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miRNA profiling of bilateral rat hippocampal CA3 by deep sequencing
Authors:Shinohara Yoshiaki  Yahagi Kazuko  Kawano Mitsuoki  Nishiyori Hiromi  Kawazu Chika  Suzuki Naoko  Manabe Ri-ichiroh  Hirase Hajime
Institution:aDepartment of Molecular & Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan;bDepartment of Biological Chemistry, Kyoto University, Graduate School of Pharmaceutical Sciences, Kyoto, Japan;cDepartment of Molecular Neurobiology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan
Abstract:Brain capillary endothelial cells (BCECs) form blood brain barrier (BBB) to maintain brain homeostasis. Cell turnover of BCECs by the balance of cell proliferation and cell death is critical for maintaining the integrity of BBB. Here we found that stimuli with tunicamycin, endoplasmic reticulum (ER) stress inducer, up-regulated inward rectifier K+ channel (Kir2.1) and facilitated cell death in t-BBEC117, a cell line derived from bovine BCECs. The activation of Kir channels contributed to the establishment of deeply negative resting membrane potential in t-BBEC117. The deep resting membrane potential increased the resting intracellular Ca2+ concentration due to Ca2+ influx through non-selective cation channels and thereby partly but significantly regulated cell death in t-BBEC117. The present results suggest that the up-regulation of Kir2.1 is, at least in part, responsible for cell death/cell turnover of BCECs induced by a variety of cellular stresses, particularly ER stress, under pathological conditions.
Keywords:Brain capillary endothelial cell  Cell death  Tunicamycin  Membrane hyperpolarization  Inward rectifier K+ channel  ER stress
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