Ventilatory dysfunction in mdx mice: Impact of tumor necrosis factor-alpha deletion
Muscular dystrophy is associated with inflammation and fiber necrosis in the diaphragm that may alter ventilatory function. The purpose of this study was to determine to what extent in vivo ventilatory function in dystrophic (mdx) mice was compromised and to assess the impact of deletion of tumor ne...
Gespeichert in:
| Veröffentlicht in: | Muscle & nerve 2003-09, Vol.28 (3), p.336-343 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 343 |
|---|---|
| container_issue | 3 |
| container_start_page | 336 |
| container_title | Muscle & nerve |
| container_volume | 28 |
| creator | Gosselin, Luc E. Barkley, Jacob E. Spencer, Melissa J. McCormick, Kathleen M. Farkas, Gaspar A. |
| description | Muscular dystrophy is associated with inflammation and fiber necrosis in the diaphragm that may alter ventilatory function. The purpose of this study was to determine to what extent in vivo ventilatory function in dystrophic (mdx) mice was compromised and to assess the impact of deletion of tumor necrosis factor–alpha (TNF‐α), a known proinflammatory cytokine, on ventilatory function, diaphragm contractility, and myosin heavy chain (MHC) distribution in 10–12‐month‐old mdx mice. Although the resting ventilatory pattern did not significantly differ between control and mdx mice, the ventilatory response to hypercapnia in mdx mice was significantly attenuated. Elimination of TNF‐α significantly improved the hypercapnic ventilatory response and diaphragm muscle maximal isometric force. Long‐term TNF‐α deletion also altered the myosin heavy chain isoform profile of the diaphragm. These data indicate that a blunted ventilatory response to hypercapnia exists in mdx mice, and that TNF‐α influences the progressive deterioration of diaphragm muscle in mdx mice. Muscle Nerve 28: 336–343, 2003 |
| doi_str_mv | 10.1002/mus.10431 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_73567939</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>73567939</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4241-45fd2e12ef590b4f94b7c586fdbf290cd5b82d3e1412ef4cceaf891b113a39c73</originalsourceid><addsrcrecordid>eNp10MtO3DAUBmCrApWBdsELIG-oxCLgEztxzA6N2inS0KoC2u4sxzkWhlymdiKYt2_CDLBi5SPrOxf9hBwCOwXG0rNmiGMhOHwgM2BKJiJTxQ6ZMRBFknP1d4_sx3jPGIMilx_JHqQqVaDEjFz_xrb3tem7sKbVOrqhtb3vWupb2lRPtPEWz-llszK2p52j_dB0gbZoQxd9pG787kJi6tWdoRXWOPV-IrvO1BE_b98Dcvvt6838e7L8ubicXywTK1IB45GuShFSdJlipXBKlNJmRe6q0qWK2Sori7TiCGIywlo0rlBQAnDDlZX8gHzZzF2F7t-AsdeNjxbr2rTYDVFLnuVScTXCkw2cro4BnV4F35iw1sD0lKAeE9TPCY72aDt0KBus3uQ2shEcb4GJ1tQumNb6-OYyJiHPJ3e2cY--xvX7G_XV7fXL6mTT4WOPT68dJjzoXHKZ6T8_FpotQcwz-KVv-H9RtZee</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>73567939</pqid></control><display><type>article</type><title>Ventilatory dysfunction in mdx mice: Impact of tumor necrosis factor-alpha deletion</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Gosselin, Luc E. ; Barkley, Jacob E. ; Spencer, Melissa J. ; McCormick, Kathleen M. ; Farkas, Gaspar A.</creator><creatorcontrib>Gosselin, Luc E. ; Barkley, Jacob E. ; Spencer, Melissa J. ; McCormick, Kathleen M. ; Farkas, Gaspar A.</creatorcontrib><description>Muscular dystrophy is associated with inflammation and fiber necrosis in the diaphragm that may alter ventilatory function. The purpose of this study was to determine to what extent in vivo ventilatory function in dystrophic (mdx) mice was compromised and to assess the impact of deletion of tumor necrosis factor–alpha (TNF‐α), a known proinflammatory cytokine, on ventilatory function, diaphragm contractility, and myosin heavy chain (MHC) distribution in 10–12‐month‐old mdx mice. Although the resting ventilatory pattern did not significantly differ between control and mdx mice, the ventilatory response to hypercapnia in mdx mice was significantly attenuated. Elimination of TNF‐α significantly