Atrophy and hypertrophy signalling of the quadriceps and diaphragm in COPD
BackgroundFactors involved in the regulation of muscle mass in chronic obstructive pulmonary disease (COPD) are still poorly understood. Comparing the signalisation involved in muscle mass regulation between two muscles with different levels of activation within the same subjects is an interesting s...
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| Veröffentlicht in: | Thorax 2010-11, Vol.65 (11), p.963-970 |
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| creator | Doucet, Mariève Dubé, Annie Joanisse, Denis R Debigaré, Richard Michaud, Annie Paré, Marie-Ève Vaillancourt, Rosaire Fréchette, Éric Maltais, François |
| description | BackgroundFactors involved in the regulation of muscle mass in chronic obstructive pulmonary disease (COPD) are still poorly understood. Comparing the signalisation involved in muscle mass regulation between two muscles with different levels of activation within the same subjects is an interesting strategy to tease out the impact of local (muscle activity) versus systemic factors in the regulation of muscle mass. A study was undertaken to measure and compare the protein levels of p-AKT, AKT, Atrogin-1, p-p70S6K, p-4E-BP1, p-GSK3β as well as the mRNA expression of Atrogin-1, MuRF1 and FoxO-1 in the quadriceps and the diaphragm of 12 patients with COPD and 7 controls with normal lung function.MethodsDiaphragm biopsies were obtained during thoracic surgery and quadriceps samples were obtained from needle biopsies. Protein content and mRNA expression were measured by western blot and quantitative PCR, respectively.ResultsIncreased mRNA expressions of Atrogin-1, MuRF1 and FoxO-1 were found in the quadriceps compared with the diaphragm only in patients with COPD. The quadriceps/diaphragm ratio for MuRF1 was higher in COPD. The protein level of p-p70S6K was decreased in the quadriceps compared with the diaphragm in patients with COPD. The quadriceps/diaphragm ratios of p-p70S6K and p-GSK3β were lower in patients with COPD than in controls.ConclusionsThese results indicate a greater susceptibility to a catabolic/anabolic imbalance favouring muscle atrophy in the quadriceps compared with the diaphragm in patients with COPD. The balance between the atrophy and hypertrophy signalling is inhomogeneous between respiratory and lower limb muscles, suggesting that local factors are likely to be involved in the regulation of muscle mass in COPD. |
| doi_str_mv | 10.1136/thx.2009.133827 |
| format | Article |
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Comparing the signalisation involved in muscle mass regulation between two muscles with different levels of activation within the same subjects is an interesting strategy to tease out the impact of local (muscle activity) versus systemic factors in the regulation of muscle mass. A study was undertaken to measure and compare the protein levels of p-AKT, AKT, Atrogin-1, p-p70S6K, p-4E-BP1, p-GSK3β as well as the mRNA expression of Atrogin-1, MuRF1 and FoxO-1 in the quadriceps and the diaphragm of 12 patients with COPD and 7 controls with normal lung function.MethodsDiaphragm biopsies were obtained during thoracic surgery and quadriceps samples were obtained from needle biopsies. Protein content and mRNA expression were measured by western blot and quantitative PCR, respectively.ResultsIncreased mRNA expressions of Atrogin-1, MuRF1 and FoxO-1 were found in the quadriceps compared with the diaphragm only in patients with COPD. The quadriceps/diaphragm ratio for MuRF1 was higher in COPD. The protein level of p-p70S6K was decreased in the quadriceps compared with the diaphragm in patients with COPD. The quadriceps/diaphragm ratios of p-p70S6K and p-GSK3β were lower in patients with COPD than in controls.ConclusionsThese results indicate a greater susceptibility to a catabolic/anabolic imbalance favouring muscle atrophy in the quadriceps compared with the diaphragm in patients with COPD. The balance between the atrophy and hypertrophy signalling is inhomogeneous between respiratory and lower limb muscles, suggesting that local factors are likely to be involved in the regulation of muscle mass in COPD.