Shuanglin Hao, MD, Ph.D.
Dr. Hao’s laboratory focuses on the neurochemical mechanisms of chronic pain and opioid abuse supported by NIH.
Infection of the nervous system with the human immunodeficiency virus type 1 (HIV-1) can lead to sensory disorders. HIV-associated sensory neuropathy (HIV-SN) is the most common form of peripheral neuropathy, affecting about 30% of people with acquired immune deficiency syndrome (AIDS). Studies suggest that chemokines and cytokines whose expression is induced by HIV envelope glycoprotein gp120 and/or NRTIs may play an important role in the pathogenesis of painful HIV-SN.
Clinical utility of opiate analgesics is often hampered by the development of hyperalgesia, tolerance/dependence. Glia is highly heterogeneous within the CNS; glial activation during chronic neuroinflammatory diseases may demonstrate regional differences in expression levels of proteins in the nervous system. Chronic administration of systemic or intrathecal morphine activates glia cells and upregulates proinflammatory factors.
We are actively pursuing neuropharmacological and viral vector gene therapy approaches for controlling such pathological pain processes and opioid tolerance and opioid withdrawal.
- Chronic pain – Neurochemical mechanisms on HIV-related neuropathic pain
- Opiate abuse – Neurogenic mechanisms on opioid abuse.
- Glia, neurons, and mitochondrial dysfunction
- Viral vectors expressing targeted proteins to treat neuropathic pain and opiate abuse (gene therapy).
Hao S. Anti-inflammatory cytokines mediated by HSV vector reduces morphine tolerance and physical withdrawal. Symposium 2, International Narcotics Research Conference 2012, Kansas City, MO,
Hao S. The Molecular Mechanisms of HIV- related Neuropathy and Pain, Symposium 327, The 31st Annual Scientific Meeting of the American Pain Society 2012 • Honolulu, HI
Selected PublicationsOuyang H, Liu S, Zeng W, Levitt RC, Candiotti KA, Hao S. An emerging new paradigm in opioid withdrawal: a critical role for glia-neuron signaling in the periaqueductal gray. ScientificWorldJournal. 2012;2012:940613. , Sun J, Liu S, Mata M, Fink DJ, Hao S. Transgene-mediated expression of tumor necrosis factor soluble receptor attenuates morphine tolerance in rats. Gene Ther. 2012;19(1):101-8 Chattopadhyay M, Zhou Z, Hao S, Mata M, Fink DJ. Reduction of voltage gated sodium channel protein in DRG by vector mediated miRNA reduces pain in rats with painful diabetic neuropathy. Mol Pain. 2012 Mar 22;8(1):17. Zheng W, Zheng X, Liu S, Ouyang H, Levitt RC, Candiotti KA, Hao S. TNFα and IL-1β are mediated by both TLR4 and Nod1 pathways in the cultured HAPI cells stimulated by LPS. Biochem Biophys Res Commun. 2012 Apr 20;420(4):762-7. Zheng X, Zheng W, Liu S, Patel HM, Xia X, Ouyang H, Levitt RC, Candiotti KA, Hao S. Crosstalk Between JNK and NF-κB in the KDO2-Mediated Production of TNFα in HAPI Cells. Cell Mol Neurobiol. 2012 Jul 27. Zheng W, Ouyang H, Zheng X, Liu S, Mata M, Fink DJ, Hao S. Glial TNFα in the spinal cord regulates neuropathic pain induced by HIV gp120 application in rats. Mol Pain. 2011 May 20;7:40. Zheng X, Ouyang H, Liu S, Mata M, Fink DJ, Hao S. TNFα is involved in neuropathic pain induced by nucleoside reverse transcriptase inhibitor in rats. Brain Behav Immun. 2011; 25(8): 1668-76 Hao S, Liu S, Zheng X, Zheng W, Ouyang H, Mata M, Fink DJ. The Role of TNFα in the Periaqueductal Gray During Naloxone-Precipitated Morphine Withdrawal in Rats. Neuropsychopharmacology. 2011; 36(3):664-76. Hao S, Mata M, Wolfe D, Glorioso JC and Fink D. Gene Transfer of Glutamic acid decarboxylase to dorsal horn ganglion produces an antinociceptive effect in Neuropathic pain. Annual of Neurology. 57:914-8, 2005
Grants and Contracts
NIH/NINDS R01 (1R01NS066792)
HIV AND NRTI’S-INDUCED PAINFUL PATHOGENIC MECHANISMS AND GENE THERAPY