improved the hypercapnic ventilatory response and diaphragm muscle maximal isometric force. Long‐term TNF‐α deletion also altered the myosin heavy chain isoform profile of the diaphragm. These data indicate that a blunted ventilatory response to hypercapnia exists in mdx mice, and that TNF‐α influences the progressive deterioration of diaphragm muscle in mdx mice. Muscle Nerve 28: 336–343, 2003</description><identifier>ISSN: 0148-639X</identifier><identifier>EISSN: 1097-4598</identifier><identifier>DOI: 10.1002/mus.10431</identifier><identifier>PMID: 12929194</identifier><identifier>CODEN: MUNEDE</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Biological and medical sciences ; contractile properties ; diaphragm ; Diaphragm - pathology ; Diaphragm - physiopathology ; Disease Models, Animal ; Diseases of striated muscles. Neuromuscular diseases ; Hypercapnia - genetics ; Hypercapnia - physiopathology ; Immunohistochemistry ; Medical sciences ; Mice ; Mice, Inbred mdx ; Muscle Contraction - genetics ; Muscle Contraction - physiology ; Muscle Fibers, Skeletal - pathology ; Muscle Fibers, Skeletal - physiology ; muscular dystrophy ; Muscular Dystrophy, Duchenne - genetics ; Muscular Dystrophy, Duchenne - physiopathology ; Mutation - genetics ; myosin ; Myosin Heavy Chains - genetics ; Myosin Heavy Chains - physiology ; Neurology ; Protein Isoforms - genetics ; Recovery of Function - genetics ; Respiration Disorders - genetics ; Respiration Disorders - physiopathology ; tumor necrosis factor-alpha ; Tumor Necrosis Factor-alpha - deficiency ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>Muscle & nerve, 2003-09, Vol.28 (3), p.336-343</ispartof><rights>Copyright © 2003 Wiley Periodicals, Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4241-45fd2e12ef590b4f94b7c586fdbf290cd5b82d3e1412ef4cceaf891b113a39c73</citedby><cites>FETCH-LOGICAL-c4241-45fd2e12ef590b4f94b7c586fdbf290cd5b82d3e1412ef4cceaf891b113a39c73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmus.10431$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmus.10431$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15071664$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12929194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gosselin, Luc E.</creatorcontrib><creatorcontrib>Barkley, Jacob E.</creatorcontrib><creatorcontrib>Spencer, Melissa J.</creatorcontrib><creatorcontrib>McCormick, Kathleen M.</creatorcontrib><creatorcontrib>Farkas, Gaspar A.</creatorcontrib><title>Ventilatory dysfunction in mdx mice: Impact of tumor necrosis factor-alpha deletion</title><title>Muscle & nerve</title><addtitle>Muscle Nerve</addtitle><description>Muscular dystrophy is associated with inflammation and fiber necrosis in the diaphragm that may alter ventilatory function. The purpose of this study was to determine to what extent in vivo ventilatory function in dystrophic (mdx) mice was compromised and to assess the impact of deletion of tumor necrosis factor–alpha (TNF‐α), a known proinflammatory cytokine, on ventilatory function, diaphragm contractility, and myosin heavy chain (MHC) distribution in 10–12‐month‐old mdx mice. Although the resting ventilatory pattern did not significantly differ between control and mdx mice, the ventilatory response to hypercapnia in mdx mice was significantly attenuated. Elimination of TNF‐α significantly improved the hypercapnic ventilatory response and diaphragm muscle maximal isometric force. Long‐term TNF‐α deletion also altered the myosin heavy chain isoform profile of the diaphragm. These data indicate that a blunted ventilatory response to hypercapnia exists in mdx mice, and that TNF‐α influences the progressive deterioration of diaphragm muscle in mdx mice. Muscle Nerve 28: 336–343, 2003</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>contractile properties</subject><subject>diaphragm</subject><subject>Diaphragm - pathology</subject><subject>Diaphragm - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Diseases of striated muscles. Neuromuscular diseases</subject><subject>Hypercapnia - genetics</subject><subject>Hypercapnia - physiopathology</subject><subject>Immunohistochemistry</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred mdx</subject><subject>Muscle Contraction - genetics</subject><subject>Muscle Contraction - physiology</subject><subject>Muscle Fibers, Skeletal - pathology</subject><subject>Muscle Fibers, Skeletal - physiology</subject><subject>muscular dystrophy</subject><subject>Muscular Dystrophy, Duchenne - genetics</subject><subject>Muscular Dystrophy, Duchenne - physiopathology</subject><subject>Mutation - genetics</subject><subject>myosin</subject><subject>Myosin Heavy Chains - genetics</subject><subject>Myosin Heavy Chains - physiology</subject><subject>Neurology</subject><subject>Protein Isoforms - genetics</subject><subject>Recovery of Function - genetics</subject><subject>Respiration Disorders - genetics</subject><subject>Respiration Disorders - physiopathology</subject><subject>tumor necrosis factor-alpha</subject><subject>Tumor Necrosis Factor-alpha - deficiency</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>0148-639X</issn><issn>1097-4598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10MtO3DAUBmCrApWBdsELIG-oxCLgEztxzA6N2inS0KoC2u4sxzkWhlymdiKYt2_CDLBi5SPrOxf9hBwCOwXG0rNmiGMhOHwgM2BKJiJTxQ6ZMRBFknP1d4_sx3jPGIMilx_JHqQqVaDEjFz_xrb3tem7sKbVOrqhtb3vWupb2lRPtPEWz-llszK2p52j_dB0gbZoQxd9pG787kJi6tWdoRXWOPV-IrvO1BE_b98Dcvvt6838e7L8ubicXywTK1IB45GuShFSdJlipXBKlNJmRe6q0qWK2Sori7TiCGIywlo0rlBQAnDDlZX8gHzZzF2F7t-AsdeNjxbr2rTYDVFLnuVScTXCkw2cro4BnV4F35iw1sD0lKAeE9TPCY72aDt0KBus3uQ2shEcb4GJ1tQumNb6-OYyJiHPJ3e2cY--xvX7G_XV7fXL6mTT4WOPT68dJjzoXHKZ6T8_FpotQcwz-KVv-H9RtZee</recordid><startdate>200309</startdate><enddate>200309</enddate><creator>Gosselin, Luc E.</creator><creator>Barkley, Jacob E.</creator><creator>Spencer, Melissa J.</creator><creator>McCormick, Kathleen M.</creator><creator>Farkas, Gaspar A.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>BSCLL</scope><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>200309</creationdate><title>Ventilatory dysfunction in mdx mice: Impact of tumor necrosis factor-alpha deletion</title><author>Gosselin, Luc E. ; Barkley, Jacob E. ; Spencer, Melissa J. ; McCormick, Kathleen M. ; Farkas, Gaspar A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4241-45fd2e12ef590b4f94b7c586fdbf290cd5b82d3e1412ef4cceaf891b113a39c73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>contractile properties</topic><topic>diaphragm</topic><topic>Diaphragm - pathology</topic><topic>Diaphragm - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Diseases of striated muscles. Neuromuscular diseases</topic><topic>Hypercapnia - genetics</topic><topic>Hypercapnia - physiopathology</topic><topic>Immunohistochemistry</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred mdx</topic><topic>Muscle Contraction - genetics</topic><topic>Muscle Contraction - physiology</topic><topic>Muscle Fibers, Skeletal - pathology</topic><topic>Muscle Fibers, Skeletal - physiology</topic><topic>muscular dystrophy</topic><topic>Muscular Dystrophy, Duchenne - genetics</topic><topic>Muscular Dystrophy, Duchenne - physiopathology</topic><topic>Mutation - genetics</topic><topic>myosin</topic><topic>Myosin Heavy Chains - genetics</topic><topic>Myosin Heavy Chains - physiology</topic><topic>Neurology</topic><topic>Protein Isoforms - genetics</topic><topic>Recovery of Function - genetics</topic><topic>Respiration Disorders - genetics</topic><topic>Respiration Disorders - physiopathology</topic><topic>tumor necrosis factor-alpha</topic><topic>Tumor Necrosis Factor-alpha - deficiency</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gosselin, Luc E.</creatorcontrib><creatorcontrib>Barkley, Jacob E.