Overexpression of SERCA1a in the mdx Diaphragm Reduces Susceptibility to Contraction-Induced Damage
Although the precise pathophysiological mechanism of muscle damage in dystrophin-deficient muscle remains disputed, calcium appears to be a critical mediator of the dystrophic process. Duchenne muscular dystrophy patients and mouse models of dystrophin deficiency exhibit extensive abnormalities of c...
Gespeichert in:
| Veröffentlicht in: | Human gene therapy 2010-12, Vol.21 (12), p.1735-1739 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1739 |
|---|---|
| container_issue | 12 |
| container_start_page | 1735 |
| container_title | Human gene therapy |
| container_volume | 21 |
| creator | MORINE, Kevin J SLEEPER, Meg M BARTON, Elisabeth R SWEENEY, H. Lee |
| description | Although the precise pathophysiological mechanism of muscle damage in dystrophin-deficient muscle remains disputed, calcium appears to be a critical mediator of the dystrophic process. Duchenne muscular dystrophy patients and mouse models of dystrophin deficiency exhibit extensive abnormalities of calcium homeostasis, which we hypothesized would be mitigated by increased expression of the sarcoplasmic reticulum calcium pump. Neonatal adeno-associated virus gene transfer of sarcoplasmic reticulum ATPase 1a to the mdx diaphragm decreased centrally located nuclei and resulted in reduced susceptibility to eccentric contraction-induced damage at 6 months of age. As the diaphragm is the mouse muscle most representative of human disease, these results provide impetus for further investigation of therapeutic strategies aimed at enhanced cytosolic calcium removal. |
| doi_str_mv | 10.1089/hum.2010.077 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2999573</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A245254974</galeid><sourcerecordid>A245254974</sourcerecordid><originalsourceid>FETCH-LOGICAL-c578t-b857ae94cd0934764704f0b7a2b13384f06529bb7cf3b4b7981bf0be71a8375a3</originalsourceid><addsrcrecordid>eNqFkt9rFDEQx4Motp6--SwBEV_cMz83yYtwXKsWCoVWn0OSzd5Fdjdrslva_94sd1YLguQhM5nPfMkMXwBeY7TGSKqP-7lfE1QyJMQTcIo5F5VghDwtMWK0QpSRE_Ai5x8IYcpr8RycEMQZqlF9CtzVrU_-bkw-5xAHGFt4c3693WADwwCnvYd9cwfPghn3yex6eO2b2fkMb-bs_DgFG7ow3cMpwm0cpmTcVFSqi2GhGnhmerPzL8Gz1nTZvzreK_D98_m37dfq8urLxXZzWTku5FRZyYXxirkGKcpEzQRiLbLCEIsplSWuOVHWCtdSy6xQEttS9wIbSQU3dAU-HXTH2fa-cX75UKfHFHqT7nU0QT-uDGGvd_FWE6UUF7QIvD8KpPhz9nnSfShjdp0ZfJyzlhwzQWoh_09iWTPEyiAr8PZA7kzndRjauGxpofWGME44U4IVav0PqpzG98HFwbehvD9q-HBocCnmnHz7MCZGevGFLr7Qiy908UXB3_y9mgf4txEK8O4ImOxM1yYzuJD_cLSWtWCY_gKM1r-J</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>818640409</pqid></control><display><type>article</type><title>Overexpression of SERCA1a in the mdx Diaphragm Reduces Susceptibility to Contraction-Induced Damage</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>MORINE, Kevin J ; SLEEPER, Meg M ; BARTON, Elisabeth R ; SWEENEY, H. Lee</creator><creatorcontrib>MORINE, Kevin J ; SLEEPER, Meg M ; BARTON, Elisabeth R ; SWEENEY, H. Lee</creatorcontrib><description>Although the precise pathophysiological mechanism of muscle damage in dystrophin-deficient muscle remains disputed, calcium appears to be a critical mediator of the dystrophic process. Duchenne muscular dystrophy patients and mouse models of dystrophin deficiency exhibit extensive abnormalities of calcium homeostasis, which we hypothesized would be mitigated by increased expression of the sarcoplasmic reticulum calcium pump. Neonatal adeno-associated virus gene transfer of sarcoplasmic reticulum ATPase 1a to the mdx diaphragm decreased centrally located nuclei and resulted in reduced susceptibility to eccentric contraction-induced damage at 6 months of age. As the diaphragm is the mouse muscle most representative of human disease, these results provide impetus for further investigation of therapeutic strategies aimed at enhanced cytosolic calcium removal.