</description><identifier>ISSN: 0040-6376</identifier><identifier>EISSN: 1468-3296</identifier><identifier>DOI: 10.1136/thx.2009.133827</identifier><identifier>PMID: 20965933</identifier><identifier>CODEN: THORA7</identifier><language>eng</language><publisher>London: BMJ Publishing Group</publisher><subject>Aged ; Atrophy ; Biological and medical sciences ; Biopsy ; Cardiology. Vascular system ; Chronic illnesses ; Chronic obstructive pulmonary disease ; Chronic obstructive pulmonary disease, asthma ; Diaphragm (Anatomy) ; Diaphragm - metabolism ; Diaphragm - pathology ; Female ; Forced Expiratory Volume - physiology ; Gene Expression Regulation ; Humans ; Hypertrophy - etiology ; Hypertrophy - pathology ; Hypotheses ; Insulin-like growth factors ; Male ; Medical sciences ; Middle Aged ; Muscle Proteins - biosynthesis ; Muscle Proteins - genetics ; Muscular Atrophy - etiology ; Muscular Atrophy - metabolism ; Muscular Atrophy - pathology ; Muscular Atrophy - physiopathology ; Musculoskeletal system ; Nutritional status ; Ostomy ; Pneumology ; Proteins ; Pulmonary Disease, Chronic Obstructive - complications ; Pulmonary Disease, Chronic Obstructive - metabolism ; Pulmonary Disease, Chronic Obstructive - physiopathology ; Quadriceps Muscle - metabolism ; Quadriceps Muscle - pathology ; RNA, Messenger - genetics ; Steroids ; Vital Capacity - physiology</subject><ispartof>Thorax, 2010-11, Vol.65 (11), p.963-970</ispartof><rights>2010, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright: 2010 (c) 2010, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b430t-883bc6f176ae3453aa531f9aeffe8c79b66369492f6a5c0751b2e871671f1d113</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://thorax.bmj.com/content/65/11/963.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttps://thorax.bmj.com/content/65/11/963.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,777,781,3183,23552,27905,27906,77349,77380</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23366947$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20965933$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Doucet, Mariève</creatorcontrib><creatorcontrib>Dubé, Annie</creatorcontrib><creatorcontrib>Joanisse, Denis R</creatorcontrib><creatorcontrib>Debigaré, Richard</creatorcontrib><creatorcontrib>Michaud, Annie</creatorcontrib><creatorcontrib>Paré, Marie-Ève</creatorcontrib><creatorcontrib>Vaillancourt, Rosaire</creatorcontrib><creatorcontrib>Fréchette, Éric</creatorcontrib><creatorcontrib>Maltais, François</creatorcontrib><title>Atrophy and hypertrophy signalling of the quadriceps and diaphragm in COPD</title><title>Thorax</title><addtitle>Thorax</addtitle><description>BackgroundFactors involved in the regulation of muscle mass in chronic obstructive pulmonary disease (COPD) are still poorly understood. Comparing the signalisation involved in muscle mass regulation between two muscles with different levels of activation within the same subjects is an interesting strategy to tease out the impact of local (muscle activity) versus systemic factors in the regulation of muscle mass. A study was undertaken to measure and compare the protein levels of p-AKT, AKT, Atrogin-1, p-p70S6K, p-4E-BP1, p-GSK3β as well as the mRNA expression of Atrogin-1, MuRF1 and FoxO-1 in the quadriceps and the diaphragm of 12 patients with COPD and 7 controls with normal lung function.MethodsDiaphragm biopsies were obtained during thoracic surgery and quadriceps samples were obtained from needle biopsies. Protein content and mRNA expression were measured by western blot and quantitative PCR, respectively.ResultsIncreased mRNA expressions of Atrogin-1, MuRF1 and FoxO-1 were found in the quadriceps compared with the diaphragm only in patients with COPD. The quadriceps/diaphragm ratio for MuRF1 was higher in COPD. The protein level of p-p70S6K was decreased in the quadriceps compared with the diaphragm in patients with COPD. The quadriceps/diaphragm ratios of p-p70S6K and p-GSK3β were lower in patients with COPD than in controls.ConclusionsThese results indicate a greater susceptibility to a catabolic/anabolic imbalance favouring muscle atrophy in the quadriceps compared with the diaphragm in patients with COPD. The balance between the atrophy and hypertrophy signalling is inhomogeneous between respiratory and lower limb muscles, suggesting that local factors are likely to be involved in the regulation of muscle mass in COPD.