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Enhanced matrix metalloproteinase activity in skeletal muscles of rats with congestive heart failure
Patients with congestive heart failure (CHF) are prone to increased skeletal muscle fatigue. Elevated circulatory concentrations of tumor necrosis factor (TNF)-{alpha} and monocyte chemoattractant protein-1, which may stimulate matrix metalloproteinase (MMP) activity and, thereby, contribute to skel...
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Published in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2005-08, Vol.58 (2), p.R389-R394 |
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creator | SCHIØTZ THORUD, Hanne M STRANDA, Annicke BIRKELAND, Jon-Arne LUNDE, Per K SJAASTAD, Ivar KOLSET, Svein O SEJERSTED, Ole M IVERSEN, Per O |
description | Patients with congestive heart failure (CHF) are prone to increased skeletal muscle fatigue. Elevated circulatory concentrations of tumor necrosis factor (TNF)-{alpha} and monocyte chemoattractant protein-1, which may stimulate matrix metalloproteinase (MMP) activity and, thereby, contribute to skeletal muscle dysfunction, are frequently found in CHF. However, whether skeletal muscle MMP activity is altered in CHF is unknown. Hence, we have used a gelatinase assay to assess the activity of MMP and tissue inhibitors of MMP in single skeletal muscles of rats with CHF 6 wk after induction of myocardial infarction. Sham-operated (Sham) rats were used as controls. We also measured the gene expression and protein contents of MMP-2 and MMP-9 in skeletal muscles of these rats. Plasma MMP activity was nearly seven times higher (P < 0.05) in CHF than in Sham rats. Concomitantly, the MMP activity within single slow- and fast-twitch skeletal muscles of CHF rats increased two- to fourfold compared with Sham animals, whereas tissue inhibitor of MMP activity did not differ (P > 0.05). Preformed MMP-2 and MMP-9 were probably activated in CHF, because neither their gene expression nor protein levels were altered (P > 0.05). Serum concentrations of TNF-{alpha} and monocyte chemoattractant protein-1 remained unchanged (P > 0.05) between CHF and Sham rats during the 6-wk observation period. We conclude that development of CHF in rats enhances MMP activity, which in turn may distort the normal contractile function of skeletal muscle, thereby contributing to increased skeletal muscle fatigue. [PUBLICATION ABSTRACT] |
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Elevated circulatory concentrations of tumor necrosis factor (TNF)-{alpha} and monocyte chemoattractant protein-1, which may stimulate matrix metalloproteinase (MMP) activity and, thereby, contribute to skeletal muscle dysfunction, are frequently found in CHF. However, whether skeletal muscle MMP activity is altered in CHF is unknown. Hence, we have used a gelatinase assay to assess the activity of MMP and tissue inhibitors of MMP in single skeletal muscles of rats with CHF 6 wk after induction of myocardial infarction. Sham-operated (Sham) rats were used as controls. We also measured the gene expression and protein contents of MMP-2 and MMP-9 in skeletal muscles of these rats. Plasma MMP activity was nearly seven times higher (P < 0.05) in CHF than in Sham rats. Concomitantly, the MMP activity within single slow- and fast-twitch skeletal muscles of CHF rats increased two- to fourfold compared with Sham animals, whereas tissue inhibitor of MMP activity did not differ (P > 0.05). Preformed MMP-2 and MMP-9 were probably activated in CHF, because neither their gene expression nor protein levels were altered (P > 0.05). Serum concentrations of TNF-{alpha} and monocyte chemoattractant protein-1 remained unchanged (P > 0.05) between CHF and Sham rats during the 6-wk observation period. We conclude that development of CHF in rats enhances MMP activity, which in turn may distort the normal contractile function of skeletal muscle, thereby contributing to increased skeletal muscle fatigue. [PUBLICATION ABSTRACT]</description><identifier>ISSN: 0363-6119</identifier><identifier>EISSN: 1522-1490</identifier><identifier>CODEN: AJPRDO</identifier><language>eng</language><publisher>Bethesda, MD: American