Michael R. Due
Indiana University
16 Papers
190 Citations
Michael R. Due is an academic researcher from Indiana University. The author has contributed to research in topics: Neuropathic pain & Hyperalgesia. The author has an hindex of 13, co-authored 15 publications. Previous affiliations of Michael R. Due include Icahn School of Medicine at Mount Sinai.
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Papers
Suppression of inflammatory and neuropathic pain by uncoupling CRMP-2 from the presynaptic Ca2+ channel complex
Joel M. Brittain,Djane B. Duarte,Sarah M. Wilson,Weiguo Zhu,Carrie J. Ballard,Philip L. Johnson,Nai-Kui Liu,Wenhui Xiong,Matthew S. Ripsch,Yuying Wang,Jill C. Fehrenbacher,Stephanie D. Fitz,May Khanna,Chul Park,Brian S. Schmutzler,Bo M. Cheon,Michael R. Due,Tatiana Brustovetsky,Nicole M. Ashpole,Andy Hudmon,Samy O. Meroueh,Cynthia M. Hingtgen,Nickolay Brustovetsky,Ru-Rong Ji,Joyce H. Hurley,Xiaoming Jin,Anantha Shekhar,Xiao Ming Xu,Gerry Stephen Oxford,Michael R. Vasko,Fletcher A. White,Rajesh Khanna +31 more
TL;DR: By preventing CRMP-2–mediated enhancement of CaV2.2 function, TAT-CBD3 alleviated inflammatory and neuropathic hypersensitivity, an approach that may prove useful in managing chronic pain.
Neuroexcitatory effects of morphine-3-glucuronide are dependent on Toll-like receptor 4 signaling.
Michael R. Due,Andrew D. Piekarz,Natalie M. Wilson,Polina Feldman,Matthew S. Ripsch,Sherry A. Chavez,Hang Yin,Rajesh Khanna,Fletcher A. White +8 more
TL;DR: Evidence is provided that M3G may play a role in OIH via the TLR4/MD-2 heterodimer complex and biophysical properties of tetrodotoxin-sensitive and tetrodOToxin-resistant NaV currents.
The persistent release of HMGB1 contributes to tactile hyperalgesia in a rodent model of neuropathic pain
TL;DR: The use of the anti-inflammatory compound and known inhibitor of HMGB1, glycyrrhizin, has the ability to diminish persistent pain behavior in a model of peripheral neuropathy, presumably through its ability to neutralize the cyotkine.
Identification of a functional interaction of HMGB1 with Receptor for Advanced Glycation End-products in a model of neuropathic pain.
Yohance M. Allette,Michael R. Due,Sarah M. Wilson,Polina Feldman,Matthew S. Ripsch,Rajesh Khanna,Fletcher A. White +6 more
TL;DR: It is demonstrated that at-HMGB1 activation of nociceptive neurons is dependent on RAGE and not TLR4, and may be responsible for sensory neuron sensitization and mechanical hyperalgesia associated with chronic neuropathic pain states.
Acrolein involvement in sensory and behavioral hypersensitivity following spinal cord injury in the rat.
Michael R. Due,Jonghyuck Park,Lingxing Zheng,Michael K. Walls,Yohance M. Allette,Fletcher A. White,Riyi Shi,Riyi Shi +7 more
TL;DR: In this paper, the authors showed that there are enhanced levels of acrolein and increased neuronal sensitivity to the aldehyde for at least 14 days after spinal cord injury, and that the increased expression of TRPA1 in the lumbar (L3-L6) sensory ganglia was associated with increased sensitivity to tactile and thermal stimuli.
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