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Junfang  Wu

Junfang Wu B.M., Ph.D.

Academic Title: Associate Professor
Primary Appointment: Anesthesiology
Secondary Appointments: Anatomy and Neurobiology
Location: BRB, 6-009
Phone: 410-706-5189
Lab: 410-706-5762

Personal History:

Junfang Wu, PhD, is an Assistant Professor of Anesthesiology and Faculty Member at the Center for Shock, Trauma and Anesthesiology Research (STAR) at the University of Maryland School of Medicine, Baltimore, Maryland. Dr. Wu obtained her PhD in Neuropharmacology in 1995 at the Department of Pharmacology, Nanjing Medical University, China. She pursued postdoctoral training and was then recruited as associate Professor at the Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China. In 2000 Dr. Wu was recruited to the NIH to perform further postdoctoral training. She joined the faculty of Georgetown University Medical Center in 2007 and then moved to the University of Maryland School of Medicine in February 2010 and is currently Assistant Professor of Anesthesiology.

Research Interests:

Dr. Wu's research is focused on examining secondary injury processes following traumatic spinal cord injury (SCI) and pharmacological/gene therapeutic interventions for SCI. More specifically, she examines the pathophysiological role of cell cycle pathways, microglia and astrocytes at both injured spinal cord and supratentorial sites following SCI using complementary genetic and pharmacological strategies. She also studies nocifensive behaviors and central pain regulation after experimental SCI and traumatic brain injury.

Active Research Grants:

Cell Cycle Pathway Inhibition Decreases Peripheral Neuropathic Pain (Renn/Wu)
NIH R21 NR014053
Role: Multiple Principle Investigator
Period: 05/09/2013 - 04/30/2015

Genetics of Spinal Cord Injury Induced Chronic Pain (Wu)
NIH P30 NR014129
Role: Principle Investigator for Subproject
Period: 09/01/2012 - 08/31/2017

Spinal Mechanisms Underlying SCI-induced Pain: Implications for Targeted Therapy
NIH R01 NR013601
Role: Co-Investigator Period: 03/21/2012 - 02/28/2017


Selected Publications

Wu J, Li J, Huang KP and Huang FL (2002) Attenuation of protein kinase C and cAMP-dependent protein kinase signal transduction in the neurogranin knockout mouse. Journal of Biological Chemistry, 277(22): 19498-19505.

Wu J, Huang KP and Huang FL (2003) Participation of NMDA-mediated phosphorylation and oxidation of neurogranin in the regulation of Ca2+- and Ca2+/calmodulin-dependent neuronal signaling in the hippocampus. Journal of Neurochemistry, 86: 1524-1533.

Huang FL, Huang KP, Wu J, Boucheron C (2006) Environmental enrichment enhances neurogranin expression and hippocampal learning and memory but fails to rescue the impairments of neurogranin null mutant mice. Journal of Neuroscience, 26(23): 6230-6237.

Chen J, Wu J, Irintchev A, Apostolova I, Kuegler S, Skup M, Schachner M (2007) Adeno-associated virus-mediated adhesion molecule L1 expression ameliorates inhibitory glial scar formation and promotes axonal regeneration and functional recovery after spinal cord injury in adult mice. Brain, 130: 954-969.

Jakovceyski I, Wu J * (co-first author), Karl N, Leshchynsâ?Tka 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.

Kolata S, Wu J, Light K, Schachner M, Matzel LD (2008) Impaired working memory duration but normal learning abilities found in mice that are conditionally deficient in the close homolog of L1. Journal of Neuroscience, 28(50): 13505-13510.

Wu J # (correspondent), Wrathall JR, Schachner M (2010) Phosphatidylinositol 3-kinase/protein kinase Cδ activation induces close homolog of adhesion molecule L1 (CHL1) expression in cultured astrocytes. GLIA, 58(3): 315-328.

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.

