For years, the majority of research on reactive oxygen species (ROS) – ions or very small molecules that include free radicals – has focused on how they damage cell structure and their potential link to stroke, cardiovascular disease, and other illnesses.
However, researchers at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research have shown for the first time that neural stem cells, the cells that give rise to neurons, maintain high levels of ROS to help regulate normal self-renewal and differentiation.
The findings may have significant implications for brain repair and abnormal brain development.
“Everyone thinks of ROS as things that kill cells, and they do,” said Dr. Harley Kornblum, a professor at the Intellectual and Developmental Disabilities Research Center in the Semel Institute of Neuroscience and Behavior and senior author of the study. “Stem cells generally have been thought to maintain low levels of ROS to protect against damage, so our findings were surprising and we hope to be able to exploit this to promote neural repair and explore diseases such as autism and brain cancer.”
The study also found that the neural stem cells were highly responsive to ROS stimulation, which increased their growth and differentiation. Conversely, diminishing cellular levels of ROS in the neural stem cells interfered with normal cell function in mice and in human and mouse cell lines.
“It wasn’t just that neural stem cells maintained high ROS levels” said Janel Le Belle, an assistant researcher in Kornblum’s lab and lead author of the study. “Changes in cellular ROS can affect how the stem cells function. This study could lead to an understanding of how elevated ROS due to environmental factors might play a role in brain overgrowth, such as occurs in some cases of autism."
Illustration: Microsoft clipart.
University of California, Los Angeles Eli & Edythe Broad Center of Regenerative Medicine & Stem Cell Research News Release (01/07/11)
Abstract (Cell Stem Cell; Vol. 8, Issue 1, 59-71 (01/07/11))