Research | Deng Lab

Our Research

The neuroprotective effect of hypothermia has been demonstrated in both experimental and human spinal cord injury studies. Clinical trials have been initiated. However, the efficacy of the clinical application of hyperthermia to treat spinal cord injury remains significantly limited by delayed initiation of hypothermia in clinical practice. Dr. Deng has applied an FDA-approved and widely used clinic sedative drug rapidly induce up to 16 hours of moderate general hypothermia in ordinary ambient temperature without using any auxiliary cooling equipment. This early onset and long-lasting effect of hypothermia greatly improved both locomotor and bladder voiding functions. The current study focuses on verifying if this drug is superior to the conventional hypothermia in neuroprotection after spinal cord injury; uncovering the neuroprotective mechanism; and optimizing the therapeutic protocol of drug-induced hypothermia.

Bladder voiding dysfunction resulting from spinal cord injury can lead to severe complications such as renal failure, which is the major cause of morbidity and mortality among spinal cord injury patients. Recovery of bladder voiding is a top priority for spinal cord injury patients. So far, few effective therapies are available to target bladder function recovery. One major reason is the limited understanding of the mechanisms for both spontaneous and therapeutic functional recovery after spinal cord injury. Dr. Deng’s lab is working toward verifying a hypothesis that one population of propriospinal neurons participate in a spinal circuit to modulate external urethral sphincter activity and mediate the spontaneous recovery of external urethral sphincter function after spinal cord injury. Also, neuroinflammation is a principal secondary change following SCI and crucially modulates the acute and chronic pathological progression. Yet it is still unclear what regional and longitudinal profiles of this trauma-induced process contribute to bladder dysfunction. Taken together, this project will advance our understanding of both the short-term and long-term role of trauma-associated neuroinflammation and provide succinct translational insights into a model of bladder dysfunction associated with SCI.

Supraspinal axonal regeneration and innervation are both indispensable prerequisites for satisfactory urination functional recovery. Schwann cells are one of the most promising candidates facilitating axonal regeneration. Locomotor training prevents the dendritic atrophy of injured motoneuron. Dr. Deng’s strategy is to combine Schwann cell transplantation with locomotor training to promote supraspinal axonal regeneration and reinnervation on motoneurons to restore neural circuitry.

Published spinal cord injury studies in animals largely have employed a single sex design. Few reports in comparison have examined whether sex affects biochemical, anatomical or functional outcomes following spinal cord injury or have evaluated sex-based differences in response to therapy. Dr. Deng has found that male and female rats with spinal cord injury respond differently to the locomotor training. The mechanism responsible for this difference is unknown. His lab will apply large-molecule microdialysis to uncover sex-based different dynamic changes of these large-molecule factors in the process of locomotor training-affiliated functional recovery after spinal cord injury.

Research Funding

Inflammasome activation following spinal cord injury and associated bladder dysfunction

Showalter Trust

Plasticity of spinal L3 propriospinal neurons in urination recovery after thoracic SCI
NINDS

Synergistically enhanced neuroprotection via Dexmedetomidine induced early hypothermia and ERK activation after spinal cord injury
Department of Defense

Changes in inflammatory biomarkers from locomotor exercise-induced sex-based recovery after contusive spinal cord injury
Indiana Department of Health