</creatorcontrib><creatorcontrib>Spencer, Melissa J.</creatorcontrib><creatorcontrib>McCormick, Kathleen M.</creatorcontrib><creatorcontrib>Farkas, Gaspar A.</creatorcontrib><collection>Istex</collection><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>Muscle & nerve</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gosselin, Luc E.</au><au>Barkley, Jacob E.</au><au>Spencer, Melissa J.</au><au>McCormick, Kathleen M.</au><au>Farkas, Gaspar A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ventilatory dysfunction in mdx mice: Impact of tumor necrosis factor-alpha deletion</atitle><jtitle>Muscle & nerve</jtitle><addtitle>Muscle Nerve</addtitle><date>2003-09</date><risdate>2003</risdate><volume>28</volume><issue>3</issue><spage>336</spage><epage>343</epage><pages>336-343</pages><issn>0148-639X</issn><eissn>1097-4598</eissn><coden>MUNEDE</coden><abstract>Muscular dystrophy is associated with inflammation and fiber necrosis in the diaphragm that may alter ventilatory function. The purpose of this study was to determine to what extent in vivo ventilatory function in dystrophic (mdx) mice was compromised and to assess the impact of deletion of tumor necrosis factor–alpha (TNF‐α), a known proinflammatory cytokine, on ventilatory function, diaphragm contractility, and myosin heavy chain (MHC) distribution in 10–12‐month‐old mdx mice. Although the resting ventilatory pattern did not significantly differ between control and mdx mice, the ventilatory response to hypercapnia in mdx mice was significantly attenuated. Elimination of TNF‐α significantly improved the hypercapnic ventilatory response and diaphragm muscle maximal isometric force. Long‐term TNF‐α deletion also altered the myosin heavy chain isoform profile of the diaphragm. These data indicate that a blunted ventilatory response to hypercapnia exists in mdx mice, and that TNF‐α influences the progressive deterioration of diaphragm muscle in mdx mice. Muscle Nerve 28: 336–343, 2003</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>12929194</pmid><doi>10.1002/mus.10431</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0148-639X |
| ispartof | Muscle & nerve, 2003-09, Vol.28 (3), p.336-343 |
| issn | 0148-639X 1097-4598 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_73567939 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Biological and medical sciences contractile properties diaphragm Diaphragm - pathology Diaphragm - physiopathology Disease Models, Animal Diseases of striated muscles. Neuromuscular diseases Hypercapnia - genetics Hypercapnia - physiopathology Immunohistochemistry Medical sciences Mice Mice, Inbred mdx Muscle Contraction - genetics Muscle Contraction - physiology Muscle Fibers, Skeletal - pathology Muscle Fibers, Skeletal - physiology muscular dystrophy Muscular Dystrophy, Duchenne - genetics Muscular Dystrophy, Duchenne - physiopathology Mutation - genetics myosin Myosin Heavy Chains - genetics Myosin Heavy Chains - physiology Neurology Protein Isoforms - genetics Recovery of Function - genetics Respiration Disorders - genetics Respiration Disorders - physiopathology tumor necrosis factor-alpha Tumor Necrosis Factor-alpha - deficiency Tumor Necrosis Factor-alpha - genetics |
| title | Ventilatory dysfunction in mdx mice: Impact of tumor necrosis factor-alpha deletion |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-21T10%3A37%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Ventilatory%20dysfunction%20in%20mdx%20mice:%20Impact%20of%20tumor%20necrosis%20factor-alpha%20deletion&rft.jtitle=Muscle%20&%20nerve&rft.au=Gosselin,%20Luc%20E.&rft.date=2003-09&rft.volume=28&rft.issue=3&rft.spage=336&rft.epage=343&rft.pages=336-343&rft.issn=0148-639X&rft.eissn=1097-4598&rft.coden=MUNEDE&rft_id=info:doi/10.1002/mus.10431&rft_dat=%3Cproquest_cross%3E73567939%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=73567939&rft_id=info:pmid/12929194&rfr_iscdi=true |