Discovery of prostamide F 2α and its role in inflammatory pain and dorsal horn nociceptive neuron hyperexcitability

PLoS ONE

Volumn 7, Issue 2, 2012, Pages

  Gatta, Luisa ^a   Piscitelli, Fabiana ^b   Giordano, Catia ^a   Boccella, Serena ^a   Lichtman, Aron ^c   Maione, Sabatino ^a   Di Marzo, Vincenzo ^b  

^a SECOND UNIVERSITY OF NAPLES   (Italy)

^b CNR   (Italy)

^c VIRGINIA COMMONWEALTH UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

11 FLUORO 9,15 DIHYDROXY 15 (2 INDANYL) 16,17,18,19,20 PENTANORPROSTA 5,13 DIENOIC ACID; 2 ARACHIDONOYLGLYCEROL; 5 (4 CHLOROPHENYL) 1 (4 METHOXYPHENYL) 3 TRIFLUOROMETHYL 1H PYRAZOLE; AGN 211336; ANANDAMIDE; CARRAGEENAN; CYCLOOXYGENASE 2; ENDOCANNABINOID; INDOMETACIN; KAOLIN; N (2 CYCLOHEXYLOXY 4 NITROPHENYL)METHANESULFONAMIDE; PROSTAGLANDIN DERIVATIVE; PROSTAGLANDIN F2 ALPHA; PROSTAMIDE F2ALPHA; PROSTAMIDE F2ALPHA RECEPTOR ANTAGONIST; PROSTANOID; PROSTANOID RECEPTOR ANTAGONIST; RECEPTOR BLOCKING AGENT; UNCLASSIFIED DRUG; AMIDE; ARACHIDONIC ACID DERIVATIVE; CYCLOOXYGENASE 1; DRUG DERIVATIVE; MEMBRANE PROTEIN; PROSTAGLANDIN E2; PROSTAGLANDIN F2ALPHA ETHANOLAMIDE; PTGS1 PROTEIN, RAT; PTGS2 PROTEIN, RAT;

ANALGESIC ACTIVITY; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; EXPERIMENTAL MODEL; INFLAMMATION; MALE; MOUSE; NERVE CELL; NERVE CELL EXCITABILITY; NERVE CELL MEMBRANE POTENTIAL; NOCICEPTIVE NEURON; NONHUMAN; PAIN; SPINAL CORD; SPINAL CORD DORSAL HORN; ACTION POTENTIAL; ANIMAL; CHEMISTRY; DRUG EFFECT; EVOKED RESPONSE; HINDLIMB; LIQUID CHROMATOGRAPHY; MASS SPECTROMETRY; METABOLISM; NOCICEPTIVE RECEPTOR; PATHOLOGY; PATHOPHYSIOLOGY; PHYSIOLOGY; POSTERIOR HORN CELL; RAT;

ACTION POTENTIALS; ANIMALS; ARACHIDONIC ACIDS; CHROMATOGRAPHY, LIQUID; CYCLOOXYGENASE 1; CYCLOOXYGENASE 2; DINOPROST; DINOPROSTONE; ENDOCANNABINOIDS; EVOKED POTENTIALS; HINDLIMB; INFLAMMATION; MASS SPECTROMETRY; MEMBRANE PROTEINS; MICE; NOCICEPTORS; PAIN; POLYUNSATURATED ALKAMIDES; POSTERIOR HORN CELLS; RATS;

EID: 84857382479     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0031111     Document Type: Article

References (30)

