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Neuropeptide Y mitigates ER stress–induced neuronal cell death by activating the PI3K–XBP1 pathway
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The unfolded protein response (UPR) is an evolutionary conserved adaptive reaction for increasing cell survival under endoplasmic reticulum (ER) stress conditions. The UPR signaling pathway is a cellular defense system for dealing ER stress but switches to apoptosis when ER stress is prolonged. The ER stress-associated neuronal cell death pathways have been recognized in the pathogenesis of neurodegenerative diseases, including Alzheimer’s, Parkinson’s, and Huntington’s disease. Neuropeptide Y (NPY) has an important role in neuroprotection against neurodegenerative diseases. In this study, we investigated whether NPY has a protective role in ER stress-induced neuronal cell death in SK-N-SH human neuroblastoma cells. An ER stress-inducing chemical, tunicamycin, increased the activities of caspase-3 and -4, whereas pre-treatment with NPY reduced the caspase-3 and -4 activities during ER stress response. In addition, NPY suppressed the activation of three major ER stress sensors in tunicamycin-induced ER stress response. NPY-mediated activation of PI3K increased the nuclear translocation of XBP-1s, which in turn induced the expression of Grp78/Bip. Taken together, our data indicated that NPY has a protective role in ER stress-induced neuronal cell death through activation of the PI3K-XBP1 pathway, and NPY signaling can serve as therapeutic target for ER stress-mediated neurodegenerative diseases.
Neuropeptide Y; ER stress; XBP1; PI3K; Grp78/BiP
Journal Title
European Journal of Cell Biology
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7. KISTI 연구성과 > 학술지 발표논문
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