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Dr Xuenong Bo MB, MSc, PhD
Non-clinical Senior Lecturer in Neurosurgery

 

 

Contact details:

Tel: +44 20 7882 2294
Fax: +44 20 7882 2180
Email: x.bo@qmul.ac.uk
Address:

Centre for Neuroscience and Trauma,
Barts and The London School of Medicine and Dentistry,
4 Newark Street,
London E1 2AT,
United Kingdom

 

 

 

 

 

 

 

Biography

Xuenong Bo obtained his MB degree in 1983 and MSc degree in pharmacology in 1986 in the Third Military Medical University in China . He joined the Department of Anatomy and Developmental Biology in University College London as a Visiting Scientist in 1987 and was awarded a PhD degree in neurobiology from University of London in 1992. He continued to work as a Research Fellow and then Senior Research Fellow in University College London. During this period he spent one and half years in the MRC Laboratory of Molecular Biology in Cambridge as a Visiting Fellow. From 1995 to 2001 he mainly based his research work in the Wellcome Laboratory for Molecular Pharmacology in University College London. In 2001 he worked as a Senior Research Fellow in the Institute of Molecular Physiology in the University of Sheffield . In 2002 he was appointed as a Non-Clinical Lecturer in the Academic Department of Neurosurgery in Barts and the London School of Medicine and Dentistry. In 2008 he was promoted to Senior Lecturer.

 

Research Activity

The current research mainly focuses on using gene-targeting techniques to promote axonal regeneration of injured neurons in the central nervous system (CNS). As the lack of regeneration capacity of injured CNS neurons, presence of myelin-associated inhibitory molecules, and the formation of glial scars are the main obstacles for successful regeneration of CNS axons, strategies have been developed to overcome such obstacles. One of them is to block the effect of the inhibitory molecules by targeting a key molecule in their common signal pathway, the Rho kinase, using lentiviral vector to deliver a dominant negative mutant. Another strategy is to express a secretable non-functional receptor for the inhibitory molecules to neutralize their effects. The third strategy is to co-express neurotrophic factors to stimulate the regeneration mechanism of the injured neurons. The forth strategy is to express permissive agent such as polysialic acid at the gial scar and at the injury site to modify the inhibitory environment. Transplantation of genetically modified Schwann cells into the injured CNS is also used to promote neural regeneration. The final goal is to develop gene and/or cell therapy for the treatment of injuries to spinal cord and brain.

 

Key Publications

  1. Bo X, Wu DS, Yeh J, Zhang Y. (2011) Gene therapy approaches to facilitate axonal regeneration after spinal cord and spinal root injuries. Current Gene Therapy (in press).
  2. Luo J, Bo X, Wu D, Yeh J, Richardson PM, Zhang Y. (2011) Promoting the survival, migration, and integration of transplanted Schwann cells by over-expressing polysialic acid. Glia 59: 424-434
  3. Richardson PM, Miao T, Wu D, Yeh, J, Zhang Y, Bo X. (2009) Responses of the nerve cell body to axotomy. Neurosurgery 65: Suppl A74-A79.
  4. Zhang Y, Yeh J, Richardson PM, Bo X. (2008) Cell adhesion molecules of the immunoglobulin superfamily in axonal regeneration and neural repair. Restorative Neurology and Neuroscience 26: 81-96.
  5. Wu D, Yang P, Zhang X, Luo J, Haque ME, Yeh J, Richardson PM, Zhang Y, Bo X. (2009) Targeting a dominant negative Rho kinase to neurons promotes axonal outgrowth and partial functional recovery after rat rubrospinal tract lesion. Molecular Therapy. 17: 2020-2030.
  6. Zhang Y, Zhang X, Wu D, Verhaagen J, Richardson PM, Yeh J, Bo X. (2007) Lentiviral-mediated expression of polysialic acid in spinal cord and conditioning lesion promote regeneration of sensory axons into spinal cord. Molecular Therapy. 15: 1796-1804.
  7. Zhang Y, Ghadiri-Sani M, Zhang X, Richardson PM, Yeh J, Bo X. (2007) Induced expression of polysialic acid in the spinal cord promotes regeneration of sensory axons. Molecular and Cellular Neuroscience. 35: 109-119.
  8. Zhang Y, Zhang X, Yeh J, Richardson P, Bo X. (2007) Engineered expression of polysialic acid enhances Purkinje cell axonal regeneration in L1/GAP-43 double transgenic mice. European Journal of Neuroscience. 25: 351-361.
  9. Zhang Y, Bo X, Schoepfer R, Holtmaat AJDG, Verhaagen J, Emson PC, Lieberman AR, Anderson PN. (2005) GAP-43 and L1 act synergistically to promote regeneration of Purkinje cell axons in vivo. Proceedings of the National Academy of Sciences of USA. 102: 14883-14888.
  10. Bo X, Jiang LH, Wilson HL, Kim M, Burnstock G, Surprenant A, North RA. (2003) Pharmacological and biophysical properties of the human P2X5 receptor. Molecular Pharmacology. 63:1407-1416.
  11. Bo X, Schoepfer R, Burnstock G. (2000) Molecular cloning and characterization of novel subtype of ATP P2X receptors from embryonic chick skeletal muscle. Journal of Biological Chemistry. 275:14401-14407.

>> Publications since 2001

 

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