Physiological Society</publisher><subject>Biological and medical sciences ; Fatigue ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Heart ; Heart failure ; Muscular system ; Proteins ; Rodents ; Striated muscle. Tendons ; Vertebrates: cardiovascular system ; Vertebrates: osteoarticular system, musculoskeletal system</subject><ispartof>American journal of physiology. Regulatory, integrative and comparative physiology, 2005-08, Vol.58 (2), p.R389-R394</ispartof><rights>2006 INIST-CNRS</rights><rights>Copyright American Physiological Society Aug 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16968643$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>SCHIØTZ THORUD, Hanne M</creatorcontrib><creatorcontrib>STRANDA, Annicke</creatorcontrib><creatorcontrib>BIRKELAND, Jon-Arne</creatorcontrib><creatorcontrib>LUNDE, Per K</creatorcontrib><creatorcontrib>SJAASTAD, Ivar</creatorcontrib><creatorcontrib>KOLSET, Svein O</creatorcontrib><creatorcontrib>SEJERSTED, Ole M</creatorcontrib><creatorcontrib>IVERSEN, Per O</creatorcontrib><title>Enhanced matrix metalloproteinase activity in skeletal muscles of rats with congestive heart failure</title><title>American journal of physiology. Regulatory, integrative and comparative physiology</title><description>Patients with congestive heart failure (CHF) are prone to increased skeletal muscle fatigue. Elevated circulatory concentrations of tumor necrosis factor (TNF)-{alpha} and monocyte chemoattractant protein-1, which may stimulate matrix metalloproteinase (MMP) activity and, thereby, contribute to skeletal muscle dysfunction, are frequently found in CHF. However, whether skeletal muscle MMP activity is altered in CHF is unknown. Hence, we have used a gelatinase assay to assess the activity of MMP and tissue inhibitors of MMP in single skeletal muscles of rats with CHF 6 wk after induction of myocardial infarction. Sham-operated (Sham) rats were used as controls. We also measured the gene expression and protein contents of MMP-2 and MMP-9 in skeletal muscles of these rats. Plasma MMP activity was nearly seven times higher (P < 0.05) in CHF than in Sham rats. Concomitantly, the MMP activity within single slow- and fast-twitch skeletal muscles of CHF rats increased two- to fourfold compared with Sham animals, whereas tissue inhibitor of MMP activity did not differ (P > 0.05). Preformed MMP-2 and MMP-9 were probably activated in CHF, because neither their gene expression nor protein levels were altered (P > 0.05). Serum concentrations of TNF-{alpha} and monocyte chemoattractant protein-1 remained unchanged (P > 0.05) between CHF and Sham rats during the 6-wk observation period. We conclude that development of CHF in rats enhances MMP activity, which in turn may distort the normal contractile function of skeletal muscle, thereby contributing to increased skeletal muscle fatigue. [PUBLICATION ABSTRACT]</description><subject>Biological and medical sciences</subject><subject>Fatigue</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Heart</subject><subject>Heart failure</subject><subject>Muscular system</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Striated muscle. Tendons</subject><subject>Vertebrates: cardiovascular system</subject><subject>Vertebrates: osteoarticular system, musculoskeletal system</subject><issn>0363-6119</issn><issn>1522-1490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNotj0tLxDAYRYMoWEf_QxBcFvJq0ixlGB8w4Gb2JU2_2IzpwyRV599bcVZ3c7j33AtU0IqxkgpNLlFBuOSlpFRfo5uUjoQQwQUvULcbezNa6PBgcvQ_eIBsQpjmOGXwo0mAjc3-y-cT9iNOHxD-ADwsyQZIeHI4mpzwt889ttP4DmmlAfdgYsbO-LBEuEVXzoQEd-fcoMPT7rB9Kfdvz6_bx305V4qXmkuiqGaa1IpXrQVQtXASgEHtoIOaq7pSqqWWKqKs7YACCCplqzrGWso36P6_dpX_XFaR5jgtcVwXG8a0UkJQvkIPZ8gka4KL63ufmjn6wcRTQ6WWtRSc_wLGqWCw</recordid><startdate>20050801</startdate><enddate>20050801</enddate><creator>SCHIØTZ THORUD, Hanne M</creator><creator>STRANDA, Annicke</creator><creator>BIRKELAND, Jon-Arne</creator><creator>LUNDE, Per K</creator><creator>SJAASTAD, Ivar</creator><creator>KOLSET, Svein O</creator><creator>SEJERSTED, Ole M</creator><creator>IVERSEN, Per O</creator><general>American Physiological Society</general><scope>IQODW</scope><scope>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20050801</creationdate><title>Enhanced