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TISSUE-SPECIFIC STEM CELLS

A High Concentration of Epidermal Growth Factor Increases the Growth and Survival of Neurogenic Radial Glial Cells Within Human Neurosphere Cultures

Department of Anatomy and Neurology, Neuroscience Training Program, and Waisman Center, University of Wisconsin-Madison, Madison, Wisconsin, USA

Key Words. Epidermal growth factor • Neurogenesis • Cortical progenitor • Stem cell • Cerebral cortex • Development

Correspondence: Correspondence: Clive N. Svendsen, Ph.D., Waisman Center, University of Wisconsin-Madison, 1500 Highland Avenue, Madison, Wisconsin 53705-2280, USA. Telephone: 608-265-8668; Fax: 608-263-5267; e-mail: svendsen{at}waisman.wisc.edu

Received on April 23, 2007; accepted for publication on November 13, 2007.

First published online in STEM CELLS EXPRESS  November 21, 2007.


Human neural progenitor cells (hNPC) isolated from the fetal cortex can be expanded as aggregates of cells termed neurospheres. Traditional methods have used 20 ng/ml epidermal growth factor (EGF) to drive the proliferation of these cells. Here, we show that 100 ng/ml EGF can significantly increase growth rates of hNPC at later passages. This was through increased survival of dividing cells rather than increased proliferation and associated with prolonged activation of ErbB2 and phosphorylated Akt. High EGF also resulted in a larger proportion of elongated "radial glial"-like cells within the growing neurospheres and increased expression of the radial glial markers. The number of new neurons generated from cultures maintained in 100 ng/ml EGF was significantly higher than from 20 ng/ml EGF. Thus, high concentrations of EGF increase the survival of a highly neurogenic human radial glial cell.

Disclosure of potential conflicts of interest is found at the end of this article.

This article has been cited by other articles:

				H.-J. Kim, E. McMillan, F. Han, and C. N. Svendsen Regionally Specified Human Neural Progenitor Cells Derived from the Mesencephalon and Forebrain Undergo Increased Neurogenesis Following Overexpression of ASCL1 Stem Cells, February 1, 2009; 27(2): 390 - 398. [Abstract] [Full Text] [PDF]