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
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. My ultimate goal is to understand the cellular and molecular mechanism of functional recovery after CNS trauma and to develop potentially therapeutic strategies. Specifically, my research dedicates to: (1) Elucidating molecular mechanisms responsible for SCI/TBI-induced CNS neuroinflammation and neurological dysfunction. (2) Addressing 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 NOX2. This may lead to effective therapeutic interventions that limit post-SCI cognitive decline and depression.
Spinal cord injury, brain injury, inflammation, autophagy-lysosomal, neuropathic pain, Hv1/NOX2, cell cycle pathway, microRNA, motor function, cognition, depression, neurons, astrocytes, microglia
1. Sabirzhanov B, Li Y, Coll-Miro M, Matyas JJ, He J, Kumar A, Ward N, Yu J, Faden AI, Wu J (2019) Inhibition of NOX2 signaling limits pain-related behavior and improves motor function in male mice after spinal cord injury: participation of IL-10/miR-155 pathways. Brain, Behavior, and Immunity, 80: 73-87. PMID: 30807841.
2. Li Y, Jones JW, M C Choi H, Sarkar C, Kane MA, Koh EY, Lipinski MM, Wu J (2019) cPLA2 activation contributes to lysosomal defects leading to impairment of autophagy after spinal cord injury. Cell Death & Disease, 10(7):531. PMID: 31296844.
3. Matyas JJ, O’Driscoll CM, Yu L, Coll-Miro M, Daugherty S, Renn CL, Faden AI, Dorsey SG, Wu J (2017) Truncated TrkB.T1-mediated astrocytes dysfunction contributes to impaired motor function and neuropathic pain after spinal cord injury. Journal of Neuroscience. 37(14): 3956-3971. PubMed PMID: 28270575.
4. Liu S, Sarkar C, Dinizo M, Faden AI, Koh EY, Lipinski MM, Wu J (2015). Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death. Cell Death & Disease. 6: e1582. PubMed PMID: 25569099; PubMed Central PMCID: PMC4669738.
5. Wu J # (correspondent), Zhao Z, Sabirzhanov B, Stoica BA, Kumar A, Luo T, Skovira J, Fade AI (2014). Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways. Journal of Neuroscience, 34(33): 10989-11006. PubMed PMID: 25122899; PubMed Central PMCID: PMC4131014.
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Selected review articles and book chapters:
<Modern Neuroscience Methods>. Wu JF and Liu M. Editor in chief. The Publisher of Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P.R.China. (1100 pages with A4 paper)
- Wu J, Stoica B, Faden AI (2011) Cell cycle activation and spinal cord injury. Neurotherapeutics, 8(2):221- 228.
- Zhao Z, Wu J (2012). Emotional and anxiety assessments in CNS disorders In: Animal models of acute neurological injuries II: Injury and Mechanistic Assessments. (Chen J, Xu XM, Xu Z, Zhang J. eds). Springer. p255-263.
- Lipinski MM, Wu J, Faden AI, Sarkar C (2015) Function and mechanisms of autophagy in brain and spinal cord trauma. Antioxidants & Redox Signaling, 23(6):565-77.
- Lipinski MM, Wu J (2015) Modification of autophagy-lysosomal pathway as a treatment after spinal cord injury. Neural Regeneration Research, 10(6):892-3. (perspective)
- Faden AI, Wu J, Stoica BA, Loane DJ (2016) Progressive inflammatory-mediated neurodegeneration after traumatic brain or spinal cord injury. British Journal of Pharmacology. 2016 Feb; 173(4): 681-91.
- Wu J* (correspondent) and Lipinski MM (2019) Autophagy in neurotrauma: good or bad or dysregulated. Cells, Jul 10; 8(7). PMID: 31295858.
Additional Publication Highlighted:
- Wu J# (correspondent), Zhao Z, Kumar A, Lipinski MM, Loane DJ, Stoica BA, Faden AI (2016) ER stress and disrupted neurogenesis in the brain are associated with cognitive impairment and depressive-like behavior after spinal cord injury. Journal of Neurotrauma, 33(21):1919-1935.
- Skovira JW*, Wu J*# (co-first author & correspondent), Matyas JJ, Kumar A, Hanscom M, Kabadi SV, Ray Fang, Faden AI (2016) Cell cycle inhibition limits inflammatory responses, neuronal loss and cognitive deficits induced by hypobaria exposure following traumatic brain injury. Journal of Neuroinflammation. 2016 Dec 1;13(1): 299
- Luo T, Wu J*(co-first author), Kabadi SV, Sabirzhanov B, Guanciale K, Hanscom M, Faden J, Cardiff K, Bengson CJ, Faden AI (2013). Propofol Limits Microglial Activation after Experimental Brain Trauma through Inhibition of Nicotinamide Adenine Dinucleotide Phosphate Oxidase. Anesthesiology, 119(6):1370- 88. PMID: 24121215
- Jakovceyski I, Wu J* (co-first author), Karl N, Leshchyns’ka I, Sytnyk V, Chen J, Irintchev A, Schachner M (2007) Glial scar expression of CHL1, the close homolog of the adhesion molecule CHL1 limits recovery after spinal cord injury. Journal of Neuroscience, 27(27): 7222-7233.
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.
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 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.
3. 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.
4. 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.
5. 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.
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).
- Yun Li, PhD, Post-doctoral Fellow
- Tuoxin Cao, PhD, Post-doctoral Fellow
- Junyun He, PhD, Post-doctoral Fellow
- Lulu Liu, MS, Research Assistant
- Niaz Khan, Graduate Student for MD, PhD.