorcontrib><creatorcontrib>Hakucho, Ayako</creatorcontrib><title>Angiotensinase C mRNA and Protein Downregulations Are Involved in Ethanol-Deteriorated Left Ventricular Systolic Dysfunction in Spontaneously Hypertensive Rats</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>The influences of angiotensinase C on ethanol-induced left ventricular (LV) systolic function were assessed in spontaneously hypertensive rats (SHRs). SHRs were fed by a liquid diet with or without ethanol for 49 days. The normotensive Wistar Kyoto rats (WKY) were fed by the liquid diet without ethanol and used as control. We evaluated LV systolic function, angiotensinase C mRNA and protein expressions, activation of the renin-angiotensin system (RAS), and the gene expressions of LV collagen (Col) III a1 and matrix metalloproteinases- (MMP-) 9. Compared to the WKY, LV systolic dysfunction (expressed by decreased fractional shortening and ejection fraction) was observed in the SHRs before ethanol treatment and further deteriorated by ethanol treatment. In the ethanol-treated SHRs, the following were observed: downregulations of angiotensinase C mRNA and protein, increased RAS activity with low collagen production as evidenced by angiotensin II and angiotensin type 1 receptor (AT1R) protein upregulation, A T 1 a R mRNA downregulation, and an MMP-9 mRNA expression upregulation trend with the downregulation of Col III a1 mRNA expression in LV. We conclude that chronic ethanol regimen is sufficient to promote the enhanced RAS activity-induced decrease in the production of cardiac collagen via downregulated angiotensinase C, leading to the further deterioration of LV systolic dysfunction in SHRs.</description><subject>Angiotensin</subject><subject>Animals</subject><subject>Arterial Pressure</subject><subject>Biomedical research</subject><subject>Blood Pressure</subject><subject>Carboxypeptidases - metabolism</subject><subject>Collagen Type III - metabolism</subject><subject>Disease Models, Animal</subject><subject>Ethanol</subject><subject>Ethanol - chemistry</subject><subject>Gene Expression Regulation</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Heart attacks</subject><subject>Heart Rate</subject><subject>Heart Ventricles</subject><subject>Hypertension</subject><subject>Male</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Messenger RNA</subject><subject>Methods</subject><subject>Myocardium - pathology</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Renin-Angiotensin System</subject><subject>RNA sequencing</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Studies</subject><subject>Systole - drug effects</subject><subject>Ventricular Dysfunction, Left - chemically induced</subject><subject>Ventricular Dysfunction, Left - metabolism</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkk1vEzEQhlcIRKvSE3dkiQsChfp7dy9IUVJopQhQC1wtr3c2cbWxU9ubKr-Gv4qXlFA41RdbM8-8mhm_RfGS4PeECHFGMRFnHNdM4CfFMWWETyTh5OnhzdhRcRrjDc6nIhLX8nlxRKXAdS4_Ln5O3dL6BC5apyOgGVpffZ4i7Vr0NeS4dWju71yA5dDrZL2LaBoAXbqt77fQopw_TyvtfD-ZQ4JgfdApxxfQJfQDXArW5MqArncx-d4aNN_FbnBm1BqrrzfeJe3AD7HfoYvdBsLvbraArnSKL4pnne4jnN7fJ8X3j-ffZheTxZdPl7PpYmIErdKkgrrJ82opGyhbYJSbklYgeQcMC9awuu1k0-hSti3FopKGs7LttKk63BhC2EnxYa-7GZo1tGbsXPdqE-xah53y2qp_M86u1NJvFc8rLcs6C7y5Fwj-doCY1NpGA32_n02RUlSUSyGqR6C0oqIURGb09X_ojR-Cy5sYKVoJQTn7Sy11D8q6zucWzSiqplzkXyeMl5l6t6dM8DEG6A7TEaxGM6nRTGpvpky_eriQA_vHOhl4uwdW1rX6zj5ODTICnX4AZ6lSsF9d1d1O</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Liu, Jinyao</creator><creator>Fujimiya, Tatsuya</creator><creator>Hakucho, Ayako</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150101</creationdate><title>Angiotensinase C mRNA and Protein Downregulations Are Involved in Ethanol-Deteriorated Left Ventricular Systolic Dysfunction in Spontaneously Hypertensive Rats</title><author>Liu, Jinyao ; Fujimiya, Tatsuya ; Hakucho, Ayako</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c528t-8e9b314a66be7de324c728e64fe3053b39df6bba76dd20586c437dfac8f0bc113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Angiotensin</topic><topic>Animals</topic><topic>Arterial