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- W140533620 abstract "Alternations of ryanodine receptor type 2 (RyR-2) associate with cardiac hypertrophy and dysfunction, but the mechanism remains elusive. We here examined this by using the mice with heterozygous reduction of RyR-2 gene ( RyR-2 +/− ) and their littermate wild type ones ( RyR-2 + / + ). The mutation induced an impairing of Ca 2+ release from sarcoplasmic reticulum (SR) but did not affect growth and morphology of the cardiomyocytes at basal condition. When pressure overload was imposed, comparing to RyR-2 + / + mice, the RyR-2 +/− mice displayed an attenuated cardiac hypertrophy and contractibility, the increased death of cardiomyocytes, further down-regulated expression of RyR-2 , the different reprogramming of SR Ca 2+ -ATPase 2, L-type Ca 2+ channel and Na 1+ /Ca 2+ exchanger expressions, and a unchanged vasculature reduction in the heart at 3 weeks. Additionally, the decrease of binding of FKBP12.6 to RyR-2 and the increase in phosphorylation of RyR-2 by protein kinase A were aggravated in the loaded RyR-2 +/− heart. Furthermore, activation of protein kinase B/Akt and calcineurin by pressure overload was declined whereas that of Ca 2+ /calmudulin-dependent protein kinase II unchanged in the RyR-2 +/− heart comparing the RyR-2 + / + one. These results suggest that reduction of RyR-2 attenuated cardiac hypertrophy but accelerated the development of cardiac dysfunctions through disturbed Ca 2+ homeostasis, impaired activation of Akt and calcineurin and increased cardiomyocyte death during pressure overload." @default.
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- W140533620 date "2008-10-28" @default.
- W140533620 modified "2023-09-27" @default.
- W140533620 title "Abstract 3768: The Deficiency of Ryanodine Receptor Type 2 Accelerates Transition from Adaptive Cardiac Hypertrophy to Dysfunction during Pressure Overload" @default.
- W140533620 doi "https://doi.org/10.1161/circ.118.suppl_18.s_483-a" @default.
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