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Original Article
Dementia and Neurocognitive Disorders 2021: 20: 1: 1-8

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Glia-Like Cells from Human Mesenchymal Stem Cells Protect Neural Stem Cells in an In Vitro Model of Alzheimer's Disease by Reducing NLRP-3 Inflammasome
Mina Hwang , 1,* Se hyeon Song , 2,* Mi-Sook Chang , 2,3 Seong-Ho Koh 1,4
Department of Neurology, Hanyang University College of Medicine, Seoul, Korea 2 Laboratory of Stem Cell & Neurobiology, Department of Oral Anatomy, Dental Research Institute and School of Dentistry, Seoul National University, Seoul, Korea 3 Neuroscience Research Institute, Seoul National University, Seoul, Korea 4 Department of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul, Korea
Glia-Like Cells from Human Mesenchymal Stem Cells Protect Neural Stem Cells in an In Vitro Model of Alzheimer's Disease by Reducing NLRP-3 Inflammasome
Mina Hwang , 1,* Se hyeon Song , 2,* Mi-Sook Chang , 2,3 Seong-Ho Koh 1,4
Department of Neurology, Hanyang University College of Medicine, Seoul, Korea 2 Laboratory of Stem Cell & Neurobiology, Department of Oral Anatomy, Dental Research Institute and School of Dentistry, Seoul National University, Seoul, Korea 3 Neuroscience Research Institute, Seoul National University, Seoul, Korea 4 Department of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul, Korea
Background and Purpose: Neural stem cells (NSCs) have the ability to regenerate, proliferate, and differentiate, enabling them to play important roles in the recovery of the damaged nervous system. However, in neurodegenerative diseases such as Alzheimer's disease (AD), the NSCs are damaged as well. Glia-like cells from human mesenchymal stem cells (ghMSCs) are functionally enhanced adult stem cells. In the present study, we
investigated whether ghMSCs could protect NSCs from amyloid beta (Aβ)-mediated toxicity.Methods: Rat NSCs were obtained from E13–14 fetal rat cortices. NSCs were seeded in pre-coated plates, and the next day, cells were simultaneously treated with 20 μM Aβ and 0.4 μm pore insert well-seeded ghMSCs. After 48 hours of co-treatment, cell viability and proliferation were evaluated. After 2 hours of co-treatment, western blotting was performed to measure inflammasome-related factors, such as NOD-like receptor family pyrin domain containing 3, caspase-1, and interleukin-1β.

Results: The results showed that ghMSCs increased viability and proliferation and reduced the toxicity of NSCs injured by Aβ by reducing the NRLP3 inflammasome activation of NSCs
induced by Aβ.

Conclusions: In this study, we confirmed that ghMSCs could protect NSCs in an in vitro model of AD through the regulation of inflammatory response.
Key Words: Alzheimer's Disease; Amyloid; Neural Stem Cells; Mesenchymal Stem Cells; Inflammasomes
대한치매학회지 (Dementia and Neurocognitive Disorders)