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We are analyzing https://link.springer.com/article/10.1186/1479-5876-9-132.

Title:
SERCA2a gene transfer improves electrocardiographic performance in aged mdx mice | Journal of Translational Medicine
Description:
Background Cardiomyocyte calcium overloading has been implicated in the pathogenesis of Duchenne muscular dystrophy (DMD) heart disease. The cardiac isoform of sarcoplasmic reticulum calcium ATPase (SERCA2a) plays a major role in removing cytosolic calcium during heart muscle relaxation. Here, we tested the hypothesis that SERCA2a over-expression may mitigate electrocardiography (ECG) abnormalities in old female mdx mice, a murine model of DMD cardiomyopathy. Methods 1 Γ— 1012 viral genome particles/mouse of adeno-associated virus serotype-9 (AAV-9) SERCA2a vector was delivered to 12-m-old female mdx mice (N = 5) via a single bolus tail vein injection. AAV transduction and the ECG profile were examined eight months later. Results The vector genome was detected in the hearts of all AAV-injected mdx mice. Immunofluorescence staining and western blot confirmed SERCA2a over-expression in the mdx heart. Untreated mdx mice showed characteristic tachycardia, PR interval reduction and QT interval prolongation. AAV-9 SERCA2a treatment corrected these ECG abnormalities. Conclusions Our results suggest that AAV SERCA2a therapy may hold great promise in treating dystrophin-deficient heart disease.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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  • Health & Fitness
  • Education
  • Science

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Custom-built

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Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 8,170,236 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We don’t know how the website earns money.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {πŸ”}

sercaa, pubmed, mdx, article, mice, heart, aav, google, scholar, gene, cas, calcium, cardiac, central, duan, figure, ecg, therapy, yue, vector, expression, cardiomyopathy, dystrophy, hajjar, muscular, dmd, reticulum, bostick, muscle, dystrophindeficient, mouse, sarcoplasmic, genome, staining, failure, ther, transfer, duchenne, disease, mol, hearts, dystrophin, authors, access, viral, results, interval, trial, fibrosis, pcr,

Topics {βœ’οΈ}

duchenne muscular dystrophy stress-induced calcium influx open access article sarcoplasmic reticulum ca2+-atpase ecg profiles article download pdf cardiac fibrosis sarcoplasmic reticulum ca-atpase reduces muscular dystrophy becker muscular dystrophy muscular dystrophy association complementary dystrophin/utrophin expression myocardial fibrosis include aav-mediated expression aav1/serca2a gene transfer author information authors mdx mouse dystrophy full size image fibrosis leads stretch-activated calcium channel benefit dystrophin-deficient heart dystrophin replacement/repair therapies dongsheng duan muscle dystrophin-based cytoskeleton microdystrophin gene therapy dystrophin-deficient mdx mice muscular dystrophy cardiovascular research center mouse cftr gene related subjects aav-injected mdx mice aav gene transfer translational medicine aims sarcoplasmic reticulum ca improves sarcolemma integrity adult mdx mouse muscle gene therapy aav serca2a therapy mdx mouse heart acad nurse pract author correspondence privacy choices/manage cookies serca2a gene expression gene transfer vectors vivo gene delivery masson trichrome staining systemic aav-9 transduction aav-9 serca2a vector aav serca2a vector intracoronary gene therapy

