Characterization of regenerative potential of Baxdeficient retinal ganglion cel

Robert Nickells, PhD
Board of Regents of the University of Wisconsin System (Madison, WI)
Year Awarded:
2003
Grant Duration:
April 1, 2003 to March 31, 2005
Disease:
Glaucoma
Award Amount:
$70,000
Grant Reference ID:
G2003007
Award Type:
Standard
Award Region:
US Midwestern

Characterization of regenerative potential of Baxdeficient retinal ganglion cel

Details


Ganglion cells are one of the cell types that die in glaucoma. The cell death process often occurs in two parts—first there is the death of the axon of the cell in the optic nerve, and then the body of the cell in the retina. Advances in research have developed techniques that can help prevent the death of the cell body. Although this is a step forward, it is not sufficient to effectively treat this disease, because a cell without an axon is useless in producing vision. In this project, Dr. Nickells and his team are targeting the function of a molecule called Bax. Mice that have no Bax gene exhibit cells with extraordinary resistance to stimuli that normally kill them, and may also have an increased capacity to regenerate. To test this theory, Dr. Nickells is testing a number of treatments that are known to stimulate regeneration to find out if they work better in these "death-arrested" cells. If he can prove that Bax-deficient cells have an increased capacity to regenerate, the next step would be develop drugs to mimic this situation in human ganglion cells.

Publications

Schlamp CL, Thliveris AT, Li Y, Kohl LP, Knop C, Dietz JA, Larsen IV, Imesch P, Pinto LH, Nickells RW. Insertion of the Beta-Geo promoter trap gene into the Fem1c gene of ROSA3 mice. Mol Cell Biol 24:3794-3803, 2004.  

Nickells RW. The molecular biology of retinal ganglion cell death: caveats and controversies. Brain Res Bull 62:439-446, 2004.  

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