Decrease in sarcoglycans and dystrophin in failing heart following acute myocardial infarction
Genetic defects in several sarcoglycans (SGs) and dystrophin (Dys) play a critical role in cardiomyopathy. The present study was designed to determine whether changes in SGs and Dys might occur in animals with chronic heart failure (CHF) induced by acute myocardial infarction (AMI), which have no ge...
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| Veröffentlicht in: | Cardiovascular research 2003-08, Vol.59 (2), p.419-427 |
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| creator | YOSHIDA, Hiroyuki TAKAHASHI, Masaya KOSHIMIZU, Miki TANONAKA, Kouichi OIKAWA, Ryo TOYO-OKA, Teruhiko TAKEO, Satoshi |
| description | Genetic defects in several sarcoglycans (SGs) and dystrophin (Dys) play a critical role in cardiomyopathy. The present study was designed to determine whether changes in SGs and Dys might occur in animals with chronic heart failure (CHF) induced by acute myocardial infarction (AMI), which have no genetic defects.
AMI was induced by the left coronary artery ligation (CAL) in rats. The hemodynamic parameters of the 2- and 8-week CAL (2w- and 8w-CAL) rats were measured and the myocardial SGs, Dys, calpain, and calpastatin levels were determined by the Western blot method. Myocardial calpain-like protease activity was evaluated as caseinolysis activity.
Increases in left ventricular end-diastolic pressure (LVEDP) and right ventricular systolic pressure, and a decrease in +/-dP/dt were observed at the 2nd week, whereas cardiac output index (COI) was preserved. In contrast, the 8w-CAL rats showed a further increment in LVEDP with low COI. alpha-SG of the viable left ventricle (LV), and septum (Sep) of the 8w-CAL rat decreased (60-70% of the control). The alpha- and beta-SGs of the right ventricle (RV) of the 2w- and 8w-CAL rats were reduced, while gamma- and delta-SGs in the three regions did not change significantly. Dys in the viable LV and RV of the 8w-CAL rat decreased (75% of the control). The amount of m-calpain in the three regions of the 2w- and 8w-CAL rats increased (140-200% of the control), whereas the endogenous calpain inhibitor, calpastatin, did not change significantly. The in vitro degradation studies using purified m-calpain or cytosolic fractions of the 8w-CAL rat heart suggested a reduction in SGs and Dys by calpain.
The results suggest that a decrease in SGs and Dys may play an important role in the pathophysiology of CHF following AMI. |
| doi_str_mv | 10.1016/s0008-6363(03)00385-7 |
| format | Article |
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AMI was induced by the left coronary artery ligation (CAL) in rats. The hemodynamic parameters of the 2- and 8-week CAL (2w- and 8w-CAL) rats were measured and the myocardial SGs, Dys, calpain, and calpastatin levels were determined by the Western blot method. Myocardial calpain-like protease activity was evaluated as caseinolysis activity.
Increases in left ventricular end-diastolic pressure (LVEDP) and right ventricular systolic pressure, and a decrease in +/-dP/dt were observed at the 2nd week, whereas cardiac output index (COI) was preserved. In contrast, the 8w-CAL rats showed a further increment in LVEDP with low COI. alpha-SG of the viable left ventricle (LV), and septum (Sep) of the 8w-CAL rat decreased (60-70% of the control). The alpha- and beta-SGs of the right ventricle (RV) of the 2w- and 8w-CAL rats were reduced, while gamma- and delta-SGs in the three regions did not change significantly. Dys in the viable LV and RV of the 8w-CAL rat decreased (75% of the control). The amount of m-calpain in the three regions of the 2w- and 8w-CAL rats increased (140-200% of the control), whereas the endogenous calpain inhibitor, calpastatin, did not change significantly. The in vitro degradation studies using purified m-calpain or cytosolic fractions of the 8w-CAL rat heart suggested a reduction in SGs and Dys by calpain.
