Dysregulation of sphingolipid metabolism contributes to bortezomib-induced neuropathic pain

  • Katherine Stockstill
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1
  • Timothy M. Doyle
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1
  • Xisheng Yan
    Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, GA 2
  • Zhoumou Chen
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1
  • Kali Janes
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1
  • Joshua W. Little
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1
  • Kathryn Braden
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1
  • Filomena Lauro
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1
  • Luigino Antonio Giancotti
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1
  • Caron Mitsue Harada
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1
  • Ruchi Yadav
    Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, GA 2
  • Wen Hua Xiao
    Department of Anesthesiology, University of California, San Diego, La Jolla, CA 4
  • Jack M. Lionberger
    Department of Internal Medicine, Division of Hematology, Oncology, and Cellular Therapeutics, Saint Louis University School of Medicine, St. Louis, MO 5
  • William L. Neumann
    Department of Pharmaceutical Sciences, School of Pharmacy, Southern Illinois University Edwardsville, Edwardsville, IL 6
  • Gary J. Bennett
    Department of Anesthesiology, University of California, San Diego, La Jolla, CA 4
  • Han-Rong Weng
    Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, GA 2
  • Sarah Spiegel
    Department of Biochemistry and Molecular Biology, Virginia Commonwealth University, School of Medicine, Richmond, VA 7
  • Daniela Salvemini
    Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO 1

書誌事項

公開日
2018-04-27
権利情報
  • http://www.rupress.org/terms/
  • https://creativecommons.org/licenses/by-nc-sa/4.0/
DOI
  • 10.1084/jem.20170584
公開者
Rockefeller University Press

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説明

<jats:p>The development of chemotherapy-induced painful peripheral neuropathy is a major dose-limiting side effect of many chemotherapeutics, including bortezomib, but the mechanisms remain poorly understood. We now report that bortezomib causes the dysregulation of de novo sphingolipid metabolism in the spinal cord dorsal horn to increase the levels of sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) ligands, S1P and dihydro-S1P. Accordingly, genetic and pharmacological disruption of S1PR1 with multiple S1PR1 antagonists, including FTY720, blocked and reversed neuropathic pain. Mice with astrocyte-specific alterations of S1pr1 did not develop neuropathic pain and lost their ability to respond to S1PR1 inhibition, strongly implicating astrocytes as a primary cellular substrate for S1PR1 activity. At the molecular level, S1PR1 engaged astrocyte-driven neuroinflammation and altered glutamatergic homeostasis, processes blocked by S1PR1 antagonism. Our findings establish S1PR1 as a target for therapeutic intervention and provide insight into cellular and molecular pathways. As FTY720 also shows promising anticancer potential and is FDA approved, rapid clinical translation of our findings is anticipated.</jats:p>

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