Treatment for joint pain in rheumatoid arthritis (RA) continues to be a challenge and represents a large unmet medical need. Although RA pain is often thought to result from inflammation, it often persists even after optimal control of inflammation with currently available therapies, indicating the involvements of other non-inflammatory mechanisms. Our lab is exploring the potential inflammation-independent mechanisms of RA pain using mouse genetics and behavioral/physiological approaches. Moreover, to visualize and analyze the alterations of the activity of joint sensory neurons, we recently developed two powerful approaches, including in vivo dorsal root ganglion (DRG) neuron imaging and in vivo electrophysiological recordings on the intact DRG. The long-term goal of my research is to illuminate a novel peripheral neural mechanism underlying RA pain independent of joint inflammation and define a promising therapeutic target for RA pain that is resistant to current anti-inflammatory treatments or occurs in patients for whom such treatments are infeasible or poorly tolerated.
Our lab is interested in studying the peripheral immune and neural mechanisms of arthritis pain using a combination of approaches including immunostaining, mouse behavior, in vivo and in vitro DRG electrophysiology and calcium imaging, molecular biology and transgenic mice.
Technology Expertise Keywords
arthritis pain, miRNAs, TRP channels, In Vivo and in vitro electrophysiology, In vivo DRG imaging
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Wang L, Jiang X, Zheng Q, Jeon SM, Chen T, Liu Y, Kulaga H, Reed R, Dong X, Caterina MJ, Qu L. (2019) Neuronal FcγRI mediates acute and chronic joint pain. J Clin Invest. Jun 18;130. doi: 10.1172/JCI128010. PubMed PMID: 31211699.
Qu L. and Caterina MJ. (2016).Enhanced excitability and suppression of A-type K+ currents in joint sensory neurons in a murine model of antigen-induced arthritis. Scientific Reports. 6:28899. * Corresponding author
Qu L, Fu K, Yang J, Shimada S, and LaMotte RH. (2015). CXCR3 chemokine receptor signaling mediates itch in experimental allergic contact dermatitis. Pain. Sep;156(9):1737-1746. Featured as Editor’s Choice.
Qu L, Fan N, Ma C, Wang T, Han L, Fu K, Wang Y, Shimada S, Dong X and LaMotte RH. (2014) Enhanced excitability of MrgprA3+ and MrgprD+ nociceptors in a model of inflammatory itch and pain. Brain 137(Pt 4):1039-1050.
Han L, Ma C, Liu Q, McNeil B, Wend HJ, Cui Y, Tang Z, Kim. Y, Nie H, Qu L, Patel K, Li Z, Xiao B, LaMotte RH and Dong X. (2013). A subpopulation of nociceptors specifically linked to itch. Nat: Neurosci.16(2):174-182.