</description><identifier>ISSN: 1043-0342</identifier><identifier>EISSN: 1557-7422</identifier><identifier>DOI: 10.1089/hum.2010.077</identifier><identifier>PMID: 20540606</identifier><identifier>CODEN: HGTHE3</identifier><language>eng</language><publisher>Larchmont, NY: Liebert</publisher><subject>Adeno-associated virus ; Adenosine triphosphatase ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Animals, Newborn ; Applied cell therapy and gene therapy ; Biological and medical sciences ; Biotechnology ; Brief Reports ; Dependovirus - genetics ; Diaphragm - metabolism ; Diaphragm - physiopathology ; Disease susceptibility ; Fundamental and applied biological sciences. Psychology ; Gene therapy ; Gene Transfer Techniques ; Genetic aspects ; Genetic Therapy ; Genetic Vectors ; Health. Pharmaceutical industry ; Humans ; Industrial applications and implications. Economical aspects ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Inbred mdx ; Muscle Contraction ; Muscle diseases ; Muscle Strength ; Physiological aspects ; Protein Isoforms - biosynthesis ; Recombinant Proteins - biosynthesis ; Risk factors ; Sarcoplasmic Reticulum Calcium-Transporting ATPases - biosynthesis ; Transfusions. Complications. Transfusion reactions. Cell and gene therapy ; Transgenes</subject><ispartof>Human gene therapy, 2010-12, Vol.21 (12), p.1735-1739</ispartof><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2010 Mary Ann Liebert, Inc.</rights><rights>Copyright 2010, Mary Ann Liebert, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c578t-b857ae94cd0934764704f0b7a2b13384f06529bb7cf3b4b7981bf0be71a8375a3</citedby><cites>FETCH-LOGICAL-c578t-b857ae94cd0934764704f0b7a2b13384f06529bb7cf3b4b7981bf0be71a8375a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23686741$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20540606$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MORINE, Kevin J</creatorcontrib><creatorcontrib>SLEEPER, Meg M</creatorcontrib><creatorcontrib>BARTON, Elisabeth R</creatorcontrib><creatorcontrib>SWEENEY, H. Lee</creatorcontrib><title>Overexpression of SERCA1a in the mdx Diaphragm Reduces Susceptibility to Contraction-Induced Damage</title><title>Human gene therapy</title><addtitle>Hum Gene Ther</addtitle><description>Although the precise pathophysiological mechanism of muscle damage in dystrophin-deficient muscle remains disputed, calcium appears to be a critical mediator of the dystrophic process. Duchenne muscular dystrophy patients and mouse models of dystrophin deficiency exhibit extensive abnormalities of calcium homeostasis, which we hypothesized would be mitigated by increased expression of the sarcoplasmic reticulum calcium pump. Neonatal adeno-associated virus gene transfer of sarcoplasmic reticulum ATPase 1a to the mdx diaphragm decreased centrally located nuclei and resulted in reduced susceptibility to eccentric contraction-induced damage at 6 months of age. As the diaphragm is the mouse muscle most representative of human disease, these results provide impetus for further investigation of therapeutic strategies aimed at enhanced cytosolic calcium removal.