The Moore Lab focuses on the sensory neurobiology of pain, particularly the role of calcium-mediated signaling pathways and TRP ion channels in chronic pain conditions such as migraine. Her research examines the molecular and cellular mechanisms underlying pain, with a particular emphasis on the cross-talk between trigeminal sensory neurons and non-neural cells. This underexplored interaction is thought to contribute to the release of inflammatory mediators that influence pain pathways, making it a key focus of the lab's efforts to understand and combat pathological pain.

My lab employs advanced imaging techniques, molecular biology, and genetic rodent models to investigate how TRP channels, especially TRPV4, modulate pain and inflammation. A notable research focus is on how onabotulinumtoxinA (Botox) alters TRP channel function in trigeminal sensory neurons to prevent or treat migraine, aiming to uncover the elusive mechanisms behind Botox’s therapeutic effects. The team also explores the broader impacts of TRP ion channels in diverse physiological processes, such as inflammation and neural injury.

In addition to studying migraine—a neurological disorder that disproportionately affects women—the Moore Lab is also invested in translational neuroscience, aiming to develop new therapeutic targets to alleviate chronic pain. Current projects include investigating the role of TRPV4 channels in trigeminal sensory systems and in traumatic brain injury (TBI)-induced headaches.

Dr. Moore collaborates across disciplines both within Duke and with external partners, reflecting her commitment to a collaborative, integrative approach to pain research. She is actively involved in several clinical trials, aiming to translate her findings into therapeutic advances. Her involvement in diverse, cross-disciplinary research projects enhances the translational impact of her work, bridging the gap between basic science and clinical application.

Dr. Moore's research is supported by grants from the NIH and industry partners, and she has been recognized for her leadership and scientific contributions, including being named a Rising Star among 1000 Inspiring Black Scientists by Cell Mentor. She is passionate about mentoring the next generation of scientists, and she is actively involved in initiatives aimed at fostering diversity in neuroscience.

Transient receptor potential (TRP) ion channels have been implicated in the pathophysiology of migraine, a neurological disorder with incapacitating episodic headaches. Ca2+-permeable TRP ion channels have been shown to function in many diverse physiological processes including inflammation and pain. TRP ion channels are expressed and function in trigeminal (TG) sensory neurons, in keratinocytes (KCs) and in mast cells. My research agenda includes how TRP ion channels in skin keratinocytes and mast cells regulate the secretion of inflammatory mediators onto nerve cells resulting in inflammation and pain. The underappreciated cross-talk between TG neurons and innervated non-neural cells, skin KCs and meningeal mast cells will benefit from increased scrutiny.

To better understand chronic, pathological pain at the organismal level, we use genetic rodent models. Our approaches include behavioral, structural, and molecular studies and advanced imaging. Migraine is the most common neurological disorder and affects >20% of women and 3-5% of men. For a significant number of migraineurs the onset occurs during their teenage years, and they continue to suffer thereafter, so that migraine’s impact affects migraineurs during their peak productive years and during a decisive period of their lives.

Widespread therapeutic use of onabotulinum toxin-A (botox) has exerted a powerful impact on migraine. However, botox’s mechanism of action on the trigeminal sensory system remains elusive.  In relation to migraine we study how Botox work in the regulation of TRP channels in trigeminal sensory neurons to prevent/treat migraine.

Chen Y, Wang ZL, Yeo M, Zhang QJ, López-Romero AE, Ding HP, Zhang X, Zeng Q, Morales-Lázaro SL, Moore C, Jin YA, Morstein J, Bortsov A, Krawczyk M, Lammert F, Abdelmalek M, Diehl AM, Milkiewicz P, Kremer AE, Zhang JY, Nackley A, Reeves TE, Ko MC, Ji RR, Rosenbaum T, Liedtke W. Epithelia-Sensory Neuron Cross Talk Underlies Cholestatic Itch Induced by Lysophosphatidylcholine. Gastroenterology. 2021 Jul;161(1):301-317.e16. doi: 10.1053/j.gastro.2021.03.049. Epub 2021 Apr 2. PMID: 33819485

Moore C, Gupta R, Jordt SE, Chen Y, Liedtke WB. Regulation of Pain and Itch by TRP Channels. Neuroscience Bulletin. 2018 Feb;34(1):120-142. doi: 10.1007/s12264-017-0200-8. Epub 2017 Dec 27.

Chen Y, Moore CD, Zhang JY, Hall RP 3rd, MacLeod AS, Liedtke W. TRPV4 Moves toward Center-Fold in Rosacea Pathogenesis. Journal of Investigative Dermatology. 2017 Apr;137(4):801-804. doi: 10.1016/j.jid.2016.12.013. PMID: 28340683 

Chen Y, Kanju P, Fang Q, Lee SH, Parekh PK, Lee W, Moore C, Brenner D, Gereau RW 4th, Wang F, Liedtke W. TRPV4 is necessary for trigeminal irritant pain and functions as a cellular formalin receptor. Pain. 2014 Dec;155(12):2662-2672. doi: 10.1016/j.pain.2014.09.033. Epub 2014 Oct 2. PMID: 25281928

Moore C, Cevikbas F, Pasolli HA, Chen Y, Kong W, Kempkes C, Parekh P, Lee SH, Kontchou NA, Yeh I, Jokerst NM, Fuchs E, Steinhoff M, Liedtke WB.UVB radiation generates sunburn pain and affects skin by activating epidermal TRPV4 ion channels and triggering endothelin-1 signaling. Proceedings of the National Academy of Science, U.S.A. 2013 Aug 20;110(34):E3225-34. doi: 10.1073/pnas.1312933110. Epub 2013 Aug 8. PMID: 23929777 

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