Role of p38 mitogen‐activated protein kinase in cardiac remodelling
Background and purpose: Mitogen‐activated protein kinases (MAPK) are centrally involved in several mechanisms important for heart failure such as apoptosis, activation of inflammatory responses and cell proliferation. We therefore evaluated the effect of the selective p38 MAPK inhibitor SB 239063 on...
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| Veröffentlicht in: | British journal of pharmacology 2007-01, Vol.150 (2), p.130-135 |
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| creator | Frantz, S Behr, T Hu, K Fraccarollo, D Strotmann, J Goldberg, E Ertl, G Angermann, C E Bauersachs, J |
| description | Background and purpose:
Mitogen‐activated protein kinases (MAPK) are centrally involved in several mechanisms important for heart failure such as apoptosis, activation of inflammatory responses and cell proliferation. We therefore evaluated the effect of the selective p38 MAPK inhibitor SB 239063 on progression of left ventricular remodelling after myocardial infarction (MI) in rats.
Experimental approach:
Rats were treated for 9 weeks with placebo or SB 239063 by gavage (15mg kg‐1) twice daily starting 7 days after ligation of the left anterior descending artery. Serial transthoracic echocardiography was performed at days 7, 36 and 70.
Key results:
Over the 9 weeks, mortality was not different between the groups. On echocardiography, animals after myocardial infarction exhibited significant left ventricular dilatation as expected (week 10, end‐systolic diameter, placebo sham 5.21± 0.34 vs. placebo MI 8.44± 0.57 mm). However, there was no difference between placebo and SB 239063‐treated rats (week 10, end‐systolic diameter, SB MI 7.76± 0.74mm, not significantly different from placebo MI). Haemodynamics changed accordingly. Moreover, SB 239063 had no effect on left ventricular hypertrophy. Treatment with SB 239063 significantly reduced cytokine expression of tumour necrosis factor and interleukin‐1β after myocardial infarction. However, collagen content was not influenced by the treatment.
Conclusion:
Despite a reduction of inflammation, treatment with the p38 inhibitor SB 239063 does not affect cardiac remodelling and cardiac function when treatment is started 7 days after myocardial infarction.
British Journal of Pharmacology (2007) 150, 130–135. doi:10.1038/sj.bjp.0706963 |
| doi_str_mv | 10.1038/sj.bjp.0706963 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2042905</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>68935832</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4889-fa2ae9aa7cde2b74775e50f1cc3f82f89635c807e60ecb85d750b1933fa7cd6e3</originalsourceid><addsrcrecordid>eNqFkc1u1DAUhS1ERYfCliWKkGCXwT_jvw1SqQpFqlSEYG05zvXgkMTBzhR1xyPwjH0SPJqIFjasbOl-9_gcH4SeEbwmmKnXuVs33bTGEgst2AO0Ihspas4UeYhWGGNZE6LUMXqcc4dxGUr-CB0TSaTWXKzQ-afYQxV9NTFVDWGOWxhvf_6ybg7Xdoa2mlKcIYzVtzDaDFW5OZvaYF2VYIgt9H0Yt0_Qkbd9hqfLeYK-vDv_fHZRX169_3B2elm7jVK69pZa0NZK1wJt5N4McOyJc8wr6lVJwJ3CEgQG1yjeSo4bohnz-xUB7AS9OehOu2aA1sE4J9ubKYXBphsTbTB_T8bw1WzjtaF4QzXmReDVIpDi9x3k2QwhuxLCjhB32QilGVeMFvDFP2AXd2ks4QwlkpafFKxA6wPkUsw5gf_jhGCzr8fkzpR6zFJPWXh-3_8dvvRRgJcLYLOzvU92dCHfcYozjbEuHD1wP0IPN_951rz9eEGFZr8BxDyq4Q</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>217201463</pqid></control><display><type>article</type><title>Role of p38 mitogen‐activated protein kinase in cardiac remodelling</title><source>Wiley Free Content</source><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Frantz, S ; Behr, T ; Hu, K ; Fraccarollo, D ; Strotmann, J ; Goldberg, E ; Ertl, G ; Angermann, C E ; Bauersachs, J</creator><creatorcontrib>Frantz, S ; Behr, T ; Hu, K ; Fraccarollo, D ; Strotmann, J ; Goldberg, E ; Ertl, G ; Angermann, C E ; Bauersachs, J</creatorcontrib><description>Background and purpose:
Mitogen‐activated protein kinases (MAPK) are centrally involved in several mechanisms important for heart failure such as apoptosis, activation of inflammatory responses and cell proliferation. We therefore evaluated the effect of the selective p38 MAPK inhibitor SB 239063 on progression of left ventricular remodelling after myocardial infarction (MI) in rats.
