Journal
CELL STEM CELL
Volume 8, Issue 1, Pages 59-71Publisher
CELL PRESS
DOI: 10.1016/j.stem.2010.11.028
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Funding
- 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
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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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