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- W3004768984 abstract "Previous studies found the critical role of ORAI1-STIM1 complex in regulating calcium entry, while the exact roles of TRPCs and ORAIs in mediating Ca2+ entry in response to Ca2+ store depletion and/or G-protein coupled receptor effector molecules upon receptor activation remain unclear. During cardiac hypertrophy, it's considered that TRPC-ORAI channels are responsible for intracellular calcium elevation and provides unique source of calcium to activated hypertrophy. Based on the relationship between workload and energy demand, mitochondrial energy generations regulated by mitochondrial Ca2+ uptake will adapt to hypertrophy, while the interaction between mitochondrial and TRPC/OARI channels mediated calcium entry is not well characterized. In this study we use the human pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) as a model, where the expression of ORAI 1-3 and TRPC1, 3, 4 are found through mRNA. Immunostaining further displayed the distribution and potential colocalization of ORAI and TRPC proteins inside hiPSC-CMs. Inhibition of ORAI-TRPC channels by BTP2 at 1uM showed reduced amplitude and frequency of spontaneous Ca2+ transients within 10mins. Furthermore, hiPSC-CMs exposed to Angiotensin II or Endothelin-1 upregulated TRPC and ORAI mRNAs, suggesting the involvement in mediating hypertrophy. Conversely, efficient siRNA-induced knockdown of TRPC3 significantly attenuated hypertrophy as indicated by the downregulation of ANP and BNP. The effect on the Ca2+ transients and mitochondrial energy metabolism will be further studied. Taken together, our study confirmed the important role of TRPC/ORAI channels on regulating calcium entry in hiPSC-CMs model, and specifically identified the role of TRPC3 on cardiac hypertrophy." @default.
- W3004768984 created "2020-02-14" @default.
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- W3004768984 date "2020-02-01" @default.
- W3004768984 modified "2023-09-30" @default.
- W3004768984 title "The Role of TRPC-ORAI Channels Mediated Calcium Entry in Human Induced Pluripotent Stem Cell Derived Cardiomyocytes" @default.
- W3004768984 doi "https://doi.org/10.1016/j.bpj.2019.11.2346" @default.
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