Experimental approach:
Rats were treated for 9 weeks with placebo or SB 239063 by gavage (15mg kg‐1) twice daily starting 7 days after ligation of the left anterior descending artery. Serial transthoracic echocardiography was performed at days 7, 36 and 70.
Key results:
Over the 9 weeks, mortality was not different between the groups. On echocardiography, animals after myocardial infarction exhibited significant left ventricular dilatation as expected (week 10, end‐systolic diameter, placebo sham 5.21± 0.34 vs. placebo MI 8.44± 0.57 mm). However, there was no difference between placebo and SB 239063‐treated rats (week 10, end‐systolic diameter, SB MI 7.76± 0.74mm, not significantly different from placebo MI). Haemodynamics changed accordingly. Moreover, SB 239063 had no effect on left ventricular hypertrophy. Treatment with SB 239063 significantly reduced cytokine expression of tumour necrosis factor and interleukin‐1β after myocardial infarction. However, collagen content was not influenced by the treatment.
Conclusion:
Despite a reduction of inflammation, treatment with the p38 inhibitor SB 239063 does not affect cardiac remodelling and cardiac function when treatment is started 7 days after myocardial infarction.
British Journal of Pharmacology (2007) 150, 130–135. doi:10.1038/sj.bjp.0706963</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0706963</identifier><identifier>PMID: 17179956</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Coronary heart disease ; Heart ; hypertrophy ; Imidazoles - pharmacology ; Inflammation - prevention & control ; Male ; Medical sciences ; myocardial infarction ; Myocardial Infarction - diagnostic imaging ; Myocardial Infarction - mortality ; Myocardial Infarction - physiopathology ; Myocarditis. Cardiomyopathies ; p38 ; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases - physiology ; Pharmacology. Drug treatments ; Pyrimidines - pharmacology ; Rats ; Rats, Wistar ; remodeling ; Research Papers ; Ultrasonography ; Ventricular Remodeling</subject><ispartof>British journal of pharmacology, 2007-01, Vol.150 (2), p.130-135</ispartof><rights>2007 British Pharmacological Society</rights><rights>2007 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2007</rights><rights>Copyright 2007, Nature Publishing Group 2007 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4889-fa2ae9aa7cde2b74775e50f1cc3f82f89635c807e60ecb85d750b1933fa7cd6e3</citedby><cites>FETCH-LOGICAL-c4889-fa2ae9aa7cde2b74775e50f1cc3f82f89635c807e60ecb85d750b1933fa7cd6e3</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/PMC2042905/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042905/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18539009$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17179956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Frantz, S</creatorcontrib><creatorcontrib>Behr, T</creatorcontrib><creatorcontrib>Hu, K</creatorcontrib><creatorcontrib>Fraccarollo, D</creatorcontrib><creatorcontrib>Strotmann, J</creatorcontrib><creatorcontrib>Goldberg, E</creatorcontrib><creatorcontrib>Ertl, G</creatorcontrib><creatorcontrib>Angermann, C E</creatorcontrib><creatorcontrib>Bauersachs, J</creatorcontrib><title>Role of p38 mitogen‐activated protein kinase in cardiac remodelling</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and purpose:
Mitogen‐activated protein kinases (MAPK) are centrally involved in several mechanisms important for heart failure such as apoptosis, activation of inflammatory responses and cell proliferation. We therefore evaluated the effect of the selective p38 MAPK inhibitor SB 239063 on progression of left ventricular remodelling after myocardial infarction (MI) in rats.
