Alterations in Dystrophin-Related Glycoproteins in Development of Right Ventricular Failure in Rats

DOI Web Site 参考文献73件
  • Daicho Takuya
    Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, Japan
  • Daisho Yoriko
    Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, Japan
  • Kojima Suguru
    Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, Japan
  • Takano Saori
    Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, Japan
  • Tejima Yugo
    Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, Japan
  • Marunouchi Tetsuro
    Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, Japan
  • Takagi Norio
    Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, Japan
  • Takeo Satoshi
    Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, Japan
  • Tanonaka Kouichi
    Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, Japan

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Genetic depletion of the dystrophin-related glycoprotein (DRGP) complex causes cardiomyopathy in animals and humans. The present study was undertaken to explore the possible involvement of alterations in DRGP in the development of the right ventricular failure in monocrotaline-administered rats (MCT rats). At the 6th and 8th weeks after subcutaneous administration of 60 mg/kg monocrotaline, echocardiographic examination showed that cardiac output indices were decreased and that the right ventricular Tei indices were increased, suggesting that right ventricular failure occurs, at the latest, by 6 weeks after monocrotaline-administration. The levels of α- and β-sarcoglycan and β-dystroglycan in the right ventricle of the MCT rats at the 6th and 8th weeks were markedly decreased, and these decreases were inversely related to the increase in the right ventricular Tei index of the MCT-administered animals. The content and activity of the Ca2+-activated neutral protease m-calpain in the right ventricle of the MCT rats were increased at the 4th to 8th weeks and those of matrix metalloproteinase-2, at the 6th and 8th weeks. These results suggest that m-calpain– and/or matrix metalloproteinase-2–mediated alterations in the contents of α-sarcoglycan, β-sarcoglycan, and β-dystroglycan may be involved in the development of right ventricular failure in MCT rats.<br>

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