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Inflammatory pain control by blocking oxidized phospholipid-mediated TRP channel activation.
Sci Rep. 2017 07 14; 7(1):5447.SR

Abstract

Phospholipids occurring in cell membranes and lipoproteins are converted into oxidized phospholipids (OxPL) by oxidative stress promoting atherosclerotic plaque formation. Here, OxPL were characterized as novel targets in acute and chronic inflammatory pain. Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC) and its derivatives were identified in inflamed tissue by mass spectrometry and binding assays. They elicited calcium influx, hyperalgesia and induced pro-nociceptive peptide release. Genetic, pharmacological and mass spectrometric evidence in vivo as well as in vitro confirmed the role of transient receptor potential channels (TRPA1 and TRPV1) as OxPAPC targets. Treatment with the monoclonal antibody E06 or with apolipoprotein A-I mimetic peptide D-4F, capturing OxPAPC in atherosclerosis, prevented inflammatory hyperalgesia, and in vitro TRPA1 activation. Administration of D-4F or E06 to rats profoundly ameliorated mechanical hyperalgesia and inflammation in collagen-induced arthritis. These data reveal a clinically relevant role for OxPAPC in inflammation offering therapy for acute and chronic inflammatory pain treatment by scavenging OxPAPC.

Authors+Show Affiliations

Department of Anesthesiology, University Hospital of Wuerzburg, Wuerzburg, Germany. Institute of Clinical Neurobiology, University Hospital of Wuerzburg, Wuerzburg, Germany.Institute for Physiology and Pathophysiology, Friedrich-Alexander University of Erlangen-Nuremberg, Erlangen, Germany.Department of Anesthesiology, University Hospital of Wuerzburg, Wuerzburg, Germany. Institute of Clinical Neurobiology, University Hospital of Wuerzburg, Wuerzburg, Germany.Institute for Medical Physics and Biophysics, University of Leipzig, Leipzig, Germany.Department of Anesthesiology, University Hospital of Wuerzburg, Wuerzburg, Germany. Institute of Clinical Neurobiology, University Hospital of Wuerzburg, Wuerzburg, Germany.Department of Anesthesiology, University Hospital of Wuerzburg, Wuerzburg, Germany. Institute of Clinical Neurobiology, University Hospital of Wuerzburg, Wuerzburg, Germany.Department of Anesthesiology, University Hospital of Wuerzburg, Wuerzburg, Germany.Department of Chemistry and Pharmacy, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany. University of Bordeaux, IBGC, UMR 5095, Bordeaux, France.Wolfson CARD, King's College London, Guys' Campus, London, United Kingdom. University of Granada, Department of Pharmacology, Granada, Spain.Department of Anesthesiology, University Hospital of Wuerzburg, Wuerzburg, Germany. Institute of Clinical Neurobiology, University Hospital of Wuerzburg, Wuerzburg, Germany.Department of Anesthesiology, University Hospital of Wuerzburg, Wuerzburg, Germany.Rudolf-Boehm-Institute for Pharmacology and Toxicology, University of Leipzig, Leipzig, Germany.Rudolf-Boehm-Institute for Pharmacology and Toxicology, University of Leipzig, Leipzig, Germany.Wolfson CARD, King's College London, Guys' Campus, London, United Kingdom.Institute for Physiology and Pathophysiology, Friedrich-Alexander University of Erlangen-Nuremberg, Erlangen, Germany.Department of Anesthesiology, University Hospital of Wuerzburg, Wuerzburg, Germany.Institute of Clinical Neurobiology, University Hospital of Wuerzburg, Wuerzburg, Germany.Department of Anesthesiology, University Hospital of Wuerzburg, Wuerzburg, Germany. rittner_h@ukw.de.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28710476

Citation

Oehler, Beatrice, et al. "Inflammatory Pain Control By Blocking Oxidized Phospholipid-mediated TRP Channel Activation." Scientific Reports, vol. 7, no. 1, 2017, p. 5447.
Oehler B, Kistner K, Martin C, et al. Inflammatory pain control by blocking oxidized phospholipid-mediated TRP channel activation. Sci Rep. 2017;7(1):5447.
Oehler, B., Kistner, K., Martin, C., Schiller, J., Mayer, R., Mohammadi, M., Sauer, R. S., Filipovic, M. R., Nieto, F. R., Kloka, J., Pflücke, D., Hill, K., Schaefer, M., Malcangio, M., Reeh, P. W., Brack, A., Blum, R., & Rittner, H. L. (2017). Inflammatory pain control by blocking oxidized phospholipid-mediated TRP channel activation. Scientific Reports, 7(1), 5447. https://doi.org/10.1038/s41598-017-05348-3
Oehler B, et al. Inflammatory Pain Control By Blocking Oxidized Phospholipid-mediated TRP Channel Activation. Sci Rep. 2017 07 14;7(1):5447. PubMed PMID: 28710476.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inflammatory pain control by blocking oxidized phospholipid-mediated TRP channel activation. AU - Oehler,Beatrice, AU - Kistner,Katrin, AU - Martin,Corinna, AU - Schiller,Jürgen, AU - Mayer,Rafaela, AU - Mohammadi,Milad, AU - Sauer,Reine-Solange, AU - Filipovic,Milos R, AU - Nieto,Francisco R, AU - Kloka,Jan, AU - Pflücke,Diana, AU - Hill,Kerstin, AU - Schaefer,Michael, AU - Malcangio,Marzia, AU - Reeh,Peter W, AU - Brack,Alexander, AU - Blum,Robert, AU - Rittner,Heike L, Y1 - 2017/07/14/ PY - 2017/02/10/received PY - 2017/06/01/accepted PY - 2017/7/16/entrez PY - 2017/7/16/pubmed PY - 2019/1/17/medline SP - 5447 EP - 5447 JF - Scientific reports JO - Sci Rep VL - 7 IS - 1 N2 - Phospholipids occurring in cell membranes and lipoproteins are converted into oxidized phospholipids (OxPL) by oxidative stress promoting atherosclerotic plaque formation. Here, OxPL were characterized as novel targets in acute and chronic inflammatory pain. Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC) and its derivatives were identified in inflamed tissue by mass spectrometry and binding assays. They elicited calcium influx, hyperalgesia and induced pro-nociceptive peptide release. Genetic, pharmacological and mass spectrometric evidence in vivo as well as in vitro confirmed the role of transient receptor potential channels (TRPA1 and TRPV1) as OxPAPC targets. Treatment with the monoclonal antibody E06 or with apolipoprotein A-I mimetic peptide D-4F, capturing OxPAPC in atherosclerosis, prevented inflammatory hyperalgesia, and in vitro TRPA1 activation. Administration of D-4F or E06 to rats profoundly ameliorated mechanical hyperalgesia and inflammation in collagen-induced arthritis. These data reveal a clinically relevant role for OxPAPC in inflammation offering therapy for acute and chronic inflammatory pain treatment by scavenging OxPAPC. SN - 2045-2322 UR - https://www.unboundmedicine.com/medline/citation/28710476/Inflammatory_pain_control_by_blocking_oxidized_phospholipid_mediated_TRP_channel_activation_ L2 - https://doi.org/10.1038/s41598-017-05348-3 DB - PRIME DP - Unbound Medicine ER -