The results suggest that a decrease in SGs and Dys may play an important role in the pathophysiology of CHF following AMI.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1016/s0008-6363(03)00385-7</identifier><identifier>PMID: 12909325</identifier><identifier>CODEN: CVREAU</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animals ; Biological and medical sciences ; Blood Pressure ; Blotting, Western - methods ; Calcium-Binding Proteins - analysis ; Calcium-Binding Proteins - metabolism ; Calpain - analysis ; Calpain - metabolism ; Cardiac Output, Low - metabolism ; Cardiology. Vascular system ; Coronary heart disease ; Culture Techniques ; Cytoskeletal Proteins - analysis ; Cytoskeletal Proteins - metabolism ; Cytosol - metabolism ; Dystroglycans ; Dystrophin - analysis ; Dystrophin - metabolism ; Heart ; Heart Rate ; Male ; Medical sciences ; Membrane Glycoproteins - analysis ; Membrane Glycoproteins - metabolism ; Models, Animal ; Myocardial Infarction - metabolism ; Myocardium - chemistry ; Myocardium - metabolism ; Rats ; Rats, Wistar ; Sarcoglycans ; Sarcolemma - metabolism</subject><ispartof>Cardiovascular research, 2003-08, Vol.59 (2), p.419-427</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-f42d4a5c8a0258d5bb81c31f591c041b3a8169c66bf599003b5db9b48ff64e3f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15041198$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12909325$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YOSHIDA, Hiroyuki</creatorcontrib><creatorcontrib>TAKAHASHI, Masaya</creatorcontrib><creatorcontrib>KOSHIMIZU, Miki</creatorcontrib><creatorcontrib>TANONAKA, Kouichi</creatorcontrib><creatorcontrib>OIKAWA, Ryo</creatorcontrib><creatorcontrib>TOYO-OKA, Teruhiko</creatorcontrib><creatorcontrib>TAKEO, Satoshi</creatorcontrib><title>Decrease in sarcoglycans and dystrophin in failing heart following acute myocardial infarction</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>Genetic defects in several sarcoglycans (SGs) and dystrophin (Dys) play a critical role in cardiomyopathy. The present study was designed to determine whether changes in SGs and Dys might occur in animals with chronic heart failure (CHF) induced by acute myocardial infarction (AMI), which have no genetic defects.
AMI was induced by the left coronary artery ligation (CAL) in rats. The hemodynamic parameters of the 2- and 8-week CAL (2w- and 8w-CAL) rats were measured and the myocardial SGs, Dys, calpain, and calpastatin levels were determined by the Western blot method. Myocardial calpain-like protease activity was evaluated as caseinolysis activity.
Increases in left ventricular end-diastolic pressure (LVEDP) and right ventricular systolic pressure, and a decrease in +/-dP/dt were observed at the 2nd week, whereas cardiac output index (COI) was preserved. In contrast, the 8w-CAL rats showed a further increment in LVEDP with low COI. alpha-SG of the viable left ventricle (LV), and septum (Sep) of the 8w-CAL rat decreased (60-70% of the control). The alpha- and beta-SGs of the right ventricle (RV) of the 2w- and 8w-CAL rats were reduced, while gamma- and delta-SGs in the three regions did not change significantly. Dys in the viable LV and RV of the 8w-CAL rat decreased (75% of the control). The amount of m-calpain in the three regions of the 2w- and 8w-CAL rats increased (140-200% of the control), whereas the endogenous calpain inhibitor, calpastatin, did not change significantly. The in vitro degradation studies using purified m-calpain or cytosolic fractions of the 8w-CAL rat heart suggested a reduction in SGs and Dys by calpain.
The results suggest that a decrease in SGs and Dys may play an important role in the pathophysiology of CHF following AMI.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Blotting, Western - methods</subject><subject>Calcium-Binding Proteins - analysis</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Calpain - analysis</subject><subject>Calpain - metabolism</subject><subject>Cardiac Output, Low - metabolism</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Culture Techniques</subject><subject>Cytoskeletal Proteins - analysis</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Cytosol - metabolism</subject><subject>Dystroglycans</subject><subject>Dystrophin - analysis</subject><subject>Dystrophin - metabolism</subject><subject>Heart</subject><subject>Heart Rate</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - analysis</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Models, Animal</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardium - chemistry</subject><subject>Myocardium - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Sarcoglycans</subject><subject>Sarcolemma - metabolism</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkN9LwzAQgIMobk7_BKUvij5UkybXpY8yf8LAB_XVck2TrZI1M2mR_fembDg4OC733YX7CDln9JZRlt8FSqlMc57za8pvKOUS0ukBGbMpQMozAYdk_I-MyEkI37EEmIpjMmJZQQuewZh8PWjlNQadNG0S0Cu3sBuFbUiwrZN6Ezrv1svYi2GwsU27SJYafZcYZ637HWpUfaeT1cYp9HWDNrImbuoa156SI4M26LNdnpDPp8eP2Us6f3t-nd3PUyWE7FIjslogKIk0A1lDVUmmODNQMEUFqzhKlhcqz6v4VMRjK6irohLSmFxobviEXG33rr376XXoylUTlLYWW-36UE45cBAgIghbUHkXgtemXPtmhX5TMloOYsv3wVo5WCtpjEFsHJ-Qi90HfbXS9X5qZzIClzsAg0JrPLaqCXsO4h2skPwPoGGCBQ</recordid><startdate>20030801</startdate><enddate>20030801</enddate><creator>YOSHIDA, Hiroyuki</creator><creator>TAKAHASHI, Masaya</creator><creator>KOSHIMIZU, Miki</creator><creator>TANONAKA, Kouichi</creator><creator>OIKAWA, Ryo</creator><creator>TOYO-OKA, Teruhiko</creator><creator>TAKEO, Satoshi</creator><general>Oxford