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Membrane hyperpolarization induced by endoplasmic reticulum stress facilitates Ca2+ influx to regulate cell cycle progression in brain capillary endothelial cells
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نویسنده
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kito h. ,yamamura h. ,suzuki y. ,ohya s. ,asai k. ,imaizumi y.
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منبع
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journal of pharmacological sciences - 2014 - دوره : 125 - شماره : 2 - صفحه:227 -232
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چکیده
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Upregulation of the kir2.1 channel during endoplasmic reticulum (er) stress in t-bbec117,an immortalized bovine brain endothelial cell line,caused a sustained increase in intracellular ca2+ concentration ([ca 2+]i) and a facilitation of cell death. expressions of ca2+ influx channels (trpc,orai1,stim1) were unchanged by er stress. the er stress-induced [ca2+]i increase was mainly attributed to the deeper resting membrane potential due to kir2.1 upregulation. er stress arrested at the g2/m phase and it was attenuated by an inhibitor of kir2.1. these results indicate that kir2.1 upregulation by er stress facilitates cell death via regulation of cell cycle progression in t-bbec117. © the japanese pharmacological society.
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کلیدواژه
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Brain capillary endothelial cell; Endoplasmic reticulum stress; Store operated calcium entry
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آدرس
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department of molecular and cellular pharmacology,graduate school of pharmaceutical sciences,nagoya city university,nagoya 467-8603, Japan, department of molecular and cellular pharmacology,graduate school of pharmaceutical sciences,nagoya city university,nagoya 467-8603, Japan, department of molecular and cellular pharmacology,graduate school of pharmaceutical sciences,nagoya city university,nagoya 467-8603, Japan, department of pharmacology,division of pathological sciences,kyoto pharmaceutical university,kyoto 607-8414, Japan, department of molecular neurobiology,graduate school of medical sciences,nagoya city university,nagoya 467-8601, Japan, department of molecular and cellular pharmacology,graduate school of pharmaceutical sciences,nagoya city university,nagoya 467-8603, Japan
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Authors
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