Bo Chen, PhDAssistant Professor


Room 4.212D Research Building 17
Route: 0620 | Tel: (409) 747-2214 | bochen1@utmb.edu
Research Experts

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

Research Overview
Our lab studies how spinal cord injury changes surviving neurons and the circuits that connect the brain and spinal cord. We investigate why these circuits fail, how harmful cellular changes develop, and how targeted interventions can restore function. Our research focuses on movement, bladder control, and neuropathic pain. We combine quantitative three-dimensional imaging, circuit mapping and manipulation, and functional studies in experimental models to connect cellular mechanisms with recovery. inal cord.

Restoring spinal circuit function and protecting surviving neurons

During my postdoctoral training in Zhigang He’s laboratory, Harvard Medical School, we showed that enhancing KCC2, a neuronal chloride transporter,  function in spinal inhibitory interneurons can reactivate dormant relay pathways and mprove stepping after spinal cord injury in mice. This work demonstrated that targeting dysfunctional circuits can enable spared connections to support recovery. Our lab now investigates how KCC2regulation changes across neuronal populations after injury and how these changes affect circuit function.Fluorescent microscopy images show Vglut2+ and Vgat+ neurons with L10a‑EGFP and NeuN labeling in spinal cord tissue at T8.

We also study how injury compromises the health of surviving spinal neurons. Our work shows that excitatory and inhibitory neurons develop distinct patterns of swelling and loss, and that reducing prolonged excitatory neuron swelling can improve motor recovery in mice. Combining tissue clearing, light-sheet microscopy, and quantitative three-dimensional image analysis with targeted manipulations, we investigate strategies to preserve neurons and restore their function after injury.

Restoring brain–spinal communication for bladder control

Fluorescent images of PMC brainsLoss of bladder control is a major consequence of spinal cord injury. Normal urination requires coordinated activity between the brain and spinal circuits that control bladder contraction and urethral sphincter relaxation. Spinal cord injury disrupts this communication, impairing both voluntary control and effective bladder emptying.We investigate how descending signals from the pontine micturition center (PMC) engage spinal circuits and how these connections change after injury. By mapping and testing these pathways, we aim to identify circuit mechanisms that can be targeted to restore coordinated bladder function and voluntary control.

Understanding and targeting circuits that drive neuropathic pain

A diagram illustrates Brown-Séquard syndrome from a T8 spinal cord hemisection with sensory changes shown in a human figure and rodent model.Using a spinal cord hemisection model that reproduces key sensory features of Brown-Séquard syndrome, we examine how descending pathways and spinal circuits contribute to abnormal pain processing. By identifying and testing the athways involved, we aim to develop strategies to prevent neuropathic pain and reduce pain after it has become established.

Selected Publications:

2020–2026 ( *indicates Chen Lab-led research project)

*Tai, W. et al. (2026). In vivo reprogramming of NG2 glia improves bladder function after spinal cord injury. iScience 29. 

Wang, Y. et al. (2026). Injury-transduced oligodendrocytes modulate neuroinflammation and glial activation in diseased and non-diseased central nervous system. Nat. Commun. doi:10.1038/s41467-026-76159-2.

*Henwood, M. et al. (2025). Sensory Deficits in mice with Lateral Spinal Cord Hemisection Mimic the Brown-Sequard Syndrome. J. Neurosci doi:10.1523/JNEUROSCI.2373-24.2025. 

Metwally, S., et al. (2025). Cerebellum KCC2 protein expression plasticity in response to cerebral cortical stroke. Neurochemistry International, 184, 105939.

Huang, S., et al. (2025). Anisotropic hydrogel microelectrodes for intraspinal neural recordings in vivo. Nat. Commun., 16, 1127.

*Sandoval, A., et al. (2024). Regenerative and repair strategies for the central nervous system: Progress in basic and clinical research on spinal cord injury. In Neuroimmune Pharmacology and Therapeutics (pp. 975–985).

*Li, Q., et al. (2024). Reduction of prolonged excitatory neuron swelling after spinal cord injury improves locomotor recovery in mice. Science Translational Medicine, 16, eadn7095.

*Li, Q., et al. (2023). Advancing spinal cord injury research with optical clearing, light sheet microscopy, and artificial intelligence-based image analysis. Neural Regeneration Research, 18(12), 2661–2662.

*Yu, H., et al. (2022). Pipeline for fluorescent imaging and volumetric analysis of neurons in cleared mouse spinal cords. STAR Protocols, 3, 101759.

*Brommer, B., et al. (2021). Improving hindlimb locomotor function by non-invasive AAV-mediated manipulations of propriospinal neurons in mice with complete spinal cord injury. Nat. Commun., 12, 498.

Li, Y., et al. (2020). Microglia-organized scar-free spinal cord repair in neonatal mice. Nature, 587, 613–618.

Pre-2020
Chen, B. et al. (2018). Reactivation of dormant relay pathways in injured spinal cord by KCC2 manipulations. Cell, 174, 521–535.e13.

Liu, Y. et al. (2018). Touch and tactile neuropathic pain sensitivity are set by corticospinal projections. Nature, 561, 547–550.