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Jian-Guo Cui, MD, PhD
Instructor of Neuroscience
Neuroscience Center of Excellence
New Orleans, LA 70112
Phone: (504) 599-0909
jcui@lsuhsc.edu
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| Degrees |
1993-1999: PhD, Neurosurgery and Neuroscience, Karolinska Institute, Stockholm, Sweden
1977-1982: MD, Medicine, Bengbu Medical College, Bengbu, China
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| Bio |
Awards/Honorary Lectures:
1997: Keynote speaker. Can the pain relieving effect of spinal cord stimulation be enhanced by adjuvant pharmacotherapy? The XII World Society for Stereotactic and Functional Neurosurgery, Lyon, July 2, 1997.
1999: The Year Book of Anesthesiology and Pain Management selected the paper “Spinal cord stimulation attenuates augmented dorsal horn release of excitatory amino acids in mononeuropathy via a GABAergic mechanism” published in Pain 1997 by Cui JG, et al.
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| Clinical Interests |
Current Research
Synaptic Proteins and Neurotrophins in Neuropathic Pain
Mechanisms for neuropathic pain development are complex. Little is known about the role of synaptic proteins in neuropathic pain. Our research has screened a synaptic protein, agrin, which plays an important role in mediating neuropathic pain. Agrin has several isoforms that contribute to synaptic excitability following peripheral nerve injury. A decrease in some agrin isoforms result in neuropathic pain, while an increase in some isoforms suppress neuropathic pain. These isoforms interact with NMDA receptor subunit 1 to induce phosphorylation in NR1 subunits, and then to reduce pain. Viral vectors containing agrin genes injected into the dorsal horn of Bennett and Gazelius rat models express the proteins and also suppress neuropathic pain. Two agrin over-expression transgenic mice projects are under way to further agrin–pain study. Vanilloid receptor 1 (VR1) is a member of the transient receptor potential ion channel protein family, a non-selective cation channel, and presents on a subset of sensory neurons.Resiniferatoxin (RTX), an excitotoxic agonist for VR1, is a promising candidate for intractable pain treatment. In our studies, we demonstrated that RTX, injected into the dorsal root ganglia ipsilateral to nerve injury, suppressed both tactile allodynia and thermal hyperalgesia in a dose-dependent manner. These treated rats treated with high doses of RTX had preserved touch, cold, pain, and high-heat sensations, and exhibited hypoalgesia to low-heat stimulation. After RTX treatment, nerve growth factor (NGF) and NGF receptors tyrosine kinase A (TrkA) and p75 altered their expressions from one neuronal type to another in the DRGs. NGF and p75 expression changed from the small-size neurons in neuropathic rat DRGs to the large- and medium-size neurons. TrkA was expressed in the small-size neurons in the neuropathic rat DRGs, and was drastically reduced in all size neurons after RTX treatment. Brain derived neurotrophic factor and neurotrophin-3 displayed a similar change to NGF before and after RTX treatment. These data provide basic knowledge for RTX clinical applications.
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| Research Interests |
Keywords:
Synaptic Proteins and Neurotrophins in Neuropathic Pain
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| Teaching Activities |
2002-present: Instructor of Neuroscience,
Neuroscience Center of Excellence
LSU Health Sciences Center, New Orleans, LA
2001-2002: Postdoc, Gene Therapy Department
Tulane University, New Orleans, LA
2000-2001: Postdoc, Neurology, Dalhousie University, Halifax, Canada
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| Selected Publications |
Key Recent Papers:
1. Tender GC, Li YY, and Cui JG: Vanilliond receptor 1-positive neurons mediate thermal hyperalgesia and tactile allodynia. The Spine Journal, 8 (2008) 351-58.
2. Lukiw WJ, Zhao Y, and Cui JG: An NF-kB-sensitive microRNA-146a-mediated inflammatory circuit in Alzheimer's disease and in stressed human brain cells. J Biol Chem. 2008 Sep 18. [Epub ahead of print].
3. Cui JG, Zhang X, Zhao Y, Chen C, and Bazan NG: Allodynia and hyperalgesia suppression by a novel analgesic in experimental neuropathic pain. Biochem Biophys Res Commun. 350: 358-63 (2006).
4. Lukiw WJ, Cui JG, Marcheselli VL, Boedker M, Boetkjaer A, Gotlinger K, Serhan CN, Bazan NG: A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease. J Clin Invest. 115: 2774-83 (2005).
5.Sekiya I, Larson BL, Vuoristo JT, Cui JG, Prockop DJ: Adipogenic differentiation of human adult stem cells from bone marrow stroma (MSCs). J Bone Miner Research 19:256-64 (2004).
6. Sekiya I, Larson BL, Smith JR, Pochampally R, Cui JG and Prockop DJ: Expansion of Human Adult Stem Cells from Bone Marrow Stroma: Conditions that Maximize the Yields of Early Progenitors and Evaluate Their Quality. Stem Cells. 20:530-41 (2002).
7. Cui JG, Holmin S, Mathiesen T, Meyerson BA and Linderoth B: Possible roles of inflammation mediators in tactile hypersensitivity of rat mononeuropathic models, Pain 88:239-48 (2000).
8. Cui JG, O`Connor WT, Ungerstedt U, Linderoth B and Meyerson BA: Spinal cord stimulation attenuates augmented dorsal horn release of excitatory amino acids in mononeuropathy via a GABAergic mechanism, Pain 73:87-95 (1997).
9. Cui JG, Linderoth B and Meyerson BA: Effects of spinal cord stimulation on touch-evoked allodynia involve GABAergic mechanisms: An experimental study in the mononeuropathic rat, Pain 66:287-295 (1996).
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| Additional Info |
Funding:
“The role of VR1-posiitve neurons in central sensitization: Neuropathic pain management”.
Principle Investigator: Jian-Guo Cui
Translational Research Grant from Louisiana State University Health Sciences Center.
Period: 01/01/2007 –12/31/2009
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