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
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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.
Abstract
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.
참고문헌 (22)
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