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- W2000586063 abstract "HRC is a SR luminal protein that binds to both triadin and SERCA, and affects Ca2+ cycling in the SR (Arvanitis et al. Am. J. Physiol. Heart. Circ. Physiol. 293: H1581, 2007). In the present study, we attempted to characterize the functions of HRC by AAV-mediated KD using TAC-HF model. We expected that HRC KD could recover cardiac function in failing heart (FH), because HRC KD by itself could enhance Ca2+ uptake and Ca2+ release by increased activities of SERCA2 and RyR2 in HL-1 cells. Unexpectedly, AAV9-mediated HRC KD in TAC-FH showed decreased fractional shortening and increased cardiac fibrosis compared with control TAC-FH. We found that phospho-RyR2, phospho-CaMKII, phospho-p38MAPK and phospho-PLB Thr17 were significantly up-regulated in HRC-KD TAC-FH. The cardiac cell death markers such as LC3A/B and active caspase 9 were also increased, consistent with our results of TUNEL assay. Collectively, the increased cytosolic Ca2+ level could activate CaMKII and hence phosphorylation of p38MAPK causing the enhanced mitochondrial death pathway in TAC-FH. Our results show evidence that down-regulation of HRC is linked to deterioration of cardiomyocytes in the pathological state. (Supported by Korea NRF Grant (2010-0002159), GIST Systems Biology Infrastructure Establishment Grant (2010) and KISTI-KREONET (2010)." @default.
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- W2000586063 date "2011-02-01" @default.
- W2000586063 modified "2023-09-30" @default.
- W2000586063 title "AAV Mediated Knockdown(KD) of Histidine Rich Calcium Binding Protein (HRC) Showed Deterioration of Cardiac Function after Transverse Aortic Constriction-Induced Heart Failure(TAC-HF)" @default.
- W2000586063 doi "https://doi.org/10.1016/j.bpj.2010.12.1784" @default.
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