1. Anand P, Whiteside G, Fowler CJ, Hohmann AG, (2009) Targeting CB2 receptors and the endocannabinoid system for the treatment of pain. Brain Res Rev 60: 255-266.
2. Bisogno T, Di Marzo V, (2010) Cannabinoid receptors and endocannabinoids: role in neuroinflammatory and neurodegenerative disorders. CNS Neurol Disord Drug Targets 9: 564-573.
3. Petrosino S, Di Marzo V, (2010) FAAH and MAGL inhibitors: therapeutic opportunities from regulating endocannabinoid levels. Curr Opin Investig Drugs 11: 51-62.
4. Schlosburg JE, Kinsey SG, Lichtman AH, (2009) Targeting fatty acid amide hydrolase (FAAH) to treat pain and inflammation. AAPS J 11: 39-44.
5. Ahn K, Smith SE, Liimatta MB, Beidler D, Sadagopan N, et al. (2011) Mechanistic and Pharmacological Characterization of PF-04457845: A Highly Potent and Selective Fatty Acid Amide Hydrolase Inhibitor That Reduces Inflammatory and Noninflammatory Pain. J Pharmacol Exp Ther 338: 114-124.
6. Johnson DS, Stiff C, Lazerwith SE, Kesten SR, Fay LK, et al. (2011) Discovery of PF-04457845: A Highly Potent, Orally Bioavailable, and Selective Urea FAAH Inhibitor. ACS Med Chem Lett 2: 91-96.
7. Telleria-Diaz A, Schmidt M, Kreusch S, Neubert AK, Schache F, et al. (2010) Spinal antinociceptive effects of cyclooxygenase inhibition during inflammation: Involvement of prostaglandins and endocannabinoids. Pain 148: 26-35.
8. Hu SS, Bradshaw HB, Chen JS, Tan B, Walker JM, (2008) Prostaglandin E2 glycerol ester, an endogenous COX-2 metabolite of 2-arachidonoylglycerol, induces hyperalgesia and modulates NFkappaB activity. Br J Pharmacol 153: 1538-1549.
9. Woodward DF, Carling RW, Cornell CL, Fliri HG, Martos JL, et al. (2008) The pharmacology and therapeutic relevance of endocannabinoid derived cyclo-oxygenase (COX)-2 products. Pharmacol Ther 120: 71-80.
10. Yoshikawa K, Takei S, Hasegawa-Ishii S, Chiba Y, Furukawa A, et al. (2011) Preferential localization of prostamide/prostaglandin F synthase in myelin sheaths of the central nervous system. Brain Res 1367: 22-32.
11. Weber A, Ni J, Ling KH, Acheampong A, Tang-Liu DD, et al. (2004) Formation of prostamides from anandamide in FAAH knockout mice analyzed by HPLC with tandem mass spectrometry. J Lipid Res 45: 757-763.
12. Yang W, Ni J, Woodward DF, Tang-Liu DD, Ling KH, (2005) Enzymatic formation of prostamide F2alpha from anandamide involves a newly identified intermediate metabolite, prostamide H2. J Lipid Res 46: 2745-2751.
13. Duggan KC, Hermanson DJ, Musee J, Prusakiewicz JJ, Scheib JL, et al. (2011) (R)-Profens are substrate-selective inhibitors of endocannabinoid oxygenation by COX-2. Nature Chemical Biology 7: 803-809.
14. Staniaszek LE, Norris LM, Kendall DA, Barrett DA, Chapman V, (2010) Effects of COX-2 inhibition on spinal nociception: the role of endocannabinoids. Br J Pharmacol 160: 669-676.
15. Glaser ST, Kaczocha M, (2010) Cyclooxygenase-2 mediates anandamide metabolism in the mouse brain. J Pharmacol Exp Ther 335: 380-388.
16. Straiker A, Wager-Miller J, Hu SS, Blankman JL, Cravatt BF, et al. (2011) COX-2 and FAAH can regulate the time course of depolarization induced suppression of excitation. Br J Pharmacol.
17. Kozak KR, Prusakiewicz JJ, Marnett LJ, (2004) Oxidative metabolism of endocannabinoids by COX-2. Curr Pharm Des 10: 659-667.
18. Vecchio AJ, Malkowski MG, (2011) The structural basis of endocannabinoid oxygenation by cyclooxygenase-2. J Biol Chem 286: 20736-20745.
19. Petrosino S, Palazzo E, de Novellis V, Bisogno T, Rossi F, et al. (2007) Changes in spinal and supraspinal endocannabinoid levels in neuropathic rats. Neuropharmacology 52: 415-422.
20. Vanegas H, Schaible HG, (2001) Prostaglandins and cyclooxygenases [correction of cycloxygenases] in the spinal cord. Prog Neurobiol 64: 327-363.
21. Di Marzo V, Goparaju SK, Wang L, Liu J, Batkai S, et al. (2001) Leptin-regulated endocannabinoids are involved in maintaining food intake. Nature 410: 822-825.
22. Hains BC, Waxman SG, (2006) Activated microglia contribute to the maintenance of chronic pain after spinal cord injury. J Neurosci 26: 4308-4317.
23. McGaraughty S, Chu KL, Perner RJ, Didomenico S, Kort ME, et al. (2010) TRPA1 modulation of spontaneous and mechanically evoked firing of spinal neurons in uninjured, osteoarthritic, and inflamed rats. Mol Pain 6: 14.
24. Khasabov SG, Hamamoto DT, Harding-Rose C, Simone DA, (2007) Tumor-evoked hyperalgesia and sensitization of nociceptive dorsal horn neurons in a murine model of cancer pain. Brain Res 1180: 7-19.
25. Pitcher MH, Cervero F, (2010) Role of the NKCC1 co-transporter in sensitization of spinal nociceptive neurons. Pain 151: 756-762.
26. Simone DA, Khasabov SG, Hamamoto DT, (2008) Changes in response properties of nociceptive dorsal horn neurons in a murine model of cancer pain. Sheng Li Xue Bao 60: 635-644.
27. Davidova A, Schreiberova A, Kolesar D, Capkova L, Krizanova O, et al. (2009) Spinal cord transection significantly influences nNOS-IR in neuronal circuitry that underlies the tail-flick reflex activity. Cell Mol Neurobiol 29: 879-886.
28. Griffin BW, Klimko P, Crider JY, Sharif NA, (1999) AL-8810: a novel prostaglandin F2 alpha analog with selective antagonist effects at the prostaglandin F2 alpha (FP) receptor. J Pharmacol Exp Ther 290: 1278-1284.
29. Vasquez E, Bar KJ, Ebersberger A, Klein B, Vanegas H, et al. (2001) Spinal prostaglandins are involved in the development but not the maintenance of inflammation-induced spinal hyperexcitability. J Neurosci 21: 9001-9008.
30. Hylden JL, Wilcox GL, (1980) Intrathecal morphine in mice: a new technique. Eur J Pharmacol 67: 313-316.