Acute changes of biventricular gene expression in volume and right ventricular pressure overload
We investigated the effects of acute volume and RV pressure overload on biventricular function and gene expression of BNP, pro-inflammatory cytokines (IL-6 and TNF-α), iNOS, growth factors (IGF-1, ppET-1), ACE and Ca 2+-handling proteins (SERCA2a, phospholamban and calsequestrin). Male Wistar rats (...
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creator | Roncon-Albuquerque, Roberto Vasconcelos, Mariana Lourenço, André P. Brandão-Nogueira, Ana Teles, Antónia Henriques-Coelho, Tiago Leite-Moreira, Adelino F. |
description | We investigated the effects of acute volume and RV pressure overload on biventricular function and gene expression of BNP, pro-inflammatory cytokines (IL-6 and TNF-α), iNOS, growth factors (IGF-1, ppET-1), ACE and Ca
2+-handling proteins (SERCA2a, phospholamban and calsequestrin).
Male Wistar rats (
n
=
45) instrumented with pressure tip micromanometers in right (RV) and left ventricular (LV) cavities were assigned to one of three protocols: i) Acute RV pressure overload induced by pulmonary trunk banding in order to double RV peak systolic pressure, during 120 or 360 min; ii) acute volume overload induced by dextran40 infusion (5 ml/h), during 120 or 360 min; iii) Sham. RV and LV samples were collected for mRNA quantification.
BNP upregulation was restricted to the overloaded ventricles. TNF-α, IL-6, ppET-1, SERCA2a and phospholamban gene activation was higher in volume than in pressure overload. IGF-1 overexpression was similar in both types of overload, but was limited to the RV. TNF-α and CSQ mRNA levels were increased in the non-overloaded LV after pulmonary trunk banding. No significant changes were detected in ACE or iNOS expression. RV end-diastolic pressures positively correlated with local expression of BNP, TNF-α, IL-6, IGF-1, ppET-1 and SERCA2a, while RV peak systolic pressures correlated only with local expression of IL-6, IGF-1 and ppET-1.
Acute cardiac overload alters myocardial gene expression profile, distinctly in volume and pressure overload. These changes correlate more closely with diastolic than with systolic load. Nonetheless, gene activation is also present in the non-overloaded LV of selectively RV overloaded hearts. |
doi_str_mv | 10.1016/j.lfs.2005.10.021 |
format | Article |
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2+-handling proteins (SERCA2a, phospholamban and calsequestrin).
Male Wistar rats (
n
=
45) instrumented with pressure tip micromanometers in right (RV) and left ventricular (LV) cavities were assigned to one of three protocols: i) Acute RV pressure overload induced by pulmonary trunk banding in order to double RV peak systolic pressure, during 120 or 360 min; ii) acute volume overload induced by dextran40 infusion (5 ml/h), during 120 or 360 min; iii) Sham. RV and LV samples were collected for mRNA quantification.
BNP upregulation was restricted to the overloaded ventricles. TNF-α, IL-6, ppET-1, SERCA2a and phospholamban gene activation was higher in volume than in pressure overload. IGF-1 overexpression was similar in both types of overload, but was limited to the RV. TNF-α and CSQ mRNA levels were increased in the non-overloaded LV after pulmonary trunk banding. No significant changes were detected in ACE or iNOS expression. RV end-diastolic pressures positively correlated with local expression of BNP, TNF-α, IL-6, IGF-1, ppET-1 and SERCA2a, while RV peak systolic pressures correlated only with local expression of IL-6, IGF-1 and ppET-1.
Acute cardiac overload alters myocardial gene expression profile, distinctly in volume and pressure overload. These changes correlate more closely with diastolic than with systolic load. Nonetheless, gene activation is also present in the non-overloaded LV of selectively RV overloaded hearts.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2005.10.021</identifier><identifier>PMID: 16310223</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Acute Disease ; Animals ; Biological Factors - genetics ; Biological Factors - metabolism ; Dextrans - administration & dosage ; Disease Models, Animal ; Gene expression ; Gene Expression - physiology ; Growth factors ; Heart Ventricles - metabolism ; Hemodynamics ; Hemodynamics - genetics ; Ligation - methods ; Male ; Mechanotransduction ; Mechanotransduction, Cellular - genetics ; Myocytes, Cardiac - physiology ; Pulmonary Artery - surgery ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Ventricular Dysfunction, Right - genetics ; Ventricular Dysfunction, Right - metabolism ; Ventricular Remodeling - physiology</subject><ispartof>Life sciences (1973), 2006-04, Vol.78 (22), p.2633-2642</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-9f25e2428fa5533bcd04417246220198c7da41f11abb3a56cf537d5c8dfadbd3</citedby><cites>FETCH-LOGICAL-c451t-9f25e2428fa5533bcd04417246220198c7da41f11abb3a56cf537d5c8dfadbd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lfs.2005.10.021$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16310223$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Roncon-Albuquerque, Roberto</creatorcontrib><creatorcontrib>Vasconcelos, Mariana</creatorcontrib><creatorcontrib>Lourenço, André P.</creatorcontrib><creatorcontrib>Brandão-Nogueira, Ana</creatorcontrib><creatorcontrib>Teles, Antónia</creatorcontrib><creatorcontrib>Henriques-Coelho, Tiago</creatorcontrib><creatorcontrib>Leite-Moreira, Adelino F.</creatorcontrib><title>Acute changes of biventricular gene expression in volume and right ventricular pressure overload</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>We investigated the effects of acute volume and RV pressure overload on biventricular function and gene expression of BNP, pro-inflammatory cytokines (IL-6 and TNF-α), iNOS, growth factors (IGF-1, ppET-1), ACE and Ca
2+-handling proteins (SERCA2a, phospholamban and calsequestrin).
