Junfang Wu, BM, PhD

Neuroinflammation and Neuroprotection Following CNS Trauma

The focus of research in Dr. Wu’s laboratory is to understand the cellular and molecular mechanisms of neurological dysfunction following spinal cord injury (SCI) and traumatic brain injury (TBI), with the ultimate goal of developing potential therapeutic strategies. In particular, we are interested in pathological mechanisms including disruption of autophagy and lysosomal pathway, astrocytic TrkB.T1, microglial Hv1 channel, NOX2, extracellular vesicles (EVs), and their contribution to neuroinflammation and neurodegeneration in both acute CNS trauma and aging conditions including chronic SCI/TBI and Alzheimer’s disease and related dementia (AD/ADRD).

Specifically, we focus on: (1) Demonstrating the function and the mechanisms of autophagy-lysosomal pathway in SCI. (2) Elucidating molecular mechanisms responsible for SCI-induced brain neuroinflammation and neurodegeneration. (3) Investigating the role of plasma and tissue extracellular vesicles (EVs) in secondary injury after CNS trauma. (4) Examining the function and mechanism of voltage-gated proton channels Hv1 on neuroinflammation and neuropathic pain after experimental SCI and TBI. (5) Elucidating the inflammatory mechanisms underlying olfactory dysfunction in the TBI model and its correlation with late-onset dementia-related pathology.

Multidisciplinary approaches include rodent models of SCI and TBI, diverse behavioral evaluation, characterization of EVs, quantitative image analysis, as well as molecular and cellular biology.

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