TRPC3 channels as a key regulator of cardiac plasticity
نویسندگان
چکیده
منابع مشابه
TRPC3 Channels in Cardiac Fibrosis
Cardiac stiffness, caused by interstitial fibrosis due to deposition of extracellular matrix proteins, is thought as a major clinical outcome of heart failure with preserved ejection fraction (HFpEF). Canonical transient receptor potential (TRPC) subfamily proteins are components of Ca2+-permeable non-selective cation channels activated by receptor stimulation and mechanical stress, and have be...
متن کاملMolecular engineering of the TRPC3 pore structure identifies Ca2+ permeation through TRPC3 channels as a key determinant of cardiac calcineurin/NFAT signaling
Results Elimination of Ca permeation through TRPC3 abrogated its ability to trigger NFAT translocation in both HEK293 cells and in HL-1 atrial myocytes. Wild-type TRPC3 was found capable of initiating NFAT translocation in atrial myocytes by a small, homogenous elevation of cytoplasmic Ca that was independent of voltagegated CaV1.2 channels. By contrast, a Ca 2+ impermeant TRPC3 mutant strongly...
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Tumor cell plasticity contributes to functional and morphologic heterogeneity. To uncover the underlying mechanisms of this plasticity, we examined glioma stem-like cells (GSC) where we found that the biologic interconversion between GSCs and differentiated non-GSCs is functionally plastic and accompanied by gain or loss of polycomb repressive complex 2 (PRC2), a complex that modifies chromatin...
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T helper type 17 (Th17) lymphocytes, characterized by the production of interleukin-17 and other pro-inflammatory cytokines, are present in intestinal lamina propria and have been described as important players driving intestinal inflammation. Recent evidence, supporting the notion of a functional and phenotypic instability of Th17 cells, has shown that Th17 differentiate into type 1 regulatory...
متن کاملTRPC3 as a key player in electrical remodelling of atrial myocardium
Recent evidence suggests involvement of transient receptor potential (TRP)-related cation channels in cardiac physiology and pathophysiology, with TRPC3 as one potential key player in cardiac hypertrophy. It has been suggested that TRPC3 is upregulated in hypertrophy development and contributes to Ca2+ signals that govern pathological remodelling. As TRPC proteins form nonselective cation chann...
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ژورنال
عنوان ژورنال: Proceedings for Annual Meeting of The Japanese Pharmacological Society
سال: 2018
ISSN: 2435-4953
DOI: 10.1254/jpssuppl.wcp2018.0_sy4-3