Faculty > Beebe

David C. Beebe, Ph.D.

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Janet and Bernard Becker Professor, Ophthalmology and Visual Sciences
Professor, Cell Biology and Physiology
(314) 362-1621

B. S. Zoology, University of Rhode Island (1966); M. S. Biomedical Sciences, Brown University (1969); Ph.D. Biology, University of Virginia (1974); Fellow, Molecular Genetics, NICHHD, NIH, Bethesda, MD (1974-1976)

Research Area: Cataract, Cornea

Research Interests:

Molecular and cellular biology of eye development ; mechanism of nuclear cataract formation

My laboratory uses conditional gene knockouts, transgenic mice and microarrays to define the signaling pathways that are required for the normal development of the eye. We also study human subjects to identify the causes of, and design preventions for, age-related cataracts, the most common cause of blindness in the world.

Current projects:

  1. Using tissue-specific deletion of receptors and signal transducers in the transforming growth factor-ß (TGFß) superfamily (BMP/TGFß/activin) to define the functions of these pathways in eye development
  2. Deleting fibroblast growth factor family (FGF) receptors from the lens to test the functions of FGF signaling alone and together with members of the TGFß superfamily in lens development.
  3. Vascular endothelial growth factor (VEGF) is produced constitutively and VEGF receptors are activated in the lenses of several species, including humans. We are using conditional deletion of the VEGF gene from the lens and mice that express specific isoforms of VEGF to examine the importance of VEGF signaling for lens function.
  4. Our studies suggest that increased exposure to oxygen from the retina causes human nuclear cataracts. We are further testing this hypothesis and are determining the factors that normally protect the lens from oxygen exposure.
  5. We found that intraocular oxygen levels regulate postnatal growth of the lens and that HIF1a, the major hypoxia-regulated transcription factor, mediates the effect of oxygen on lens growth. We are using HIF1 conditional knockout and transgenic mice to identify the molecular pathway by which HIF and hypoxia regulate lens growth.

Selected publications:

  1. Garcia CM, Yu K, Zhao H, et al. Signaling through FGF receptor-2 is required for lens cell survival and for withdrawal from the cell cycle during lens fiber cell differentiation. Dev Dyn 2005. Jun;233(2):516-27.
  2. Holekamp , NM , Shui Y-B, Beebe DC . Vitrectomy surgery increases oxygen exposure to the lens: A possible mechanism for nuclear cataract formation. Am J Ophthalmol 2005 139:302-310.
  3. Beebe D, Garcia C, Wang, X. et al. Contributions by members of the TGFß superfamily to lens development. Int J Dev Biol 2004 48:845-56.
  4. Harocopos GJ, Shui YB, McKinnon M, et al. Importance of vitreous liquefaction in age-related cataract. Invest Ophthalmol Vis Sci 2004 45(1):77-85.
  5. Shui YB, Wang X, Hu JS, et al. Vascular endothelial growth factor expression and signaling in the lens. Invest Ophthalmol Vis Sci 2003 44(9):3911-3919.

Belecky -Adams TL, Adler R, Beebe DC. Bone morphogenetic protein signaling and the initiation of lens fiber cell differentiation. Development 2002 129:3795-3802.



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