matrix metalloproteinase activity in skeletal muscles of rats with congestive heart failure</title><author>SCHIØTZ THORUD, Hanne M ; STRANDA, Annicke ; BIRKELAND, Jon-Arne ; LUNDE, Per K ; SJAASTAD, Ivar ; KOLSET, Svein O ; SEJERSTED, Ole M ; IVERSEN, Per O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p573-93607192908735bcee784f6ee2e8fede8378577b1c1707ccde1ee4166b7d22b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Biological and medical sciences</topic><topic>Fatigue</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>Heart</topic><topic>Heart failure</topic><topic>Muscular system</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Striated muscle. Tendons</topic><topic>Vertebrates: cardiovascular system</topic><topic>Vertebrates: osteoarticular system, musculoskeletal system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SCHIØTZ THORUD, Hanne M</creatorcontrib><creatorcontrib>STRANDA, Annicke</creatorcontrib><creatorcontrib>BIRKELAND, Jon-Arne</creatorcontrib><creatorcontrib>LUNDE, Per K</creatorcontrib><creatorcontrib>SJAASTAD, Ivar</creatorcontrib><creatorcontrib>KOLSET, Svein O</creatorcontrib><creatorcontrib>SEJERSTED, Ole M</creatorcontrib><creatorcontrib>IVERSEN, Per O</creatorcontrib><collection>Pascal-Francis</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SCHIØTZ THORUD, Hanne M</au><au>STRANDA, Annicke</au><au>BIRKELAND, Jon-Arne</au><au>LUNDE, Per K</au><au>SJAASTAD, Ivar</au><au>KOLSET, Svein O</au><au>SEJERSTED, Ole M</au><au>IVERSEN, Per O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced matrix metalloproteinase activity in skeletal muscles of rats with congestive heart failure</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><date>2005-08-01</date><risdate>2005</risdate><volume>58</volume><issue>2</issue><spage>R389</spage><epage>R394</epage><pages>R389-R394</pages><issn>0363-6119</issn><eissn>1522-1490</eissn><coden>AJPRDO</coden><abstract>Patients with congestive heart failure (CHF) are prone to increased skeletal muscle fatigue. Elevated circulatory concentrations of tumor necrosis factor (TNF)-{alpha} and monocyte chemoattractant protein-1, which may stimulate matrix metalloproteinase (MMP) activity and, thereby, contribute to skeletal muscle dysfunction, are frequently found in CHF. However, whether skeletal muscle MMP activity is altered in CHF is unknown. Hence, we have used a gelatinase assay to assess the activity of MMP and tissue inhibitors of MMP in single skeletal muscles of rats with CHF 6 wk after induction of myocardial infarction. Sham-operated (Sham) rats were used as controls. We also measured the gene expression and protein contents of MMP-2 and MMP-9 in skeletal muscles of these rats. Plasma MMP activity was nearly seven times higher (P < 0.05) in CHF than in Sham rats. Concomitantly, the MMP activity within single slow- and fast-twitch skeletal muscles of CHF rats increased two- to fourfold compared with Sham animals, whereas tissue inhibitor of MMP activity did not differ (P > 0.05). Preformed MMP-2 and MMP-9 were probably activated in CHF, because neither their gene expression nor protein levels were altered (P > 0.05). Serum concentrations of TNF-{alpha} and monocyte chemoattractant protein-1 remained unchanged (P > 0.05) between CHF and Sham rats during the 6-wk observation period. We conclude that development of CHF in rats enhances MMP activity, which in turn may distort the normal contractile function of skeletal muscle, thereby contributing to increased skeletal muscle fatigue. [PUBLICATION ABSTRACT]</abstract><cop>Bethesda, MD</cop><pub>American Physiological Society</pub></addata></record> |
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subjects | Biological and medical sciences Fatigue Fundamental and applied biological sciences. Psychology Gene expression Heart Heart failure Muscular system Proteins Rodents Striated muscle. Tendons Vertebrates: cardiovascular system Vertebrates: osteoarticular system, musculoskeletal system |
title | Enhanced matrix metalloproteinase activity in skeletal muscles of rats with congestive heart failure |
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