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Angiotensin II Causes Apoptosis of Adult Hippocampal Neural Stem Cells and Memory Impairment Through the Action on AMPK-PGC1 alpha Signaling in Heart Failure

Title
Angiotensin II Causes Apoptosis of Adult Hippocampal Neural Stem Cells and Memory Impairment Through the Action on AMPK-PGC1 alpha Signaling in Heart Failure
Authors
Kim, Min-SeokLee, Geun-HeeKim, Yong-MinLee, Byoung-WookNam, Hae YunSim, U-CheolChoo, Suk-JungYu, Seong-WoonKim, Jae-JoongKwon, Yunhee KimKim, Seong Who
DGIST Authors
Yu, Seong-Woon
Issue Date
2017-06
Citation
Stem Cells Translational Medicine, 6(6), 1491-1503
Type
Article
Article Type
Article
Keywords
AngiotensinBrainCardiacCell BiologyCognitive ImpairmentMitochondrial BiogenesisNeural Stem CellNeurogenesisRat
ISSN
2157-6564
Abstract
Data are limited on the mechanisms underlying memory impairment in heart failure (HF). We hypothesized that angiotensin II (Ang II) may determine the fate of adult hippocampal neural stem cells (HCNs), a cause of memory impairment in HF. HCNs with neurogenesis potential were isolated and cultured from adult rat hippocampi. Ang II decreased HCN proliferation in dose- and timedependent manners. Moreover, Ang II treatment (1 μM) for 48 hours induced apoptotic death, which was attenuated by pretreatment with Ang II receptor blockers (ARBs). Ang II increased mitochondrial reactive oxygen species (ROS) levels, which was related to mitochondrial morphological changes and functional impairment. Moreover, ROS activated the AMP-activated protein kinase (AMPK) and consequent peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) expression, causing cell apoptosis. In the HF rat model induced by left anterior descending artery ligation, ARB ameliorated the spatial memory ability which decreased 10 weeks after ischemia. In addition, neuronal cell death, especially of newly born mature neurons, was observed in HF rat hippocampi. ARB decreased cell death and promoted the survival of newly born neural precursor cells and mature neurons. In conclusion, Ang II caused HCN apoptosis through mitochondrial ROS formation and subsequent AMPK-PGC1α signaling. ARB improved learning and memory behaviors impaired by neuronal cell death in the HF animal model. These findings suggest that HCN is one treatment target for memory impairment in HF and that ARBs have additional benefits in HF combined with memory impairment. © 2017 The Authors.
URI
http://hdl.handle.net/20.500.11750/4167
DOI
10.1002/sctm.16-0382
Publisher
AlphaMed Press
Related Researcher
Files:
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Collection:
Brain and Cognitive SciencesETC1. Journal Articles


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