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Dong Feng Chen, Ph.D., M.D.

Assistant Professor of Ophthalmology

Schepens Eye Research Institute
20 Staniford St.
Boston, MA 02114
Telephone: 617 912-7490
Fax: 617- 912-0174
Email: dfchen@vision.eri.harvard.edu
Predocs: 0 Postdocs: 5 Completed PhD's: 1

 Dong Feng Chen

Why cannot neurons in the mature retina or central nervous system (CNS) of mammals be regenerated after injury? Is the regenerative failure driven by intrinsic mechanisms of neurons or neural stem cells, or is it a result of changes in the CNS environment? These are not only fundamental issues in basic neurobiology research, but also critical questions in clinical applications.

One part of our work has been dedicated to study the molecular mechanisms that prevent CNS axon regeneration. At a certain point in development, axons in the mammalian CNS lose their ability to regenerate after injury. Using the optic nerve model, we have shown that the absence of intrinsic, Bcl-2-supported mechanisms of axonal growth and the induction of reactive glial cells after injury are two essential elements in adult CNS regenerative failure. Our current efforts aim to combine these paradigms to design therapeutic strategies for treating diseases and damages involving optic nerve or spinal cord damage.

In addition, many neurodegenerative diseases, such as Alzheimer’s disease, Parkingson’s disease, glaucoma, and age-related macular degeneration, share a common tragic feature – neurons die; hence the functions carried out by these neurons are lost. Previously, it is believed that neural stem cells present only in restricted regions in the brain, and the rest of the CNS has very limited ability to regenerate. Recent findings resulted from our research suggest that endogenous neural stem cells are distributed widely throughout the CNS, including the retina, brain and spinal cord, and they can be activated to generate new neurons and enhance CNS function. Currently, my group is devising strategies to activate the dormant capacity of these stem cells in the adult brain and retina. The results of these studies will have important implications for the development of therapies to repair the CNS/retina after trauma, stroke, and other insults and diseases.

 

References:

  • Kinouchi R, Takeda M, Yang L, Wilhelmsson U, A. Lundkvist, Pekny M, and Chen DF. (2003) Robust neural integration from retinal transplants in mice deficient in GFAP and vimentin. Nature Neurosci. 6, 863-868.
  • Liu Y, Bula D, Arroyo JG, and Chen DF. (2004) Preventing retinal detachment-associated photoreceptor cell loss in Bax-deficient mice. Invest. Ophthalmol. Vis. Sci. 45, 648-654.
  • Cho K-S, Ma HF, Yang L, Lu B, Pekny M, and Chen DF. (2005) Re-establishing the regenerative potential of CNS axons in adult mice. J. Cell Sci. 118, 863-872.
  • Jiao J, Huang XA, Feit-Leithman RA, Neve RL, Snider W, Dartt DA, and Chen DF. (2005) Bcl-2 enhances Ca2+ signaling to support the intrinsic regenerative capacity of CNS axons. EMBO J. 24, 1068-1078.
  • Koprivica V, Cho KS, Park JB, Yiu G, Atwal J, Gore B, Kim JA, Lin E, Tesser-Lavigne M, Chen DF, and He Z. (2005) EGFR Activation Mediates Inhibition of Axon Regeneration by Myelin and Chondroitin Sulfate Proteoglycans. Science 310,106-10.