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Donald Fox

Department
University of Houston
Houston, Texas 77204-

Office: JDA 2156
Phone: 713-743-1964
dafox@uh.edu


My laboratory's NIH funded research interests focus on the areas of mammalian retinal cell biology/biochemistry, molecular biology and neurotoxicology.  We have two main interrelated areas of basic physiological, biochemical, and cellular and molecular investigation. First, we are interested in the processes that regulate the apoptotic cell death in the normal developing retina and how these processes are altered by calcium, lead, pharmacological and toxicological compounds, and neurodegenerative diseases.  Second, we are interested in the short-term and long-term regulation of the retinal energy metabolism as it relates to mitochondria ATP production and the Na ,K -pump.


Exposure to lead during development leads to rod-mediated visual deficits and apoptotic cell death in rod photoreceptors.  The overall goal of my research is to determine the cellular mechanisms underlying these developmental defects.  To this end, we are examining lead-induced abnormalities in fundamental and interrelated cellular processes in freshly isolated and cultured retinas, in isolated rod photoreceptors, on isolated enzymes and, on mRNA and DNA isolated from retinas.  More specifically, we are investigating (1) the role of mitochondria in the apoptotic process and in intracellular calcium cell signaling, (2) various pharmacological and transgenic models of cytoprotection against the rod-mediated apoptosis, and (3) the functional properties of the rod Na ,K -pump and its regulation by dopamine and selected second messengers.


Some of the tools and techniques employed in my laboratory are: microsurgery techniques; tissue culture; light and electron microscopy; histochemical and fluorescent microscopy techniques; confocal microscopy, enzyme isolation and purification; enzyme assays and determination of enzyme kinetics; ligand binding assays, absorption spectroscopy; radioisotopes; HPLC; molecular biological procedures such as Northerns, Southerns, Westerns and gel mobility shift assays; transgenic animals.

Johnson JE Jr, Perkins GA, Giddabasappa A, Chaney S, Xiao W, White AD, Brown JM, Waggoner J, Ellisman MH, Fox DA. (2007). Spatiotemporal regulation of ATP and Ca2 dynamics in vertebrate rod and cone ribbon synapses. Molecular Vision, 13:887-919.

Xiao W, Liu W, Li Z, Liang D, Li L, White LD, Fox DA, Overbeek PA, Chen Q. (2006). Gene expression profiling in embryonic mouse lenses. Molecular Vision, 12:1692-8.

Perkins GA, Ellisman MH, Fox DA. (2004). The structure-function correlates of mammalian rod and cone photoreceptor mitochondria: observations and unanswered questions. Mitochondrion, 4(5-6):695-703.

He, L., Perkins, G.A., Poblenz, A.T., Ellisman, M.H., Harris, J.B., Hung M. and Fox, D.A. (2003). Bcl-xL overexpression blocks bax-mediated mitochondrial contact site formation and apoptosis in rod photoreceptors of lead-exposed mice. Proc. Natl. Acad. S

Perkins, G.A., Ellisman, M.H. and Fox, D.A. (2003). Three-dimensional analysis of mouse rod and cone mitochondrial cristae architecture: Comparisons and bioenergetic implications. Mol. Vision 9: 60-73.

Fox, D.A., Poblenz, A.T., He, L., Harris, J.B. and Medrano, C.J. (2003). Pharmacological strategies to block rod photoreceptor apoptosis caused by calcium overload: A mechanistic target-site approach to neuroprotection. Europ J. Ophthalmol. 13 (Suppl. 3):

Rothenberg, S.J., Schnaas, L., Salgado-Valladares, M., Casanueva E., Geller, A.M., Hudnell, H.K., Fox D.A. (2002). Increased ERG a- and b-wave amplitudes in 7-10 year old children resulting from prenatal lead exposure. Invest. Ophthalmol. Vis. Sci. 43: 20

Bell W, Clapp R, Davis D, Epstein S, Farber E, Fox DA, Holub B, Jacobson MF, Lijinsky W, Millstone E, Reuber MD, Suzuki D, Temple NJ. (2002). Carcinogenicity of saccharin in laboratory animals and humans: letter to Dr. Harry Conacher of Health Canada. International Journal Of Occupational And Environmental Health : Official Journal Of The International Commission On Occupational Health, 8(4):387-93.

Kueng-Hitz, N., Grimm, C., Lansel, N., Hafezi, F., He, L. Fox, D.A., Reme, C.E., Niemeyer, G, and Wensel, A. (2000). The retina of c-fos / and c-fos-/- mice: Electrophysiological, morphological and biochemical aspects. Investig. Ophthalmol. Vis. Sci. 41:

Söderpalm, A.K., Fox, D.A., Karlsson, J.-O. van Veen, T. (2000). Retinoic acid produces rod photoreceptor selective apoptosis in the developing mammalian retina. Investig. Ophthalmol. Vis. Sci. 41: 937-947.

He, L., Poblenz, A.T., Medrano, C.J. and Fox, D.A. (2000). Lead and calcium produce photoreceptor cell apoptosis by opening the mitochondrial permeability transition pore. J. Biol. Chem. 275: 12175-12184.

He L., Campbell M.L., Srivastava D., Blocker Y.S., Harris J.R., Swaroop, A. and Fox, D.A. (1998). Spatial and temporal expression of AP-1 responsive rod photoreceptor genes and bZIP transcription factors during development of the rat retina. Mol. Vis. 4:

Fox, D. A., M. L. Campbell and Y. S. Blocker. 1997. Functional alterations and apoptotic cell death in the retina following developmental or adult lead exposure. NeuroToxicology 18: 645-654.

Shulman, L. M. and D. A. Fox. 1996. Dopamine inhibits mammalian photoreceptor Na ,K -ATPase via a selective effect on the a3 isozyme. Proc. Natl. Acad. Sci. USA. 93:8034-8039.

Srivastava, D., R. L. Hurwitz and D. A. Fox. 1995. Lead and calcium-mediated inhibition of bovine rod cGMP phosphodiesterase: Interactions with magnesium. Toxicol. Appl. Pharmacol. 134:43-52

Medrano, C. J. and D. A. Fox. 1994. Concentration-dependent and substrate-dependent effects of calcium on retinal mitochondrial respiration: Physiological and toxicological studies. Toxicol. Appl. Pharmacol. 125:309-321.