</description><subject>Adeno-associated virus</subject><subject>Adenosine triphosphatase</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Applied cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Brief Reports</subject><subject>Dependovirus - genetics</subject><subject>Diaphragm - metabolism</subject><subject>Diaphragm - physiopathology</subject><subject>Disease susceptibility</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene therapy</subject><subject>Gene Transfer Techniques</subject><subject>Genetic aspects</subject><subject>Genetic Therapy</subject><subject>Genetic Vectors</subject><subject>Health. Pharmaceutical industry</subject><subject>Humans</subject><subject>Industrial applications and implications. Economical aspects</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred mdx</subject><subject>Muscle Contraction</subject><subject>Muscle diseases</subject><subject>Muscle Strength</subject><subject>Physiological aspects</subject><subject>Protein Isoforms - biosynthesis</subject><subject>Recombinant Proteins - biosynthesis</subject><subject>Risk factors</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases - biosynthesis</subject><subject>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><subject>Transgenes</subject><issn>1043-0342</issn><issn>1557-7422</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkt9rFDEQx4Motp6--SwBEV_cMz83yYtwXKsWCoVWn0OSzd5Fdjdrslva_94sd1YLguQhM5nPfMkMXwBeY7TGSKqP-7lfE1QyJMQTcIo5F5VghDwtMWK0QpSRE_Ai5x8IYcpr8RycEMQZqlF9CtzVrU_-bkw-5xAHGFt4c3693WADwwCnvYd9cwfPghn3yex6eO2b2fkMb-bs_DgFG7ow3cMpwm0cpmTcVFSqi2GhGnhmerPzL8Gz1nTZvzreK_D98_m37dfq8urLxXZzWTku5FRZyYXxirkGKcpEzQRiLbLCEIsplSWuOVHWCtdSy6xQEttS9wIbSQU3dAU-HXTH2fa-cX75UKfHFHqT7nU0QT-uDGGvd_FWE6UUF7QIvD8KpPhz9nnSfShjdp0ZfJyzlhwzQWoh_09iWTPEyiAr8PZA7kzndRjauGxpofWGME44U4IVav0PqpzG98HFwbehvD9q-HBocCnmnHz7MCZGevGFLr7Qiy908UXB3_y9mgf4txEK8O4ImOxM1yYzuJD_cLSWtWCY_gKM1r-J</recordid><startdate>20101201</startdate><enddate>20101201</enddate><creator>MORINE, Kevin J</creator><creator>SLEEPER, Meg M</creator><creator>BARTON, Elisabeth R</creator><creator>SWEENEY, H. Lee</creator><general>Liebert</general><general>Mary Ann Liebert, Inc</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><scope>7QO</scope><scope>7QP</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20101201</creationdate><title>Overexpression of SERCA1a in the mdx Diaphragm Reduces Susceptibility to Contraction-Induced Damage</title><author>MORINE, Kevin J ; SLEEPER, Meg M ; BARTON, Elisabeth R ; SWEENEY, H. Lee</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c578t-b857ae94cd0934764704f0b7a2b13384f06529bb7cf3b4b7981bf0be71a8375a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adeno-associated virus</topic><topic>Adenosine triphosphatase</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Applied cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Brief Reports</topic><topic>Dependovirus - genetics</topic><topic>Diaphragm - metabolism</topic><topic>Diaphragm - physiopathology</topic><topic>Disease susceptibility</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene therapy</topic><topic>Gene Transfer Techniques</topic><topic>Genetic aspects</topic><topic>Genetic Therapy</topic><topic>Genetic Vectors</topic><topic>Health. Pharmaceutical industry</topic><topic>Humans</topic><topic>Industrial applications and implications. Economical aspects</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred mdx</topic><topic>Muscle Contraction</topic><topic>Muscle diseases</topic><topic>Muscle Strength</topic><topic>Physiological aspects</topic><topic>Protein Isoforms - biosynthesis</topic><topic>Recombinant Proteins - biosynthesis</topic><topic>Risk factors</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases - biosynthesis</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><topic>Transgenes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MORINE, Kevin J</creatorcontrib><creatorcontrib>SLEEPER, Meg M</creatorcontrib><creatorcontrib>BARTON, Elisabeth