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Junfang Wu, BM, PhD

Academic Title:


Primary Appointment:


Secondary Appointment(s):

Anatomy Neurobiology


MSTF, 6-34D

Phone (Primary):

(410) 706-5189


(410) 706-1639

Education and Training

BM (Medicine): Jiangxi Medical College, China
MS (Pharmacology): Jiangxi Medical College, China
PhD (Neuropharmacology): Nanjing Medical University, China
Postdoctoral training: Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
Postdoctoral training: National Institutes of Health, Bethesda, MD


The focus of research in my lab is to understand the cellular and molecular mechanism of neurological dysfunction following spinal cord injury (SCI) and traumatic brain injury (TBI), with the ultimate goal of developing potentially therapeutic strategies. In particular, we are interested in pathological mechanisms including disruption of autophagy/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). The research tools used in my lab include rodent models of SCI and TBI, animal behavior testing (for motor function, pain, cognition, depression, olfaction), characterization of extracellular vesicles using Nanoparticle Tracking Analysis and ExoViewTM, advanced flow cytometry technology, quantitative image analysis, stereological cellular assessments, in vivo administration of therapeutics, as well as primary neuronal and glial culture.

Research/Clinical Keywords

Spinal cord injury, traumatic brain injury, aging, inflammation, neuroprotection, autophagy-lysosomal, neuropathic pain, Hv1/NOX2/ROS, TrkB.T1, microRNA, motor function, cognition, depression, neurons, astrocytes, microglia

Highlighted Publications

1. Ritzel RM, He J, Li Y, Cao T, Khan N, Shim B, Sabirzhanov B, Aubrecht T, Stoica BA, Faden AI, Wu L-J, Wu J. Proton extrusion during oxidative burst in microglia exacerbates pathological acidosis following traumatic brain injury. Glia, 2021 Mar;69(3):746-764. PMID: 33090575.

2. Ritzel RM, Li Y, He J, Khan N, Doran S, Faden AI, and Wu J. Sustained neuronal and microglial alterations are associated with diverse neurobehavioral dysfunction long after experimental brain injury. Neurobiology of Disease, 2020; 136:104713. PMID: 31843705

3. Li Y, Ritzel RM, Khan N, Cao T, He J, Matyas JJ, Sabirzhanov B, Liu S, Li H, Stoica BA, Loane DJ, Faden AI, Wu J. Delayed microglial depletion after spinal cord injury reduces chronic inflammation and neurodegeneration in the brain and improves neurological recovery in male mice. Theranostics, 2020; 10(25): 11376-11403. PMID: 33052221.

4. Khan N, Cao T, He J, Ritzel RM, Li Y, Henry RJ, Colson C, Stoica1 BA, Faden AI, Wu J. Spinal cord injury alters microRNA and CD81+ exosome levels in plasma extracellular nanoparticles with neuroinflammatory potential. Brain, Behavior, and Immunity, 2020 Dec 8:S0889-1591(20)32450-8. Online ahead of print. PMID: 33307173

5. Li Y, Ritzel RM, He J, Cao T, Sabirzhanov B, Li H, Liu S, Wu L-J, Wu J. The voltage-gated proton channel Hv1 plays a detrimental role in contusion spinal cord injury via extracellular acidosis-mediated neuroinflammation. Brain, Behavior, and Immunity, 2021 Jan; 91: 267-283. PMID: 33039662.

6. Li Y, Jones JW, M C Choi H, Sarkar C, Kane MA, Koh EY, Lipinski MM, Wu J. cPLA2 activation contributes to lysosomal defects leading to impairment of autophagy after spinal cord injury. Cell Death & Disease, 2019, 10(7):531. PMID: 31296844.

7. Matyas JJ, O’Driscoll CM, Yu L, Coll-Miro M, Daugherty S, Renn CL, Faden AI, Dorsey SG, Wu J. Truncated TrkB.T1-mediated astrocytes dysfunction contributes to impaired motor function and neuropathic pain after spinal cord injury. Journal of Neuroscience. 2017, 37(14): 3956-3971. PMID: 28270575.

8. Dutta D, Khan N, Wu J #, Jay SM #. Extracellular Vesicles as an Emerging Frontier in Spinal Cord Injury Pathobiology and Therapy. Trends in Neuroscience, in press, Jan, 2021. (# correspondent)