University Press</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>7X8</scope></search><sort><creationdate>20030801</creationdate><title>Decrease in sarcoglycans and dystrophin in failing heart following acute myocardial infarction</title><author>YOSHIDA, Hiroyuki ; TAKAHASHI, Masaya ; KOSHIMIZU, Miki ; TANONAKA, Kouichi ; OIKAWA, Ryo ; TOYO-OKA, Teruhiko ; TAKEO, Satoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-f42d4a5c8a0258d5bb81c31f591c041b3a8169c66bf599003b5db9b48ff64e3f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Blotting, Western - methods</topic><topic>Calcium-Binding Proteins - analysis</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Calpain - analysis</topic><topic>Calpain - metabolism</topic><topic>Cardiac Output, Low - metabolism</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Culture Techniques</topic><topic>Cytoskeletal Proteins - analysis</topic><topic>Cytoskeletal Proteins - metabolism</topic><topic>Cytosol - metabolism</topic><topic>Dystroglycans</topic><topic>Dystrophin - analysis</topic><topic>Dystrophin - metabolism</topic><topic>Heart</topic><topic>Heart Rate</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - analysis</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Models, Animal</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardium - chemistry</topic><topic>Myocardium - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Sarcoglycans</topic><topic>Sarcolemma - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YOSHIDA, Hiroyuki</creatorcontrib><creatorcontrib>TAKAHASHI, Masaya</creatorcontrib><creatorcontrib>KOSHIMIZU, Miki</creatorcontrib><creatorcontrib>TANONAKA, Kouichi</creatorcontrib><creatorcontrib>OIKAWA, Ryo</creatorcontrib><creatorcontrib>TOYO-OKA, Teruhiko</creatorcontrib><creatorcontrib>TAKEO, Satoshi</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>MEDLINE - Academic</collection><jtitle>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YOSHIDA, Hiroyuki</au><au>TAKAHASHI, Masaya</au><au>KOSHIMIZU, Miki</au><au>TANONAKA, Kouichi</au><au>OIKAWA, Ryo</au><au>TOYO-OKA, Teruhiko</au><au>TAKEO, Satoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decrease in sarcoglycans and dystrophin in failing heart following acute myocardial infarction</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>2003-08-01</date><risdate>2003</risdate><volume>59</volume><issue>2</issue><spage>419</spage><epage>427</epage><pages>419-427</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><coden>CVREAU</coden><abstract>Genetic defects in several sarcoglycans (SGs) and dystrophin (Dys) play a critical role in cardiomyopathy. The present study was designed to determine whether changes in SGs and Dys might occur in animals with chronic heart failure (CHF) induced by acute myocardial infarction (AMI), which have no genetic defects.
AMI was induced by the left coronary artery ligation (CAL) in rats. The hemodynamic parameters of the 2- and 8-week CAL (2w- and 8w-CAL) rats were measured and the myocardial SGs, Dys, calpain, and calpastatin levels were determined by the Western blot method. Myocardial calpain-like protease activity was evaluated as caseinolysis activity.
Increases in left ventricular end-diastolic pressure (LVEDP) and right ventricular systolic pressure, and a decrease in +/-dP/dt were observed at the 2nd week, whereas cardiac output index (COI) was preserved. In contrast, the 8w-CAL rats showed a further increment in LVEDP with low COI. alpha-SG of the viable left ventricle (LV), and septum (Sep) of the 8w-CAL rat decreased (60-70% of the control). The alpha- and beta-SGs of the right ventricle (RV) of the 2w- and 8w-CAL rats were reduced, while gamma- and delta-SGs in the three regions did not change significantly. Dys in the viable LV and RV of the 8w-CAL rat decreased (75% of the control). The amount of m-calpain in the three regions of the 2w- and 8w-CAL rats increased (140-200% of the control), whereas the endogenous calpain inhibitor, calpastatin, did not change significantly. The in vitro degradation studies using purified m-calpain or cytosolic fractions of the 8w-CAL rat heart suggested a reduction in SGs and Dys by calpain.
The results suggest that a decrease in SGs and Dys may play an important role in the pathophysiology of CHF following AMI.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>12909325</pmid><doi>10.1016/s0008-6363(03)00385-7</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences Blood Pressure Blotting, Western - methods Calcium-Binding Proteins - analysis Calcium-Binding Proteins - metabolism Calpain - analysis Calpain - metabolism Cardiac Output, Low - metabolism Cardiology. Vascular system Coronary heart disease Culture Techniques Cytoskeletal Proteins - analysis Cytoskeletal Proteins - metabolism Cytosol - metabolism Dystroglycans Dystrophin - analysis Dystrophin - metabolism Heart Heart Rate Male Medical sciences Membrane Glycoproteins - analysis Membrane Glycoproteins - metabolism Models, Animal Myocardial Infarction - metabolism Myocardium - chemistry Myocardium - metabolism Rats Rats, Wistar Sarcoglycans Sarcolemma - metabolism |
| title | Decrease in sarcoglycans and dystrophin in failing heart following acute myocardial infarction |
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