Male Wistar rats (
n
=
45) instrumented with pressure tip micromanometers in right (RV) and left ventricular (LV) cavities were assigned to one of three protocols: i) Acute RV pressure overload induced by pulmonary trunk banding in order to double RV peak systolic pressure, during 120 or 360 min; ii) acute volume overload induced by dextran40 infusion (5 ml/h), during 120 or 360 min; iii) Sham. RV and LV samples were collected for mRNA quantification.
BNP upregulation was restricted to the overloaded ventricles. TNF-α, IL-6, ppET-1, SERCA2a and phospholamban gene activation was higher in volume than in pressure overload. IGF-1 overexpression was similar in both types of overload, but was limited to the RV. TNF-α and CSQ mRNA levels were increased in the non-overloaded LV after pulmonary trunk banding. No significant changes were detected in ACE or iNOS expression. RV end-diastolic pressures positively correlated with local expression of BNP, TNF-α, IL-6, IGF-1, ppET-1 and SERCA2a, while RV peak systolic pressures correlated only with local expression of IL-6, IGF-1 and ppET-1.
Acute cardiac overload alters myocardial gene expression profile, distinctly in volume and pressure overload. These changes correlate more closely with diastolic than with systolic load. Nonetheless, gene activation is also present in the non-overloaded LV of selectively RV overloaded hearts.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Biological Factors - genetics</subject><subject>Biological Factors - metabolism</subject><subject>Dextrans - administration & dosage</subject><subject>Disease Models, Animal</subject><subject>Gene expression</subject><subject>Gene Expression - physiology</subject><subject>Growth factors</subject><subject>Heart Ventricles - metabolism</subject><subject>Hemodynamics</subject><subject>Hemodynamics - genetics</subject><subject>Ligation - methods</subject><subject>Male</subject><subject>Mechanotransduction</subject><subject>Mechanotransduction, Cellular - genetics</subject><subject>Myocytes, Cardiac - physiology</subject><subject>Pulmonary Artery - surgery</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Ventricular Dysfunction, Right - genetics</subject><subject>Ventricular Dysfunction, Right - metabolism</subject><subject>Ventricular Remodeling - physiology</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1v2zAQhomiReM4_QFdAk7d5PJIUR_oZBhJEyBAF-8sRR5tGrLokJKR_PvSsYF2SqfD3T3vOzyEfAW2AAbV992id2nBGZN5XzAOH8gMmrotWCXgI5kxxstCcCavyHVKO5ZBWYvP5Aryn3EuZuT30kwjUrPVwwYTDY52_ojDGL2Zeh3pBgek-HKImJIPA_UDPYZ-2iPVg6XRb7Yj_Zd_A6eINBwx9kHbG_LJ6T7hl8uck_X93Xr1UDz9-vm4Wj4VppQwFq3jEnnJG6elFKIzlpUl1LysOGfQNqa2ugQHoLtOaFkZJ0VtpWms07azYk6-nWsPMTxPmEa198lg3-sBw5RUVTdNCcD-C0Lb1tlMk0E4gyaGlCI6dYh-r-OrAqZO-tVOZf3qpP90yvpz5vZSPnV7tH8TF98Z-HEGMKs4eowqGY-DQesjmlHZ4N-p_wN_2pbw</recordid><startdate>20060425</startdate><enddate>20060425</enddate><creator>Roncon-Albuquerque, Roberto</creator><creator>Vasconcelos, Mariana</creator><creator>Lourenço, André P.</creator><creator>Brandão-Nogueira, Ana</creator><creator>Teles, Antónia</creator><creator>Henriques-Coelho, Tiago</creator><creator>Leite-Moreira, Adelino F.</creator><general>Elsevier Inc</general><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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20060425</creationdate><title>Acute changes of biventricular gene expression in volume and right ventricular pressure overload</title><author>Roncon-Albuquerque, Roberto ; Vasconcelos, Mariana ; Lourenço, André P. ; Brandão-Nogueira, Ana ; Teles, Antónia ; Henriques-Coelho, Tiago ; Leite-Moreira, Adelino F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-9f25e2428fa5533bcd04417246220198c7da41f11abb3a56cf537d5c8dfadbd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Biological Factors - genetics</topic><topic>Biological Factors - metabolism</topic><topic>Dextrans - administration & dosage</topic><topic>Disease Models, Animal</topic><topic>Gene expression</topic><topic>Gene Expression - physiology</topic><topic>Growth factors</topic><topic>Heart Ventricles - metabolism</topic><topic>Hemodynamics</topic><topic>Hemodynamics - genetics</topic><topic>Ligation - methods</topic><topic>Male</topic><topic>Mechanotransduction</topic><topic>Mechanotransduction, Cellular - genetics</topic><topic>Myocytes, Cardiac - physiology</topic><topic>Pulmonary Artery - surgery</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Ventricular Dysfunction, Right - genetics</topic><topic>Ventricular Dysfunction, Right - metabolism</topic><topic>Ventricular Remodeling - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Roncon-Albuquerque, Roberto</creatorcontrib><creatorcontrib>Vasconcelos, Mariana</creatorcontrib><creatorcontrib>Lourenço, André P.</creatorcontrib><creatorcontrib>Brandão-Nogueira, Ana</creatorcontrib><creatorcontrib>Teles, Antónia</creatorcontrib><creatorcontrib>Henriques-Coelho, Tiago</creatorcontrib><creatorcontrib>Leite-Moreira, Adelino F.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Roncon-Albuquerque, Roberto</au><au>Vasconcelos, Mariana</au><au>Lourenço, André P.</au><au>Brandão-Nogueira, Ana</au><au>Teles, Antónia</au><au>Henriques-Coelho, Tiago</au><au>Leite-Moreira, Adelino F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acute changes of biventricular gene expression in volume and right ventricular pressure overload</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2006-04-25</date><risdate>2006</risdate><volume>78</volume><issue>22</issue><spage>2633</spage><epage>2642</epage><pages>2633-2642</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>We investigated the effects of acute volume and RV pressure overload on biventricular function and gene expression of BNP, pro-inflammatory cytokines (IL-6 and TNF-α), iNOS, growth factors (IGF-1, ppET-1), ACE and Ca
2+-handling proteins (SERCA2a, phospholamban and calsequestrin).
Male Wistar rats (
n
=
45) instrumented with pressure tip micromanometers in right (RV) and left ventricular (LV) cavities were assigned to one of three protocols: i) Acute RV pressure overload induced by pulmonary trunk banding in order to double RV peak systolic pressure, during 120 or 360 min; ii) acute volume overload induced by dextran40 infusion (5 ml/h), during 120 or 360 min; iii) Sham. RV and LV samples were collected for mRNA quantification.
BNP upregulation was restricted to the overloaded ventricles. TNF-α, IL-6, ppET-1, SERCA2a and phospholamban gene activation was higher in volume than in pressure overload. IGF-1 overexpression was similar in both types of overload, but was limited to the RV. TNF-α and CSQ mRNA levels were increased in the non-overloaded LV after pulmonary trunk banding. No significant changes were detected in ACE or iNOS expression. RV end-diastolic pressures positively correlated with local expression of BNP, TNF-α, IL-6, IGF-1, ppET-1 and SERCA2a, while RV peak systolic pressures correlated only with local expression of IL-6, IGF-1 and ppET-1.
Acute cardiac overload alters myocardial gene expression profile, distinctly in volume and pressure overload. These changes correlate more closely with diastolic than with systolic load. Nonetheless, gene activation is also present in the non-overloaded LV of selectively RV overloaded hearts.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>16310223</pmid><doi>10.1016/j.lfs.2005.10.021</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acute Disease Animals Biological Factors - genetics Biological Factors - metabolism Dextrans - administration & dosage Disease Models, Animal Gene expression Gene Expression - physiology Growth factors Heart Ventricles - metabolism Hemodynamics Hemodynamics - genetics Ligation - methods Male Mechanotransduction Mechanotransduction, Cellular - genetics Myocytes, Cardiac - physiology Pulmonary Artery - surgery Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Ventricular Dysfunction, Right - genetics Ventricular Dysfunction, Right - metabolism Ventricular Remodeling - physiology |
title | Acute changes of biventricular gene expression in volume and right ventricular pressure overload |
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