Experimental approach:
Rats were treated for 9 weeks with placebo or SB 239063 by gavage (15mg kg‐1) twice daily starting 7 days after ligation of the left anterior descending artery. Serial transthoracic echocardiography was performed at days 7, 36 and 70.
Key results:
Over the 9 weeks, mortality was not different between the groups. On echocardiography, animals after myocardial infarction exhibited significant left ventricular dilatation as expected (week 10, end‐systolic diameter, placebo sham 5.21± 0.34 vs. placebo MI 8.44± 0.57 mm). However, there was no difference between placebo and SB 239063‐treated rats (week 10, end‐systolic diameter, SB MI 7.76± 0.74mm, not significantly different from placebo MI). Haemodynamics changed accordingly. Moreover, SB 239063 had no effect on left ventricular hypertrophy. Treatment with SB 239063 significantly reduced cytokine expression of tumour necrosis factor and interleukin‐1β after myocardial infarction. However, collagen content was not influenced by the treatment.
Conclusion:
Despite a reduction of inflammation, treatment with the p38 inhibitor SB 239063 does not affect cardiac remodelling and cardiac function when treatment is started 7 days after myocardial infarction.
British Journal of Pharmacology (2007) 150, 130–135. doi:10.1038/sj.bjp.0706963</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Heart</subject><subject>hypertrophy</subject><subject>Imidazoles - pharmacology</subject><subject>Inflammation - prevention & control</subject><subject>Male</subject><subject>Medical sciences</subject><subject>myocardial infarction</subject><subject>Myocardial Infarction - diagnostic imaging</subject><subject>Myocardial Infarction - mortality</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>p38</subject><subject>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>p38 Mitogen-Activated Protein Kinases - physiology</subject><subject>Pharmacology. Drug treatments</subject><subject>Pyrimidines - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>remodeling</subject><subject>Research Papers</subject><subject>Ultrasonography</subject><subject>Ventricular Remodeling</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkc1u1DAUhS1ERYfCliWKkGCXwT_jvw1SqQpFqlSEYG05zvXgkMTBzhR1xyPwjH0SPJqIFjasbOl-9_gcH4SeEbwmmKnXuVs33bTGEgst2AO0Ihspas4UeYhWGGNZE6LUMXqcc4dxGUr-CB0TSaTWXKzQ-afYQxV9NTFVDWGOWxhvf_6ybg7Xdoa2mlKcIYzVtzDaDFW5OZvaYF2VYIgt9H0Yt0_Qkbd9hqfLeYK-vDv_fHZRX169_3B2elm7jVK69pZa0NZK1wJt5N4McOyJc8wr6lVJwJ3CEgQG1yjeSo4bohnz-xUB7AS9OehOu2aA1sE4J9ubKYXBphsTbTB_T8bw1WzjtaF4QzXmReDVIpDi9x3k2QwhuxLCjhB32QilGVeMFvDFP2AXd2ks4QwlkpafFKxA6wPkUsw5gf_jhGCzr8fkzpR6zFJPWXh-3_8dvvRRgJcLYLOzvU92dCHfcYozjbEuHD1wP0IPN_951rz9eEGFZr8BxDyq4Q</recordid><startdate>200701</startdate><enddate>200701</enddate><creator>Frantz, S</creator><creator>Behr, T</creator><creator>Hu, K</creator><creator>Fraccarollo, D</creator><creator>Strotmann, J</creator><creator>Goldberg, E</creator><creator>Ertl, G</creator><creator>Angermann, C E</creator><creator>Bauersachs, J</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><general>Nature Publishing Group</general><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>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</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>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200701</creationdate><title>Role of p38 mitogen‐activated protein kinase in cardiac remodelling</title><author>Frantz, S ; Behr, T ; Hu, K ; Fraccarollo, D ; Strotmann, J ; Goldberg, E ; Ertl, G ; Angermann, C E ; Bauersachs, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4889-fa2ae9aa7cde2b74775e50f1cc3f82f89635c807e60ecb85d750b1933fa7cd6e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Heart</topic><topic>hypertrophy</topic><topic>Imidazoles - pharmacology</topic><topic>Inflammation - prevention & control</topic><topic>Male</topic><topic>Medical sciences</topic><topic>myocardial infarction</topic><topic>Myocardial Infarction - diagnostic imaging</topic><topic>Myocardial Infarction - mortality</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>p38</topic><topic>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>p38 Mitogen-Activated Protein Kinases - physiology</topic><topic>Pharmacology. Drug treatments</topic><topic>Pyrimidines - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>remodeling</topic><topic>Research Papers</topic><topic>Ultrasonography</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Frantz, S</creatorcontrib><creatorcontrib>Behr, T</creatorcontrib><creatorcontrib>Hu, K</creatorcontrib><creatorcontrib>Fraccarollo, D</creatorcontrib><creatorcontrib>Strotmann, J</creatorcontrib><creatorcontrib>Goldberg, E</creatorcontrib><creatorcontrib>Ertl, G</creatorcontrib><creatorcontrib>Angermann, C E</creatorcontrib><creatorcontrib>Bauersachs, J</creatorcontrib><collection>Pascal-Francis</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>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech 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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Frantz, S</au><au>Behr, T</au><au>Hu, K</au><au>Fraccarollo, D</au><au>Strotmann, J</au><au>Goldberg, E</au><au>Ertl, G</au><au>Angermann, C E</au><au>Bauersachs, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of p38 mitogen‐activated protein kinase in cardiac remodelling</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2007-01</date><risdate>2007</risdate><volume>150</volume><issue>2</issue><spage>130</spage><epage>135</epage><pages>130-135</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Background and purpose:
Mitogen‐activated protein kinases (MAPK) are centrally involved in several mechanisms important for heart failure such as apoptosis, activation of inflammatory responses and cell proliferation. We therefore evaluated the effect of the selective p38 MAPK inhibitor SB 239063 on progression of left ventricular remodelling after myocardial infarction (MI) in rats.
Experimental approach:
Rats were treated for 9 weeks with placebo or SB 239063 by gavage (15mg kg‐1) twice daily starting 7 days after ligation of the left anterior descending artery. Serial transthoracic echocardiography was performed at days 7, 36 and 70.
Key results:
Over the 9 weeks, mortality was not different between the groups. On echocardiography, animals after myocardial infarction exhibited significant left ventricular dilatation as expected (week 10, end‐systolic diameter, placebo sham 5.21± 0.34 vs. placebo MI 8.44± 0.57 mm). However, there was no difference between placebo and SB 239063‐treated rats (week 10, end‐systolic diameter, SB MI 7.76± 0.74mm, not significantly different from placebo MI). Haemodynamics changed accordingly. Moreover, SB 239063 had no effect on left ventricular hypertrophy. Treatment with SB 239063 significantly reduced cytokine expression of tumour necrosis factor and interleukin‐1β after myocardial infarction. However, collagen content was not influenced by the treatment.
Conclusion:
Despite a reduction of inflammation, treatment with the p38 inhibitor SB 239063 does not affect cardiac remodelling and cardiac function when treatment is started 7 days after myocardial infarction.
British Journal of Pharmacology (2007) 150, 130–135. doi:10.1038/sj.bjp.0706963</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17179956</pmid><doi>10.1038/sj.bjp.0706963</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Cardiology. Vascular system Coronary heart disease Heart hypertrophy Imidazoles - pharmacology Inflammation - prevention & control Male Medical sciences myocardial infarction Myocardial Infarction - diagnostic imaging Myocardial Infarction - mortality Myocardial Infarction - physiopathology Myocarditis. Cardiomyopathies p38 p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - physiology Pharmacology. Drug treatments Pyrimidines - pharmacology Rats Rats, Wistar remodeling Research Papers Ultrasonography Ventricular Remodeling |
| title | Role of p38 mitogen‐activated protein kinase in cardiac remodelling |
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