Qing Lin, M.D., Ph.D., Associate Professor
- Affiliations: Department of Neuroscience & Cell Biology
- Route: 1069, 2.138A Medical Research Building (MRB)
- Tel: (409) 772-2404
- Fax: (409) 772-2789
- qilin@utmb.edu
Qing Lin, M.D., Ph.D.
Education
1980 Doctor of Medicine, Fujian Medical University, China
1986 Master of Medical Sciences, Fujian Medical University, China
1991 Doctor of Philosophy, Shanghai Medical University, China
1992-1996 Visiting Scientist (Postdoctoral Training), University of Texas Medical Branch, USA
Honors
Guest Professor - Vice-Chairman, Research Center of Neurobiology, Fujian Medical University, Fuzhou, China
Guest Professor - Shantou University Medical School, Shantou, China
Lecture Professor - Capital Medical University, Beijing, China
Research Interests
Mechanisms of Neurogenic Inflammation Induced Pain - The National Institute of Health (NIH) funded research project
Neurogenic inflammation is the process by which inflammatory mediators released from sensory nerve terminals produce inflammation in their target tissue. This process exacerbates pain. Neurogenic inflammation contributes to many clinically relevant states, including arthritis, inflammatory bowel disease, chronic bronchitis, migraine and interstitial cystitis. One of the mechanisms by which neurogenic inflammation is induced is the effector function of primary nociceptive afferent fibers. It is hypothesized that antidromic activity in primary afferents triggers the release of inflammatory mediators from these terminals when peripheral tissue is damaged, which helps develop neurogenic inflammatory pain. An increasing number of studies demonstrate that the antidromic activity of primary afferent fibers is centrally mediated by way of dorsal root reflexes (DRRs). In order to investigate its mechanisms, we have experimentally established an acute model of neurogenic inflammation by using an intradermal capsaicin (CAP) injection. The long-term goal of the proposed studies is to elucidate how neurogenic inflammation is initiated by action of the peripheral nociceptive molecule, the transient receptor potential vanilloid-1 (TRPV1) activated by CAP, then maintained by triggering the centrally mediated antidromic activity, DRRs, to exacerbate inflammatory pain, and how the released inflammatory mediators driven by DRRs participate in the process of pain sensation. Currently, our specific goals are 1) to determine if neurogenic inflammation following CAP injection involves triggering DRRs that cause the release of calcitonin gene-related peptide and/or substance P from primary afferent nociceptors and if this process would in turn enhance the CAP-induced sensitization of primary afferent nociceptors, as well as analyze if this process is initiated by activation of TRPV1 receptors; 2) to examine if activation of the TRPV1 receptors in primary afferent nociceptors plays an important role in enhancing DRRs by activating GABAergic interneurons in dorsal horn circuits; 3) to determine if phosphorylation of protein kinase C (PKC) takes place in the primary afferent neurons when neurogenic inflammation is initiated and develops, and if TRPV1 receptors are up-regulated by the phosphorylation of PKC.
Electrophysiology, neuropharmacology, neurochemistry, immunocytochemistry (confocal imaging analysis), Western blots, and laser Doppler blood flow meter are utilized to perform these studies. In addition, we are currently developing molecular biological techniques, such as PCR, aiming at a deeper study of ionic and molecular targets by which the DRRs mediate inflammatory pain.
Uncovering these mechanisms will be critical for pharmaceutical manufacturers and clinicians to develop new anti-inflammatory therapies and improve the healthcare for patients.
Publications (2005-2008)
Original Research Articles (peer reviewed)
Ren Y, Zou X, Fang L and Lin Q. Sympathetic modulation of activity in Aδ and C primary afferents following intradermal injection of capsaicin in rats. J Neurophysiol 93:365-377, 2005.
Fang L, Wu J, Zhang X, Lin Q and Willis WD. Calcium/calmodulin dependent protein kinase II regulates the phosphorylation of cyclic AMP-responsive element-binding protein of spinal cord in rats following noxious stimulation. Neurosci Lett 374:1-4, 2005.
Wu J, Su G, Ma L, Zhang X, Lei Y, Li J, Lin Q, and Fang L. Protein kinases mediate increment the phophorylation of cyclic AMP-responsive element binding protein in spinal cord of rats following capsaicin injection. Molecular Pain 1:26, 2005.
Valencia De Ita S, Castañeda-Hernandez G, Lawand NB, Lin Q and Willis WD. The role of the Na+-K+-2Cl- co-transporter in the development of capsaicin-induced neurogenic inflammation. J Neurophysiol 95:3553-3561, 2006.
Ren Y, Zou X, Fang L, and Lin Q. Involvement of peripheral purinoceptors in sympathetic modulation of capsaicin-Induced sensitization of primary afferent fibers. J Neurophysiol 96:2207-2216, 2006.
Wu J, Su G, Ma L, Zhang X, Lei Y, Lin Q, Nauta HJ and Li J. The role of c-AMP-dependent protein kinase in spinal cord and post synaptic dorsal column neurons in a rat model of visceral pain. Neurochem Int 50:710-718, 2007.
Wu J, Li J, Lin Q and Fang L. Signal transduction in chronic pain. Int Anesthesiol Clin 45:73-81, 2007.
Lin Q, Li D, Xu X, Zou X, and Fang L. Roles of TRPV1 and neuropeptidergic receptors in dorsal root reflex-mediated neurogenic inflammation induced by intradermal injection of capsaicin. Mol Pain 3:30, 2007.
Xu X, Wang P, Zou X, Li D, Fang L, and Lin Q. Increases in transient receptor potential vanilloid-1 mRNA and protein in primary afferent neurons stimulated by protein kinase C and their possible role in neurogenic inflammation. J Neurosci Res 2008 (In press).
Li D, Ren Y, Xu X, Zou X, Fang L, Lin Q. Sensitization of primary afferent nociceptors induced by intradermal capsaicin involves the peripheral release of calcitonin gene-related peptide driven by dorsal root reflexes. J Pain (In press).
Selected Review Articles
Lin Q, Cervero F and Schmelz M. Pathophysiology of neurogenic inflammation. In Flor H, Kalso E and Dostrovsky JO (eds). Proceedings of the 11th World Congress on Pain. IASP Press, Seattle 2006, p155-168.