The public URL for your collection is

Research Interests

Neuroinflammation and Neuroprotection Following CNS Trauma

Dr. Wu’s laboratory studies secondary injury processes following traumatic spinal cord and brain injury (SCI/TBI) and pharmacological/gene therapeutic interventions for CNS trauma. Specifically, we focus on: (1) Elucidating molecular mechanisms responsible for SCI-induced brain neuroinflammation. This may lead to effective therapeutic interventions that limit post-SCI cognitive impairment and depression; (2) Demonstrating the function and the mechanisms of autophagy-lysosomal pathway and specific microRNAs in neuronal injury after SCI which could open a potential novel treatment avenue against SCI as well as identify candidate molecular targets for these manipulations; (3) Identifying the genetic and genomic factors that impact SCI-PAIN as well as identifying new therapeutic targets to reduce or eliminate SCI-PAIN, including a truncated isoform of the BDNF receptor tropomyosin related kinase B (trkB), trkB.T1, and NADPH oxidase pathways; (4) Examining the function and mechanism of voltage-gated proton channels Hv1 on neuroinflammation and neuropathic pain after experimental SCI and TBI. My ultimate goal is to understand the cellular and molecular mechanism of functional recovery after CNS trauma and also to develop potentially therapeutic strategies.

Grants and Contracts

1. NIH R01 NS094527       Junfang Wu (PI)       06/01/2016 - 05/31/2021

The Function and Mechanisms of Autophagy in Spinal Cord Injury

The goal of this grant is to identify mechanisms leading to inhibition of autophagy flux after spinal cord injury in mouse models, and to determine whether enhancement of autophagy can enhance functional recovery.

2. NIH R01 NS094527-05S1    Junfang Wu (PI)       06/01/2020- 05/31/2021

The New Roles of the Autophagy-lysosomal Pathway in Spinal Cord Injury-mediated Dementia

The goal of this grant is to identify whether accelerated inhibition of autophagy-lysosomal function in the aged brain after SCI contributes to brain neuroinflammation and neurodegeneration associated with dementia-like behaviors including cognitive decline and neuropsychological abnormalities.

3. NIH R01 NS110825       Junfang Wu/Long-Jun Wu (MPI)     05/15/2020 - 04/30/2025

The Function and Mechanisms of Voltage-Gated Proton Channel Hv1 in Spinal Cord Injury

The goal of this project is to target the signaling pathway of the voltage-gated proton channel Hv1, one of major ion channels expressed in microglia of the central nervous system, in order to decrease damage and increase functional recovery after SCI. 

4. NIH RF1 NS110637        Junfang Wu/Steven Jay (MPI)          09/01/2019 - 03/31/2024

Dementia after Spinal Cord Injury: Mechanisms and Therapeutic Targeting

The goal of this project is to identify how plasma exosomes-associated microRNAs drive remote brain neuroinflammation after SCI in order to allow future development of novel therapies.

5. NIH R01 2NR013601 Susan Dorsey/Junfang Wu/Alan Faden(MPI) 03/21/2012 - 06/30/2022

Spinal Mechanisms Underlying SCI-Induced Pain: Implications for Targeted Therapy

The major goals of this project are to investigate molecular mechanisms underlying neuropathic pain after spinal cord injury and novel targeted treatment strategies directed at such mechanisms.

6. NIH 1R01NS110635          Alan Faden/Junfang Wu (MPI)         04/01/2019 - 03/31/2024

Mechanism of Inflammatory Related Brain Dysfunction after Spinal Cord Injury

The major goal of this project is to understand the mechanisms responsible for microglia activation-induced inflammation in key brain centers after SCI in order to allow future development of novel therapies while focusing on SCI-triggered release of CCL21/NOX2 in key brain regions, in order to decrease damage and increase functional recovery after SCI.

7. NIH 1R01NS110567     Wei Chao/Junfang Wu/Lin Zou (MPI)    05/01/2019 - 02/29/2024

Targeting Brain Inflammation and Neurological Dysfunction in Sepsis

The major goal of this project is to examine the role of brain inflammation in neurocognitive dysfunction in sepsis and to identify potential therapeutic targets.

Lab Techniques and Equipment

A diverse array of in vivo and in vitro experimental models is used to study pathophysiological mechanisms of SCI. These include: contusion spinal cord injury (mouse & rat), controlled cortical impact (mouse), behavioral analysis (mechanical/thermal pain, facial spontaneous pain, locomotor/motor, learning and memory, depression/anxiety function), cell cultures (primary microglia, astrocytes, neurons; cell lines), adult microglia/macrophage isolation and FACS analysis, immunohistochemistry and state-of-the-art microscopy (light/fluorescence/confocal) and image analysis (stereology), biochemistry/molecular biology (qPCR, Western, etc).

Laboratory Personnel:

  • Junyun He, PhD, Research Associate
  • Yun Li, PhD, Post-doctoral Fellow
  • Rodney M. Ritzel, PhD, Post-doctoral Fellow
  • Zhuofan Lei, PhD, Post-doctoral Fellow
  • Rami A. Shahror, PhD, Post-doctoral Fellow
  • Niaz Khan, Graduate Student for MD, PhD.
  • Hui Li, BM, MS, Research Assistant
  • Courtney Colson, BA, Research Assistant