R</creatorcontrib><creatorcontrib>SWEENEY, H. Lee</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><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Human gene therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MORINE, Kevin J</au><au>SLEEPER, Meg M</au><au>BARTON, Elisabeth R</au><au>SWEENEY, H. Lee</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of SERCA1a in the mdx Diaphragm Reduces Susceptibility to Contraction-Induced Damage</atitle><jtitle>Human gene therapy</jtitle><addtitle>Hum Gene Ther</addtitle><date>2010-12-01</date><risdate>2010</risdate><volume>21</volume><issue>12</issue><spage>1735</spage><epage>1739</epage><pages>1735-1739</pages><issn>1043-0342</issn><eissn>1557-7422</eissn><coden>HGTHE3</coden><abstract>Although the precise pathophysiological mechanism of muscle damage in dystrophin-deficient muscle remains disputed, calcium appears to be a critical mediator of the dystrophic process. Duchenne muscular dystrophy patients and mouse models of dystrophin deficiency exhibit extensive abnormalities of calcium homeostasis, which we hypothesized would be mitigated by increased expression of the sarcoplasmic reticulum calcium pump. Neonatal adeno-associated virus gene transfer of sarcoplasmic reticulum ATPase 1a to the mdx diaphragm decreased centrally located nuclei and resulted in reduced susceptibility to eccentric contraction-induced damage at 6 months of age. As the diaphragm is the mouse muscle most representative of human disease, these results provide impetus for further investigation of therapeutic strategies aimed at enhanced cytosolic calcium removal.</abstract><cop>Larchmont, NY</cop><pub>Liebert</pub><pmid>20540606</pmid><doi>10.1089/hum.2010.077</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1043-0342 |
| ispartof | Human gene therapy, 2010-12, Vol.21 (12), p.1735-1739 |
| issn | 1043-0342 1557-7422 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2999573 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Adeno-associated virus Adenosine triphosphatase Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Animals, Newborn Applied cell therapy and gene therapy Biological and medical sciences Biotechnology Brief Reports Dependovirus - genetics Diaphragm - metabolism Diaphragm - physiopathology Disease susceptibility Fundamental and applied biological sciences. Psychology Gene therapy Gene Transfer Techniques Genetic aspects Genetic Therapy Genetic Vectors Health. Pharmaceutical industry Humans Industrial applications and implications. Economical aspects Medical sciences Mice Mice, Inbred C57BL Mice, Inbred mdx Muscle Contraction Muscle diseases Muscle Strength Physiological aspects Protein Isoforms - biosynthesis Recombinant Proteins - biosynthesis Risk factors Sarcoplasmic Reticulum Calcium-Transporting ATPases - biosynthesis Transfusions. Complications. Transfusion reactions. Cell and gene therapy Transgenes |
| title | Overexpression of SERCA1a in the mdx Diaphragm Reduces Susceptibility to Contraction-Induced Damage |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-19T18%3A53%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Overexpression%20of%20SERCA1a%20in%20the%20mdx%20Diaphragm%20Reduces%20Susceptibility%20to%20Contraction-Induced%20Damage&rft.jtitle=Human%20gene%20therapy&rft.au=MORINE,%20Kevin%20J&rft.date=2010-12-01&rft.volume=21&rft.issue=12&rft.spage=1735&rft.epage=1739&rft.pages=1735-1739&rft.issn=1043-0342&rft.eissn=1557-7422&rft.coden=HGTHE3&rft_id=info:doi/10.1089/hum.2010.077&rft_dat=%3Cgale_pubme%3EA245254974%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=818640409&rft_id=info:pmid/20540606&rft_galeid=A245254974&rfr_iscdi=true |