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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


2010-present   Member       Center for Shock, Trauma and Anesthesiology Research (STAR)


Research/Clinical Keywords

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

Highlighted Publications

1. Ritzel RM, Li Y, Lei Z, Carter J, He J, Choi HMC, Khan N, Li H, Allen S, Lipinski MM, Faden AI, Wu J. Functional and transcriptional profiling of microglial activation during the chronic phase of TBI identifies an age-related driver of poor outcome in old mice. GeroScience. 2022, April 22. PMID: 35451674

2. Li Y, Ritzel RM, Lei Z, Cao T, He J, Faden AI, Wu J. Sex dimorphism in neurological function after SCI is associated with disrupted neuroinflammation in both injured spinal cord and brain. Brain, Behavior, and Immunity. 2022 Mar; 101: 1-22. PMID: 34954073

3. Dutta D, Khan N, Wu J #, Jay SM #. Extracellular Vesicles as an Emerging Frontier in Spinal Cord Injury Pathobiology and Therapy. Trends Neurosci. 2021 June: 44(6): 492-506. PMID: 33581883. (# correspondent)

4. 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.

5. 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, 2021; 92:165-183. PMID: 33307173.

6. 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.

7. 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.

8. 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.

The public URL for your collection is

Additional Publication Citations

1. Jakovceyski I, Wu J * (co-first author), Karl N, Leshchyns’ka I, Sytnyk V, Chen J, Irintchev A, Schachner M. Glial scar expression of CHL1, the close homolog of the adhesion molecule CHL1 limits recovery after spinal cord injury. Journal of Neuroscience, 2007, 27(27): 7222-7233.    **Highlighted by Nature Medicine

2. Wu J, Yoo S, Wilcock D, Lytle LM, Leung PY, Colton CA, Wrathall JR. Interaction of NG2+ glial progenitors and microglia/macrophages from the injured spinal cord. GLIA, 2010, 58(4):410-422.

3. Wu J, Renn CL, Faden AI, Dorsey SG. TrkB.T1 contributes to neuropathic pain following spinal cord Injury through regulation of cell cycle pathways. Journal of Neuroscience, 2013, 33(30):12447-12463. PMID: 23884949.

4. Wu J, Zhao Z, Sabirzhanov B, Stoica BA, Kumar A, Luo T, Skovira J, Fade AI. Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways. Journal of Neuroscience, 2014, 34(33): 10989-11006. PMID: 25122899.

5. Liu S, Sarkar C, Dinizo M, Faden AI, Koh EY, Lipinski MM, Wu J. Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death. Cell Death & Disease. 2015, 6: PMID: 25569099.

6. Wu J, Zhao Z, Zhu X, Renn CL, Dorsey SG, Faden AI. Cell cycle inhibition limits development and maintenance of neuropathic pain following spinal cord injury. Pain, 2016, 157(2):488-503. PMID: 26797506.

7. Wu J and Lipinski MM. Autophagy in neurotrauma: good or bad or dysregulated. Cells, 2019 Jul 10; 8(7): 693. doi: 10.3390/cells8070693.pii: PMID: 31295858. Review.

8. Sabirzhanov B, Matyas J, Coll-Miro M, Yu L, Faden AI, Stoica BA, Wu J. Inhibition of microRNA-711 limits Ang-1 and Akt changes, tissue damage, and neurological dysfunction after contusive spinal cord injury in mice. Cell Death & Disease, 2019, 10(11):839. PMID: 31685802.

9. 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


10. 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, 91: 267-283. PMID: 33039662.


11. Zou L, He J, Gu L, Shahror RA, Li Y, Cao T, Zhu J, Wang S, Fan X, Wu J#, Chao W. Brain Innate Immune Response via Extracellular miRNA-TLR7 Sensing during Polymicrobial Sepsis. Brain, Behavior, and Immunity. 2022 Feb, 100: 10-24. PMID: 34808293. (# correspondent)








Research Interests

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 potentially 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 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.

Grants and Contracts

1. NIH 2RF1 NS094527          Wu / Lipinski               06/01/2016 - 05/31/2027

The Function and Mechanisms of Autophagy in Spinal Cord Injury

The goal of this grant is to identify whether accelerated inhibition of autophagy-lysosomal function in the ageing brain through perturbation of lysosomal lipid homeostasis, ultimately aggravating long-term pathological and functional outcomes and increasing posttraumatic dementia risk.                                 

Role: Contact PI

2. NIH R01 AG077541        Wu / Liu (PI)                 06/15/2022- 03/31/2027

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.

Role: Contact PI

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. 

Role: Contact PI

4. NIH RF1 NS110637          Wu/ 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.

Role: Contact PI

5. NIH 1R01NS110567         Chao/ Wu/ Zou (MPI)       05/01/2019 - 02/29/2025

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.

Role: PD/PI

6. NIH 1R01NS110635          Faden/ 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.

Role: PD/PI

7. NIH R01 2NR013601    Dorsey/ Wu/ Faden (MPI)     03/21/2012 - 06/30/2023

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.

Role: PD/PI

8. NIH R01NS119275    Co-I           07/01/2021 - 06/30/2026    

Using NAD+ precursor for treatment of global cerebral ischemia


Lab Techniques and Equipment

A diverse array of in vivo and in vitro experimental models is used to study pathophysiological mechanisms of SCI and TBI. 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:

  • Yun Li, PhD, Research Associate
  • Zhuofan Lei, PhD, Post-doctoral Fellow
  • Balaji Krishnamachary, PhD, Post-doctoral Fellow
  • Liwen Wei, MD, Postdoctoral Research Fellow
  • Hui Li, BM, MS, Research Assistant
  • Kavitha Brunner, BS, Research Assistant