</description><subject>Aged</subject><subject>Atrophy</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>Cardiology. Vascular system</subject><subject>Chronic illnesses</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Chronic obstructive pulmonary disease, asthma</subject><subject>Diaphragm (Anatomy)</subject><subject>Diaphragm - metabolism</subject><subject>Diaphragm - pathology</subject><subject>Female</subject><subject>Forced Expiratory Volume - physiology</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Hypertrophy - etiology</subject><subject>Hypertrophy - pathology</subject><subject>Hypotheses</subject><subject>Insulin-like growth factors</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Muscle Proteins - biosynthesis</subject><subject>Muscle Proteins - genetics</subject><subject>Muscular Atrophy - etiology</subject><subject>Muscular Atrophy - metabolism</subject><subject>Muscular Atrophy - pathology</subject><subject>Muscular Atrophy - physiopathology</subject><subject>Musculoskeletal system</subject><subject>Nutritional status</subject><subject>Ostomy</subject><subject>Pneumology</subject><subject>Proteins</subject><subject>Pulmonary Disease, Chronic Obstructive - complications</subject><subject>Pulmonary Disease, Chronic Obstructive - metabolism</subject><subject>Pulmonary Disease, Chronic Obstructive - physiopathology</subject><subject>Quadriceps Muscle - metabolism</subject><subject>Quadriceps Muscle - pathology</subject><subject>RNA, Messenger - genetics</subject><subject>Steroids</subject><subject>Vital Capacity - physiology</subject><issn>0040-6376</issn><issn>1468-3296</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkNtLwzAUh4Mobl6efZOCiCB0S5o2l8cx7wzmgz6HtE3WjN6WtOD-ezNXFXzx6XDgO7_D7wPgAsEJQphMu-JjEkHIJwhjFtEDMEYxYSGOODkEYwhjGBJMyQicOLeGEDKE6DEYRZCThGM8Bi-zzjZtsQ1knQfFtlV22J1Z1bIsTb0KGh10hQo2vcytyVTrvuDcyLawclUFpg7my9e7M3CkZenU-TBPwfvD_dv8KVwsH5_ns0WYxhh2IWM4zYhGlEiF4wRLmWCkuVRaK5ZRnhKCCY95pIlMMkgTlEaKUUQo0ij3rU_BzT63tc2mV64TlXGZKktZq6Z3giacUcoj5smrP-S66a2v5QSiDLHIa6Kemu6pzDbOWaVFa00l7VYgKHaWhbcsdpbF3rK_uBxy-7RS-Q__rdUD1wMgXSZLbWWdGffLYUx8xV3Q7Z5Lq_W_Xz8BvtqQtQ</recordid><startdate>20101101</startdate><enddate>20101101</enddate><creator>Doucet, Mariève</creator><creator>Dubé, Annie</creator><creator>Joanisse, Denis R</creator><creator>Debigaré, Richard</creator><creator>Michaud, Annie</creator><creator>Paré, Marie-Ève</creator><creator>Vaillancourt, Rosaire</creator><creator>Fréchette, Éric</creator><creator>Maltais, François</creator><general>BMJ Publishing Group</general><general>BMJ Publishing Group LTD</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20101101</creationdate><title>Atrophy and hypertrophy signalling of the quadriceps and diaphragm in COPD</title><author>Doucet, Mariève ; Dubé, Annie ; Joanisse, Denis R ; Debigaré, Richard ; Michaud, Annie ; Paré, Marie-Ève ; Vaillancourt, Rosaire ; Fréchette, Éric ; Maltais, François</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b430t-883bc6f176ae3453aa531f9aeffe8c79b66369492f6a5c0751b2e871671f1d113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Aged</topic><topic>Atrophy</topic><topic>Biological and medical sciences</topic><topic>Biopsy</topic><topic>Cardiology. Vascular system</topic><topic>Chronic illnesses</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Chronic obstructive pulmonary disease, asthma</topic><topic>Diaphragm (Anatomy)</topic><topic>Diaphragm - metabolism</topic><topic>Diaphragm - pathology</topic><topic>Female</topic><topic>Forced Expiratory Volume - physiology</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Hypertrophy - etiology</topic><topic>Hypertrophy - pathology</topic><topic>Hypotheses</topic><topic>Insulin-like growth factors</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Muscle Proteins - biosynthesis</topic><topic>Muscle Proteins - genetics</topic><topic>Muscular Atrophy - etiology</topic><topic>Muscular Atrophy - metabolism</topic><topic>Muscular Atrophy - pathology</topic><topic>Muscular Atrophy - physiopathology</topic><topic>Musculoskeletal system</topic><topic>Nutritional status</topic><topic>Ostomy</topic><topic>Pneumology</topic><topic>Proteins</topic><topic>Pulmonary Disease, Chronic Obstructive - complications</topic><topic>Pulmonary Disease, Chronic Obstructive - metabolism</topic><topic>Pulmonary Disease, Chronic Obstructive - physiopathology</topic><topic>Quadriceps Muscle - metabolism</topic><topic>Quadriceps