The Pluripotency Factor Nanog Protects against Neuronal Amyloid beta-Induced Toxicity and Oxidative Stress through Insulin Sensitivity Restoration

doi:10.3390/cells9061339

中山醫學大學機構典藏 CSMUIR > 中山醫學大學研究成果 > 期刊論文 > Item 310902500/24515

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題名:	The Pluripotency Factor Nanog Protects against Neuronal Amyloid beta-Induced Toxicity and Oxidative Stress through Insulin Sensitivity Restoration
作者:	Chang, CC;Li, HH;Tsou, SH;Hung, HC;Liu, GY;Korolenko, TA;Lai, TJ;Ho, YJ;Lin, CL
關鍵詞:	amyloid beta;insulin signaling;oxidative stress;Nanog;senescence
日期:	2020
上傳時間:	2022-08-09T08:03:36Z (UTC)
出版者:	MDPI
摘要:	Amyloid beta (A beta) is a peptide fragment of the amyloid precursor protein that triggers the progression of Alzheimer's Disease (AD). It is believed that A beta contributes to neurodegeneration in several ways, including mitochondria dysfunction, oxidative stress and brain insulin resistance. Therefore, protecting neurons from A beta-induced neurotoxicity is an effective strategy for attenuating AD pathogenesis. Recently, applications of stem cell-based therapies have demonstrated the ability to reduce the progression and outcome of neurodegenerative diseases. Particularly, Nanog is recognized as a stem cell-related pluripotency factor that enhances self-renewing capacities and helps reduce the senescent phenotypes of aged neuronal cells. However, whether the upregulation of Nanog can be an effective approach to alleviate A beta-induced neurotoxicity and senescence is not yet understood. In the present study, we transiently overexpressed Nanog-both in vitro and in vivo-and investigated the protective effects and underlying mechanisms against A beta. We found that overexpression of Nanog is responsible for attenuating A beta-triggered neuronal insulin resistance, which restores cell survival through reducing intracellular mitochondrial superoxide accumulation and cellular senescence. In addition, upregulation of Nanog expression appears to increase secretion of neurotrophic factors through activation of the Nrf2 antioxidant defense pathway. Furthermore, improvement of memory and learning were also observed in rat model of A beta neurotoxicity mediated by upregulation of Nanog in the brain. Taken together, our study suggests a potential role for Nanog in attenuating the neurotoxic effects of A beta, which in turn, suggests that strategies to enhance Nanog expression may be used as a novel intervention for reducing A beta neurotoxicity in the AD brain.
URI:	http://dx.doi.org/10.3390/cells9061339 https://www.webofscience.com/wos/woscc/full-record/WOS:000550724200001 https://ir.csmu.edu.tw:8080/handle/310902500/24515
關聯:	CELLS ,2020 ,v9 ,issue 6
顯示於類別:	[中山醫學大學研究成果] 期刊論文

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