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Article: Downregulation of Aquaporin 9 Exacerbates Beta-amyloid-induced Neurotoxicity in Alzheimer’s Disease Models In vitro and In vivo

TitleDownregulation of Aquaporin 9 Exacerbates Beta-amyloid-induced Neurotoxicity in Alzheimer’s Disease Models In vitro and In vivo
Authors
KeywordsAlzheimer's disease
aquaporin 9
APPswe/PS1dE9
beta-amyloid
apoptosis
Issue Date2018
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience
Citation
Neuroscience, 2018, v. 394, p. 72-82 How to Cite?
AbstractAlzheimer’s disease (AD) is the most common cause of dementia in the elderly, characterized by progressive cognitive dysfunction. Aquaporin 9 (AQP9) is an aquaglyceroporin membrane channel shown biophysically to conduct water, glycerol, and other small solutes. In our study, we reported for the first time an age-associated decrease in AQP9 mRNA and protein expressions in both hippocampus and cerebral cortex of APPswe/PS1dE9 (Tg) AD mice at 3, 6 and 10 months of age. Consistently, we observed a dose-dependent downregulation of AQP9 expression in PC12 cells after treatment with amyloid-beta protein 1–40 (Aβ1–40). Pre-treatment with AQP9 small interfering RNA led to a more severe neurotoxicity in PC12 cells in response to Aβ1–40. Furthermore, we corroborated that the active participation of AQP9 in AD progression is associated with Aβ-induced apoptosis both in vitro and in vivo. Taken together, our results reveal an important role of AQP9 in Aβ-induced pathogenesis of AD which deserves further investigation.
Persistent Identifierhttp://hdl.handle.net/10722/271407
ISSN
2019 Impact Factor: 3.056
2015 SCImago Journal Rankings: 1.768

 

DC FieldValueLanguage
dc.contributor.authorLIU, J-
dc.contributor.authorCHEN, XX-
dc.contributor.authorChen, HY-
dc.contributor.authorShi, J-
dc.contributor.authorLeung, GPH-
dc.contributor.authorTang, SCW-
dc.contributor.authorLao, LX-
dc.contributor.authorYip, HKF-
dc.contributor.authorLee, KF-
dc.contributor.authorSze, SCW-
dc.contributor.authorZhang, ZJ-
dc.contributor.authorZhang, KY-
dc.date.accessioned2019-06-24T01:09:16Z-
dc.date.available2019-06-24T01:09:16Z-
dc.date.issued2018-
dc.identifier.citationNeuroscience, 2018, v. 394, p. 72-82-
dc.identifier.issn0306-4522-
dc.identifier.urihttp://hdl.handle.net/10722/271407-
dc.description.abstractAlzheimer’s disease (AD) is the most common cause of dementia in the elderly, characterized by progressive cognitive dysfunction. Aquaporin 9 (AQP9) is an aquaglyceroporin membrane channel shown biophysically to conduct water, glycerol, and other small solutes. In our study, we reported for the first time an age-associated decrease in AQP9 mRNA and protein expressions in both hippocampus and cerebral cortex of APPswe/PS1dE9 (Tg) AD mice at 3, 6 and 10 months of age. Consistently, we observed a dose-dependent downregulation of AQP9 expression in PC12 cells after treatment with amyloid-beta protein 1–40 (Aβ1–40). Pre-treatment with AQP9 small interfering RNA led to a more severe neurotoxicity in PC12 cells in response to Aβ1–40. Furthermore, we corroborated that the active participation of AQP9 in AD progression is associated with Aβ-induced apoptosis both in vitro and in vivo. Taken together, our results reveal an important role of AQP9 in Aβ-induced pathogenesis of AD which deserves further investigation.-
dc.languageeng-
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience-
dc.relation.ispartofNeuroscience-
dc.subjectAlzheimer's disease-
dc.subjectaquaporin 9-
dc.subjectAPPswe/PS1dE9-
dc.subjectbeta-amyloid-
dc.subjectapoptosis-
dc.titleDownregulation of Aquaporin 9 Exacerbates Beta-amyloid-induced Neurotoxicity in Alzheimer’s Disease Models In vitro and In vivo-
dc.typeArticle-
dc.identifier.emailChen, HY: haiyong@hku.hk-
dc.identifier.emailShi, J: junshi@hku.hk-
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hk-
dc.identifier.emailTang, SCW: scwtang@hku.hk-
dc.identifier.emailLao, LX: lxlao1@hku.hk-
dc.identifier.emailLee, KF: ckflee@hku.hk-
dc.identifier.emailZhang, ZJ: zhangzj@hkucc.hku.hk-
dc.identifier.emailZhang, KY: ybzhang@hku.hk-
dc.identifier.authorityChen, HY=rp01923-
dc.identifier.authorityLeung, GPH=rp00234-
dc.identifier.authorityTang, SCW=rp00480-
dc.identifier.authorityLao, LX=rp01784-
dc.identifier.authorityYip, HKF=rp00285-
dc.identifier.authorityLee, KF=rp00458-
dc.identifier.authorityZhang, ZJ=rp01297-
dc.identifier.authorityZhang, KY=rp01410-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neuroscience.2018.09.016-
dc.identifier.pmid30266683-
dc.identifier.scopuseid_2-s2.0-85055648015-
dc.identifier.hkuros297956-
dc.identifier.volume394-
dc.identifier.spage72-
dc.identifier.epage82-
dc.publisher.placeNetherlands-

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