Muscle - pathology</topic><topic>RNA, Messenger - genetics</topic><topic>Steroids</topic><topic>Vital Capacity - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Doucet, Mariève</creatorcontrib><creatorcontrib>Dubé, Annie</creatorcontrib><creatorcontrib>Joanisse, Denis R</creatorcontrib><creatorcontrib>Debigaré, Richard</creatorcontrib><creatorcontrib>Michaud, Annie</creatorcontrib><creatorcontrib>Paré, Marie-Ève</creatorcontrib><creatorcontrib>Vaillancourt, Rosaire</creatorcontrib><creatorcontrib>Fréchette, Éric</creatorcontrib><creatorcontrib>Maltais, François</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><jtitle>Thorax</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Doucet, Mariève</au><au>Dubé, Annie</au><au>Joanisse, Denis R</au><au>Debigaré, Richard</au><au>Michaud, Annie</au><au>Paré, Marie-Ève</au><au>Vaillancourt, Rosaire</au><au>Fréchette, Éric</au><au>Maltais, François</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Atrophy and hypertrophy signalling of the quadriceps and diaphragm in COPD</atitle><jtitle>Thorax</jtitle><addtitle>Thorax</addtitle><date>2010-11-01</date><risdate>2010</risdate><volume>65</volume><issue>11</issue><spage>963</spage><epage>970</epage><pages>963-970</pages><issn>0040-6376</issn><eissn>1468-3296</eissn><coden>THORA7</coden><abstract>BackgroundFactors involved in the regulation of muscle mass in chronic obstructive pulmonary disease (COPD) are still poorly understood. Comparing the signalisation involved in muscle mass regulation between two muscles with different levels of activation within the same subjects is an interesting strategy to tease out the impact of local (muscle activity) versus systemic factors in the regulation of muscle mass. A study was undertaken to measure and compare the protein levels of p-AKT, AKT, Atrogin-1, p-p70S6K, p-4E-BP1, p-GSK3β as well as the mRNA expression of Atrogin-1, MuRF1 and FoxO-1 in the quadriceps and the diaphragm of 12 patients with COPD and 7 controls with normal lung function.MethodsDiaphragm biopsies were obtained during thoracic surgery and quadriceps samples were obtained from needle biopsies. Protein content and mRNA expression were measured by western blot and quantitative PCR, respectively.ResultsIncreased mRNA expressions of Atrogin-1, MuRF1 and FoxO-1 were found in the quadriceps compared with the diaphragm only in patients with COPD. The quadriceps/diaphragm ratio for MuRF1 was higher in COPD. The protein level of p-p70S6K was decreased in the quadriceps compared with the diaphragm in patients with COPD. The quadriceps/diaphragm ratios of p-p70S6K and p-GSK3β were lower in patients with COPD than in controls.ConclusionsThese results indicate a greater susceptibility to a catabolic/anabolic imbalance favouring muscle atrophy in the quadriceps compared with the diaphragm in patients with COPD. The balance between the atrophy and hypertrophy signalling is inhomogeneous between respiratory and lower limb muscles, suggesting that local factors are likely to be involved in the regulation of muscle mass in COPD.</abstract><cop>London</cop><pub>BMJ Publishing Group</pub><pmid>20965933</pmid><doi>10.1136/thx.2009.133827</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Atrophy Biological and medical sciences Biopsy Cardiology. Vascular system Chronic illnesses Chronic obstructive pulmonary disease Chronic obstructive pulmonary disease, asthma Diaphragm (Anatomy) Diaphragm - metabolism Diaphragm - pathology Female Forced Expiratory Volume - physiology Gene Expression Regulation Humans Hypertrophy - etiology Hypertrophy - pathology Hypotheses Insulin-like growth factors Male Medical sciences Middle Aged Muscle Proteins - biosynthesis Muscle Proteins - genetics Muscular Atrophy - etiology Muscular Atrophy - metabolism Muscular Atrophy - pathology Muscular Atrophy - physiopathology Musculoskeletal system Nutritional status Ostomy Pneumology Proteins Pulmonary Disease, Chronic Obstructive - complications Pulmonary Disease, Chronic Obstructive - metabolism Pulmonary Disease, Chronic Obstructive - physiopathology Quadriceps Muscle - metabolism Quadriceps Muscle - pathology RNA, Messenger - genetics Steroids Vital Capacity - physiology |
| title | Atrophy and hypertrophy signalling of the quadriceps and diaphragm in COPD |
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