Bo Chen, PhDAssistant Professor

Bo Chen final

Department of Neuroscience, Cell Biology, & Anatomy
Room 4.212D Research Building 17
Route: 0620 | Tel: (409) 747-2214  | bochen1@utmb.edu

Education and Training

Postdoctoral training, Boston Children’s Hospital, Harvard Medical School, Boston, U.S. 
Ph.D. Applied biomedical science, University of Reading, Reading, U.K.  
M.Sc. Biomedical science, Durham University, Durham, U.K. 
B.Sc. Biological science, University of Birmingham, Birmingham, U.K.

Research Interests

The challenge: 

Achieving functional recovery for severe CNS neurotraumas (e.g., spinal cord injury) remains a challenge for both basic and clinical neuroscience. In general, spinal cord injury causes disruption/dysfunction of the axonal connections between the brain and spinal cord. My research focuses on developing novel methods to promote functional recovery through enhancing and re-establishing functional connections between the brain and the spinal cords.

Our directions: 

Many human spinal cord injuries are anatomically incomplete (i.e., with spared axonal connections) but exhibit complete paralysis. This suggests that spared connections in the incompletely transected spinal cords are functionally dormant. Previously, we demonstrated that manipulating neuronal excitability by counter acting of downregulated KCC2 in spared neurons within spinal circuits is sufficient to promote functional recovery in an SCI model (Chen et al. Cell 2018). These results suggested that injury-induced pathological changes occur in both neurons and their circuits level. More recently, taking advantage of the compromised blood-spinal cord barrier (BBB) following SCI, we collaborate with Dr. Zhigang He at the Harvard University, optimized AAV9 vectors which efficiently transduce neurons in lesion-adjacent spinal segments in mice. With this powerful tool, it allows us not only to target these neurons, but also to manipulate their neuronal excitability within the injured spinal circuits. 

Our current studies are following up these exciting findings and trying to address two questions: 1) What is the mechanism(s) to cause the injury-induced pathological changes to neurons after SCI? What happened to survived neurons? How long do they keep in pathological conditions induced by SCI? Can we cure these neurons? 2) How to activate spared pathways to promote functional recovery post-SCI? SCI interrupts descending brain signals and suppresses the sources of modulation and excitation that render lumbar spinal circuits functioning. Therefore, increasing neuronal excitation in the spinal circuits below the injury site is an important therapeutic target for SCI. However, what is the best clinical strategy to achieve this?

Our approaches: 

To answer these questions, we will use a multidisciplinary approach combining mouse genetics, electrophysiology, detailed kinematic behavior analysis, gene therapy, and in vivo calcium imaging with optogenetic and chemogenomic tools.

Selected Publications:

Brommer, B*., He, M.*, Zhang, Z., Yang, Z., Page, J.C., Su, J., Zhang, Y., Zhu, J., Gouy, E., Tang, J., Williams, P., Dai, W., Wang, Q., Solinsky, R., Chen. B.*, He, Z.* (2021). Improving hindlimb locomotor function by Non-invasive AAV-mediated manipulations of propriospinal neurons in mice with complete spinal cord injury. Nat. Commun. 2–15.

Li, Y., He, X., Kawaguchi, R., Zhang, Y., Wang. Q., Monavarfeshani, A., Yang, Z., Chen, B., Shi, Z., Meng, H., Zhou, S., Zhu, J., Jacobi, A., Swarup, V., Popvich, P., Geschwind, D. and He. Z. (2020). Microglia-organized scar-free spinal cord repair in neonatal mice. Nature. 587, 613–618.

Liu, Y., Latremoliere, A., Li, X., Zhang, Z., Chen, M., Wang, X., Fang, C., Alexandre, C., Gao, Z., Chen, B., Ding, X., Zhou, J., Zhang. Y., Chen, C., Wang, K., Woolf, C., He, Z. (2018). Touch and tactile neuropathic pain sensitivity are set by cortical spinal projections. Nature 56, 541-50.

Chen, B., Li, Y., Yu, B., Zhang, Z., Brommer, B., Williams, P.R., Liu, Y., Hegarty, S.V., Zhou, S., Zhu, J., et al. (2018). Reactivation of Dormant Relay Pathways in Injured Spinal Cord by KCC2 Manipulations. Cell 174, 521-535.e13.

Liu, Y., Wang, X., Li, W., Zhang, Q., Li, Y., Zhang, Z., Zhu, J., Chen, B., Williams, P.R., Zhang, Y., et al. (2017). A Sensitized IGF1 Treatment Restores Corticospinal Axon-Dependent Functions. Neuron 95, 817-833.e4.

Chen, B. and He, Z. (2018). Reviving dormant nerves after spinal cord injury. Homeland Defense & Security Information Analysis Center (US DoD research entity), Volume 5, issue 4, 2019.