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:SERCA2a gene transfer improves electrocardiographic performance in aged mdx mice
         description:Cardiomyocyte calcium overloading has been implicated in the pathogenesis of Duchenne muscular dystrophy (DMD) heart disease. The cardiac isoform of sarcoplasmic reticulum calcium ATPase (SERCA2a) plays a major role in removing cytosolic calcium during heart muscle relaxation. Here, we tested the hypothesis that SERCA2a over-expression may mitigate electrocardiography (ECG) abnormalities in old female mdx mice, a murine model of DMD cardiomyopathy. 1 Γ— 1012 viral genome particles/mouse of adeno-associated virus serotype-9 (AAV-9) SERCA2a vector was delivered to 12-m-old female mdx mice (N = 5) via a single bolus tail vein injection. AAV transduction and the ECG profile were examined eight months later. The vector genome was detected in the hearts of all AAV-injected mdx mice. Immunofluorescence staining and western blot confirmed SERCA2a over-expression in the mdx heart. Untreated mdx mice showed characteristic tachycardia, PR interval reduction and QT interval prolongation. AAV-9 SERCA2a treatment corrected these ECG abnormalities. Our results suggest that AAV SERCA2a therapy may hold great promise in treating dystrophin-deficient heart disease.
         datePublished:2011-08-11T00:00:00Z
         dateModified:2011-08-11T00:00:00Z
         pageStart:1
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         license:https://creativecommons.org/licenses/by/2.0
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         keywords:
            Cystic Fibrosis Transmembrane Conductance Regulator
            Duchenne Muscular Dystrophy
            Mouse Cystic Fibrosis
            Cystic Fibrosis Transmembrane Conductance Regulator Gene
            Biomedicine
            general
            Medicine/Public Health
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               name:Jin-Hong Shin
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               name:Brian Bostick
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               name:Yongping Yue
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      headline:SERCA2a gene transfer improves electrocardiographic performance in aged mdx mice
      description:Cardiomyocyte calcium overloading has been implicated in the pathogenesis of Duchenne muscular dystrophy (DMD) heart disease. The cardiac isoform of sarcoplasmic reticulum calcium ATPase (SERCA2a) plays a major role in removing cytosolic calcium during heart muscle relaxation. Here, we tested the hypothesis that SERCA2a over-expression may mitigate electrocardiography (ECG) abnormalities in old female mdx mice, a murine model of DMD cardiomyopathy. 1 Γ— 1012 viral genome particles/mouse of adeno-associated virus serotype-9 (AAV-9) SERCA2a vector was delivered to 12-m-old female mdx mice (N = 5) via a single bolus tail vein injection. AAV transduction and the ECG profile were examined eight months later. The vector genome was detected in the hearts of all AAV-injected mdx mice. Immunofluorescence staining and western blot confirmed SERCA2a over-expression in the mdx heart. Untreated mdx mice showed characteristic tachycardia, PR interval reduction and QT interval prolongation. AAV-9 SERCA2a treatment corrected these ECG abnormalities. Our results suggest that AAV SERCA2a therapy may hold great promise in treating dystrophin-deficient heart disease.
      datePublished:2011-08-11T00:00:00Z
      dateModified:2011-08-11T00:00:00Z
      pageStart:1
      pageEnd:7
      license:https://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1479-5876-9-132
      keywords:
         Cystic Fibrosis Transmembrane Conductance Regulator
         Duchenne Muscular Dystrophy
         Mouse Cystic Fibrosis
         Cystic Fibrosis Transmembrane Conductance Regulator Gene
         Biomedicine
         general
         Medicine/Public Health
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                     name:Department of Cardiology, Cardiovascular Research Center, Mount Sinai School of Medicine, New York, USA
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                  name:The University of Missouri
                  address:
                     name:Department of Molecular Microbiology and Immunology, School of Medicine, The University of Missouri, Columbia, USA
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            address:
               name:Department of Molecular Microbiology and Immunology, School of Medicine, The University of Missouri, Columbia, USA
               type:PostalAddress
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      name:Brian Bostick
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               name:Department of Molecular Microbiology and Immunology, School of Medicine, The University of Missouri, Columbia, USA
               type:PostalAddress
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      name:Yongping Yue
      affiliation:
            name:The University of Missouri
            address:
               name:Department of Molecular Microbiology and Immunology, School of Medicine, The University of Missouri, Columbia, USA
               type:PostalAddress
            type:Organization
      name:Roger Hajjar
      affiliation:
            name:Cardiovascular Research Center, Mount Sinai School of Medicine
            address:
               name:Department of Cardiology, Cardiovascular Research Center, Mount Sinai School of Medicine, New York, USA
               type:PostalAddress
            type:Organization
      name:Dongsheng Duan
      affiliation:
            name:The University of Missouri
            address:
               name:Department of Molecular Microbiology and Immunology, School of Medicine, The University of Missouri, Columbia, USA
               type:PostalAddress
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      name:Department of Molecular Microbiology and Immunology, School of Medicine, The University of Missouri, Columbia, USA
      name:Department of Molecular Microbiology and Immunology, School of Medicine, The University of Missouri, Columbia, USA
      name:Department of Cardiology, Cardiovascular Research Center, Mount Sinai School of Medicine, New York, USA
      name:Department of Molecular Microbiology and Immunology, School of Medicine, The University of Missouri, Columbia, USA

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