期刊
CELL STEM CELL
卷 8, 期 1, 页码 59-71出版社
CELL PRESS
DOI: 10.1016/j.stem.2010.11.028
关键词
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资金
- Cure Autism Now Fellowship
- Autism Speaks Basic and Clinical grant
- Autism Speaks Environmental Sciences
- Center for Autism Research and Treatment (CART) [06LEB2008]
- NIH/NICHD [11 P50-HD-055784]
- NIH [MH65756]
- Henry Singleton Brain Cancer Research Program
- James S. McDonnell Foundation
- Miriam and Sheldon Adelson Program in Neural Repair and Rehabilitation
- University of California, Cancer Research Coordinating Committee
- National Institutes of Health [CA-16042, AI-28697]
- JCCC
- UCLA AIDS Institute
- David Geffen School of Medicine at UCLA
- UCLA Chancellor's Office
The majority of research on reactive oxygen species (ROS) has focused on their cellular toxicities. Stem cells generally have been thought to maintain low levels of ROS as a protection against these processes. However, recent studies suggest that ROS can also play roles as second messengers, activating normal cellular processes. Here, we investigated ROS function in primary brain-derived neural progenitors. Somewhat surprisingly, we found that proliferative, self-renewing multipotent neural progenitors with the phenotypic characteristics of neural stem cells (NSC) maintained a high ROS status and were highly responsive to ROS stimulation. ROS-mediated enhancements in self-renewal and neurogenesis were dependent on PI3K/Akt signaling. Pharmacological or genetic manipulations that diminished cellular ROS levels also interfered with normal NSC and/or multipotent progenitor function both in vitro and in vivo. This study has identified a redox-mediated regulatory mechanism of NSC function that may have significant implications for brain injury, disease, and repair.
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