Department of Neuroscience, Cell Biology, & Anatomy
Room 2.138A Medical Research Building
Route: 1069 | Tel: (409) 772-1396 | firstname.lastname@example.org
Education and Training
Postdoctoral training, Johns Hopkins University School of Medicine, Advisor Xinzhong Dong
Ph.D. in Physiology, University of Texas Health Science Center, San Antonio, TX, Advisor Ken Hargreaves
B.S. in Biology, Centenary College of Louisiana
Our lab examines the interface between neurons and immune cells. Specifically, we study a large family of G protein-coupled receptors, called Mrgprs, and their role in pathological pain and itch. Recently, we found that the mast cell specific receptor, MrgprB2 and its human orthologue, MRGPRX2, contribute to thermal and mechanical pain.
As one of the key effector cells in the inflammatory process, mast cells are an important link between the nervous and immune systems. Mast cells can be found in close proximity to peripheral nerve endings and, due to their significant spatial advantages over other immune cells, are one of the first to respond to sensory nerve activation.
Using genetic, molecular, cellular, and behavioral approaches, we identified MrgprB2 as a link between the nervous system’s modulation of the innate immune response. We found MrgprB2 contributes to thermal and mechanical pain and is critical in recruiting immune cells. We were then able to connect these two findings by showing that the neuropeptide substance P (SP) activates MrgprB2, causing the release of proinflammatory cytokines and the recruitment of immune cells to the injury site. These findings were further confirmed using human mast cells expressing MRGPRX2. Another finding that upended previous dogma, was the finding that the canonical receptor NK1 was not involved in SP induced neurogenic inflammation and pain.
Our lab’s future research will use a multidisciplinary approach to characterize the contribution of mast cells to multiple pain pathologies, as well as the modulation of peripheral afferents by Mrgprs expressed on immune cells. Moreover, we plan to examine the role of orphan Mrgpr’s in pain conditions. Mrgprs are only found in certain neurons and immune cells, but not in any other tissues in the body, making them attractive therapeutic targets.
We are always looking for individuals who want to explore how the nervous and immune system interact with one another. Interested individuals can contact me at email@example.com
Green, D. P., Limjunyawong, N., Gour, N., Pundir, P., & Dong, X. (2019). A Mast-Cell-Specific Receptor Mediates Neurogenic Inflammation and Pain. Neuron, 101(3), 412–420.e3. PMID: 30686732
Green, D. P., & Dong, X. (2019). A Pungent and Painful Toxin. Cell, In Press. https://doi.org/10.1016/j.cell.2019.08.016
Meixiong, J., Vasavda, C., Green, D.P., Zheng, Q., Qi, L., Kwatra, S. G., … Dong, X. (2019). Identification of a bilirubin receptor that may mediate a component of cholestatic itch. eLife, 8. PMID: 30657454
Green, D. P., & Dong, X. (2016). The cell biology of acute itch. Journal of Cell Biology, 25;213(2):155-61. PMID: 27114499
Green, D. P., et al. (2016). Central activation of TRPV1 and TRPA1 by novel endogenous agonists contributes to mechanical allodynia and thermal hyperalgesia after burn injury. Molecular Pain, 12:1–9. PMID: 27411353
Green, D. P., & Dong, X. (2015). Supporting itch: a new role for astrocytes in chronic itch. Nature Medicine, 21(8), 841–2. PMID: 26248264
Eskander, M. A., Ruparel, S., Green, D. P., Chen, P. B., Por, E. D., Jeske, N. A., … Hargreaves, K. M. (2015) Persistent Nociception Triggered by Nerve Growth Factor (NGF) Is Mediated by TRPV1 and Oxidative Mechanisms. The Journal of Neuroscience 35(22), 8593–603. PMID: 26041925
Ruparel, S., Bendele, M., Wallace, A., & Green, D.P. (2015). Released lipids regulate transient receptor potential channel (TRP)-dependent oral cancer pain. Mol Pain, 11(1), 30. PMID: 26007300
Green, D. P., Ruparel, S., Roman, L., Henry, M. A. & Hargreaves, K. M. (2013) Role of endogenous TRPV1 agonists in a postburn pain model of partial-thickness injury. Pain 154, 2512-2520. PMID: 23891895
Google Scholar Page