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공공누리This item is licensed Korea Open Government License

dc.contributor.author
이도연
dc.contributor.author
유권
dc.contributor.author
김보경
dc.contributor.author
이규선
dc.contributor.author
이동석
dc.contributor.author
홍승현
dc.date.accessioned
2019-08-28T07:42:19Z
dc.date.available
2019-08-28T07:42:19Z
dc.date.issued
2018-06-29
dc.identifier.issn
0171-9335
dc.identifier.uri
https://repository.kisti.re.kr/handle/10580/14792
dc.description.abstract
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.
dc.language
eng
dc.relation.ispartofseries
European Journal of Cell Biology
dc.title
Neuropeptide Y mitigates ER stress–induced neuronal cell death by activating the PI3K–XBP1 pathway
dc.citation.endPage
348
dc.citation.startPage
339
dc.citation.volume
97
dc.subject.keyword
Neuropeptide Y
dc.subject.keyword
ER stress
dc.subject.keyword
XBP1
dc.subject.keyword
PI3K
dc.subject.keyword
Grp78/BiP
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7. KISTI 연구성과 > 학술지 발표논문
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