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Shinichi Yoshimura, Tetsuyuki Teramoto, Michael J. Whalen, Michael C. Irizarry, Yasushi Takagi, Jianhua Qiu, Jun Harada, Christian Waeber, Xandra O. Breakefield, Michael A. Moskowitz
J Clin Invest. 2003;
112(8):1202
doi:10.1172/JCI16618
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e studied the role of FGF-2 on regulation of neurogenesis and cell loss in the granule cell layer (GCL) of the hippocampal dentate gyrus after experimental traumatic brain injury (TBI). In both FGF-2–/– and FGF-2+/+ mice subjected to controlled cortical impact, the number of dividing cells labeled with BrdU, injected on posttrauma days 6 through 8, increased at 9 days after TBI, and the number of BrdU-positive cells colabeled with neuron-specific nuclear antigen significantly increased at 35 days. However, in injured FGF-2–/– mice, BrdU-positive cells and BrdU-positive neurons (days 9, 35) were fewer compared with FGF-2+/+ mice. There was also a decrease in the volume of the GCL and the number of GCL neurons after TBI in both FGF-2–/– and FGF-2+/+ mice, but the decrease in both was greater in FGF-2–/– mice at 35 days. Overexpression of FGF-2 by intracerebral injection of herpes simplex virus–1 amplicon vectors encoding this factor increased numbers of dividing cells (day 9) and BrdU-positive neurons (day 35) significantly in C57BL/6 mice. Furthermore, the decrease in GCL volume was also attenuated. These results suggest that FGF-2 upregulates neurogenesis and protects neurons against degeneration in the adult hippocampus after TBI, and that FGF-2 supplementation via gene transfer can reduce GCL degeneration after TBI.
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