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Junfang Wu, BM, PhD

Academic Title:

Associate Professor

Primary Appointment:

Anesthesiology

Secondary Appointment(s):

Anatomy Neurobiology

Location:

BRB, 6-009

Phone (Primary):

(410) 706-5189

Fax:

(410) 706-1639

Education and Training

BM (Clinical Medicine): Jiangxi Medical College, Nanchang, China
MS (Pharmacology): Jiangxi Medical College, Nanchang, China
PhD (Neuropharmacology): Nanjing Medical University, Nanjing, 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

Biosketch

The overall objective of research in my laboratory is to examine secondary injury processes following traumatic spinal cord injury (SCI) and pharmacological/gene therapeutic interventions for SCI. Specifically, we focus on: (1) Elucidating molecular mechanisms responsible for SCI-induced brain inflammation. This may lead to effective therapeutic interventions that limit post-SCI cognitive decline 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; (4) Examining the function and mechanism of NOX2 on nocifensive behaviors and central pain regulation after experimental SCI and traumatic brain injury (TBI). My ultimate goal is to understand the cellular and molecular mechanism of functional recovery after SCI and also to develop potentially therapeutic strategies.

Research/Clinical Keywords

Spinal cord injury, brain injury, inflammation, autophagy-lysosomal, neuropathic pain, NOX2, cell cycle pathway, microRNA, motor function, cognition, depression, neurons, astrocytes, microglia

Highlighted Publications

1. 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. In press.
2. 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.
3. 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.
4. Wu J, Renn CL, Faden AI, Dorsey SG (2013) TrkB.T1 contributes to neuropathic pain following spinal cord Injury through regulation of cell cycle pathways. Journal of Neuroscience, 33(30):12447-12463. PubMed PMID: 23884949; PubMed Central PMCID: PMC3721848.
5. Wu J, Yoo S, Wilcock D, Lytle LM, Leung PY, Colton CA, Wrathall JR (2010) Interaction of NG2+ glial progenitors and microglia/macrophages from the injured spinal cord. GLIA, 58(4):410-422. PubMed PMID: 19780197; PubMed Central PMCID: PMC2807472.

 The public URL for your collection is

 https://www.ncbi.nlm.nih.gov/sites/myncbi/1hWcekpAphrQm/bibliography/48103015/public/?sort=date&direction=descending

Additional Publication Citations

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)

  1. Wu J, Stoica B, Faden AI (2011) Cell cycle activation and spinal cord injury. Neurotherapeutics, 8(2):221- 228.
  2. 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.
  3. 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.
  4. 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)
  5. 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.

Additional Publication Highlighted:

  1. 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.
  2. 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
  3.  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
  4. 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.

Research Interests

The overall objective of research in my laboratory is to examine secondary injury processes following traumatic spinal cord injury (SCI) and pharmacological/gene therapeutic interventions for SCI. Specifically, we focus on: (1) Elucidating molecular mechanisms responsible for SCI-induced brain inflammation. This may lead to effective therapeutic interventions that limit post-SCI cognitive decline 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; (4) Examining the function and mechanism of NOX2 on nocifensive behaviors and central pain regulation after experimental SCI and traumatic brain injury (TBI). My ultimate goal is to understand the cellular and molecular mechanism of functional recovery after SCI and also to develop potentially therapeutic strategies.

Grants and Contracts

1. NIH R01 NS094527      PI: Junfang Wu                              

Period: 06/01/2016 - 05/31/2021                                             

Title: The Function and Mechanisms of Autophagy in Spinal Cord Injury

 

2. NIH R01 NR013601     MPI: Susan Dorsey/ Junfang Wu /Alan Faden

Period: 09/12/2017 - 06/30/2022

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

 

3. MPower Seed Grant    MPI: Junfang Wu/Steven Jay                   

Period: 07/01/2017 - 06/30/2018        

Title: Physiologically informed engineering of therapeutic exosomes for spinal cord injury repair

 

4. Craig Nielson Foundation Research (340442)  PI: Alan I. Faden   

Period: 09/01/2015 - 08/31/2018

Title: Cell Cycle Pathway Mediates SCI-induced Cognitive Impairment and Depression

Role: Co-Investigator

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:

  • Jessica J. Matyas, PhD, Post-doctoral Fellow
  • Marina Coll-Miro, PhD, Post-doctoral Fellow
  • Yun Li, PhD, Post-doctoral Fellow
  • Jingwen Yu, BA, MS, Student