Pressure</topic><topic>Biomedical research</topic><topic>Blood Pressure</topic><topic>Carboxypeptidases - metabolism</topic><topic>Collagen Type III - metabolism</topic><topic>Disease Models, Animal</topic><topic>Ethanol</topic><topic>Ethanol - chemistry</topic><topic>Gene Expression Regulation</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Heart attacks</topic><topic>Heart Rate</topic><topic>Heart Ventricles</topic><topic>Hypertension</topic><topic>Male</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Messenger RNA</topic><topic>Methods</topic><topic>Myocardium - pathology</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Renin-Angiotensin System</topic><topic>RNA sequencing</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Studies</topic><topic>Systole - drug effects</topic><topic>Ventricular Dysfunction, Left - chemically induced</topic><topic>Ventricular Dysfunction, Left - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Jinyao</creatorcontrib><creatorcontrib>Fujimiya, Tatsuya</creatorcontrib><creatorcontrib>Hakucho, Ayako</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Jinyao</au><au>Fujimiya, Tatsuya</au><au>Hakucho, Ayako</au><au>Jugdutt, Bodh I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensinase C mRNA and Protein Downregulations Are Involved in Ethanol-Deteriorated Left Ventricular Systolic Dysfunction in Spontaneously Hypertensive Rats</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>2015</volume><issue>2015</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>The influences of angiotensinase C on ethanol-induced left ventricular (LV) systolic function were assessed in spontaneously hypertensive rats (SHRs). SHRs were fed by a liquid diet with or without ethanol for 49 days. The normotensive Wistar Kyoto rats (WKY) were fed by the liquid diet without ethanol and used as control. We evaluated LV systolic function, angiotensinase C mRNA and protein expressions, activation of the renin-angiotensin system (RAS), and the gene expressions of LV collagen (Col) III a1 and matrix metalloproteinases- (MMP-) 9. Compared to the WKY, LV systolic dysfunction (expressed by decreased fractional shortening and ejection fraction) was observed in the SHRs before ethanol treatment and further deteriorated by ethanol treatment. In the ethanol-treated SHRs, the following were observed: downregulations of angiotensinase C mRNA and protein, increased RAS activity with low collagen production as evidenced by angiotensin II and angiotensin type 1 receptor (AT1R) protein upregulation, A T 1 a R mRNA downregulation, and an MMP-9 mRNA expression upregulation trend with the downregulation of Col III a1 mRNA expression in LV. We conclude that chronic ethanol regimen is sufficient to promote the enhanced RAS activity-induced decrease in the production of cardiac collagen via downregulated angiotensinase C, leading to the further deterioration of LV systolic dysfunction in SHRs.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>26509155</pmid><doi>10.1155/2015/409350</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin Animals Arterial Pressure Biomedical research Blood Pressure Carboxypeptidases - metabolism Collagen Type III - metabolism Disease Models, Animal Ethanol Ethanol - chemistry Gene Expression Regulation Genetic aspects Health aspects Heart attacks Heart Rate Heart Ventricles Hypertension Male Matrix Metalloproteinase 9 - metabolism Messenger RNA Methods Myocardium - pathology Rats Rats, Inbred SHR Rats, Inbred WKY Real-Time Polymerase Chain Reaction Receptor, Angiotensin, Type 1 - metabolism Renin-Angiotensin System RNA sequencing RNA, Messenger - metabolism Rodents Studies Systole - drug effects Ventricular Dysfunction, Left - chemically induced Ventricular Dysfunction, Left - metabolism |
| title | Angiotensinase C mRNA and Protein Downregulations Are Involved in Ethanol-Deteriorated Left Ventricular Systolic Dysfunction in Spontaneously Hypertensive Rats |
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