Wu J # (correspondent), Leung PY, Sharp A, Lee HJ, Wrathall JR (2011) Increased expression of the close homolog of the adhesion molecule L1 (CHL1) in different cell types over time after rat spinal cord contusion. Journal of Neuroscience Research, 89(5): 628-638.

Wu J # (correspondent), Stoica B, Faden AI (2011) Cell cycle activation and spinal cord injury. Neurotherapeutics, 8(2):221- 228. (review)

Whittaker MT, Zai LJ, Lee HJ, Pajoohesh-Ganji A, Wu J, Sharp A, Wyse R, Wrathall JR (2012). GGF2 (Nrg1- β3) treatment enhances NG2+ cell response and improves functional recovery after spinal cord injury. GLIA, 60(2): 281-294.

Dickey JS, Baird BJ, Redon CE, Avdoshina V, Palchik G, Wu J, Kondratyev A, Bonner WM, Martin OA (2012) Susceptibility to bystander DNA damage is influenced by replication and transcriptional activity. Nucleic Acids Res, 40(20):10274-86. PMID: 22941641

Wu J # (correspondent), Stoica BA, Dinizo M, Pajoohesh-Ganji A, Piao C, and Faden AI (2012) Delayed cell cycle pathway modulation facilitates recovery after spinal cord injury. Cell Cycle, 11(9): 1782-1795.

Wu J # (correspondent), Pajoohesh-Ganji A, Stoica BA, Dinizo M, Guanciale K, and Faden AI (2012) Delayed expression of cell cycle proteins contributes to astroglial scar formation and chronic inflammation after rat spinal cord contusion. Journal of Neuroinflammation, 9(1): 169-179.

Wu J # (correspondent), Kharebava G, Piao C, Stoica BA, Dinizo M, Sabirzhanov B, Hanscom M, Guanciale K, and Faden AI (2012) Inhibition of E2F1/CDK1 pathway attenuates neuronal apoptosis in vitro and confers neuroprotection after spinal cord injury in vivo. PLoS One, 7(7): e42129.

Lee HJ, Wu J, Chung J, Wrathall JR (2013). SOX2 expression is up-regulated in adult spinal cord after contusion injury in both glial progenitors and ependymal stem cells. Journal of Neuroscience Research, 91(2):196-210. PMID:23169458.

Piao CS, Stoica BA, Wu J, Sabirzhanov B, Zhao Z, Cabatbat R, Loane DJ, Faden AI (2013). Late exercise reduces neuroinflammation and cognitive dysfunction after traumatic brain injury. Neurobiology of Disease, 54:252-263. PMID: 23313314

Wu J # (correspondent), Raver C, Piao C, Keller A, Faden AI (2013) Cell cycle activation contributes to increased neuronal activity in the posterior thalamic nucleus and associated chronic hyperalgesia after rat spinal cord contusion. Neurotherapeutics, 10(3):520-538.

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.

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

Wu J # (correspondent), Stoica BA, Luo T, Sabirzhanov B, Zhao Z, Guanciale K, Nayar SK, Foss CA, Pomper MG, Faden AI (2014). Isolated spinal cord contusion in rats induces chronic brain neuroinflammation, neurodegeneration, and cognitive impairment: Involvement of cell cycle activation. Cell Cycle, 13(15): 2446-2458.

Sabirzhanov B, Zhao Z, Stoica BA, Loane DJ, Wu J, Borroto C, Dorsey SG, Faden AI (2014). Down-regulation of miR-23a and miR-27a following experimental traumatic brain injury induces neuronal cell death through activation of pro-apoptotic Bcl-2 proteins. Journal of Neuroscience, 34(30): 10055-10071.

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.

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, Jan 8; 6: e1582.

Zhao Z, Sabirzhanov B, Wu J, Faden AI, Stoica BA (2015) Voluntary exercise preconditioning activates multiple anti-apoptotic mechanisms and improves neurological recovery after experimental traumatic brain injury. J Neurotrauma. 2014 Nov 24. [Epub ahead of print]