Eicosanoid receptor

(Redirected from Prostanoid receptor)

Most of the eicosanoid receptors are integral membrane protein G protein-coupled receptors (GPCRs) that bind and respond to eicosanoid signaling molecules. Eicosanoids are rapidly metabolized to inactive products and therefore are short-lived. Accordingly, the eicosanoid-receptor interaction is typically limited to a local interaction: cells, upon stimulation, metabolize arachidonic acid to an eicosanoid which then binds cognate receptors on either its parent cell (acting as an autocrine signalling molecule) or on nearby cells (acting as a paracrine signalling molecule) to trigger functional responses within a restricted tissue area, e.g. an inflammatory response to an invading pathogen. In some cases, however, the synthesized eicosanoid travels through the blood (acting as a hormone-like messenger) to trigger systemic or coordinated tissue responses, e.g. prostaglandin (PG) E2 released locally travels to the hypothalamus to trigger a febrile reaction (see Fever § PGE2 release). An example of a non-GPCR receptor that binds many eicosanoids is the PPAR-γ nuclear receptor.[1]

The following is a list of human eicosanoid GPCRs grouped according to the type of eicosanoid ligand that each binds:[2][3]

Leukotriene

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Leukotrienes:

Lipoxin

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Lipoxins:

Resolvin E

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Resolvin Es:

Oxoeicosanoid

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Oxoeicosanoid:[15]

Prostanoid

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Prostanoids and Prostaglandin receptors

Prostanoids are prostaglandins (PG), thromboxanes (TX), and prostacyclins (PGI). Seven, structurally-related, prostanoid receptors fall into three categories based on the cell activation pathways and activities which they regulate. Relaxant prostanoid receptors (IP, DP1, EP2, and EP4) raise cellular cAMP levels; contractile prostanoid receptors (TP, FP, and EP1) mobilize intracellular calcium; and the inhibitory prostanoid receptor (EP3) lowers cAMP levels. A final prostanoid receptor, DP2, is structurally related to the chemotaxis class of receptors and unlike the other prostanoid receptors mediates eosinophil, basophil, and T helper cell (Th2 type) chemotactic responses. Prostanoids, particularly PGE2 and PGI2, are prominent regulators of inflammation and allergic responses as defined by studies primarily in animal models but also as suggested by studies with human tissues and, in certain cases, human subjects.[17]

References

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  1. ^ DuBois RN, Gupta R, Brockman J, Reddy BS, Krakow SL, Lazar MA (1998). "The nuclear eicosanoid receptor, PPAR-γ, is aberrantly expressed in colonic cancers". Carcinogenesis. 19 (1): 49–53. doi:10.1093/carcin/19.1.49. PMID 9472692.
  2. ^ Coleman RA, Smith WL, Narumiya S (1994). "International Union of Pharmacology classification of prostanoid receptors: properties, distribution, and structure of the receptors and their subtypes". Pharmacol. Rev. 46 (2): 205–29. PMID 7938166.
  3. ^ Brink C, Dahlén SE, Drazen J, Evans JF, Hay DW, Nicosia S, Serhan CN, Shimizu T, Yokomizo T (2003). "International Union of Pharmacology XXXVII. Nomenclature for leukotriene and lipoxin receptors". Pharmacol. Rev. 55 (1): 195–227. doi:10.1124/pr.55.1.8. PMID 12615958. S2CID 1584172.
  4. ^ a b c d Bäck M, Powell WS, Dahlén SE, Drazen JM, Evans JF, Serhan CN, Shimizu T, Yokomizo T, Rovati GE (2014). "Update on leukotriene, lipoxin and oxoeicosanoid receptors: IUPHAR Review 7". British Journal of Pharmacology. 171 (15): 3551–74. doi:10.1111/bph.12665. PMC 4128057. PMID 24588652.
  5. ^ a b Liu M, Yokomizo T (2015). "The role of leukotrienes in allergic diseases". Allergology International. 64 (1): 17–26. doi:10.1016/j.alit.2014.09.001. PMID 25572555.
  6. ^ Kanaoka Y, Maekawa A, Austen KF (2013). "Identification of GPR99 protein as a potential third cysteinyl leukotriene receptor with a preference for leukotriene E4 ligand". J. Biol. Chem. 288 (16): 10967–72. doi:10.1074/jbc.C113.453704. PMC 3630866. PMID 23504326.
  7. ^ Bankova LG, Lai J, Yoshimoto E, Boyce JA, Austen KF, Kanaoka Y, Barrett NA (2016). "Leukotriene E4 elicits respiratory epithelial cell mucin release through the G-protein-coupled receptor, GPR99". Proceedings of the National Academy of Sciences of the United States of America. 113 (22): 6242–7. Bibcode:2016PNAS..113.6242B. doi:10.1073/pnas.1605957113. PMC 4896673. PMID 27185938.
  8. ^ Marucci G, Dal Ben D, Lambertucci C, Santinelli C, Spinaci A, Thomas A, Volpini R, Buccioni M (2016). "The G Protein-Coupled Receptor GPR17: Overview and Update". ChemMedChem. 11 (23): 2567–2574. doi:10.1002/cmdc.201600453. hdl:11581/394099. PMID 27863043. S2CID 10935349.
  9. ^ Fumagalli M, Lecca D, Abbracchio MP (2016). "CNS remyelination as a novel reparative approach to neurodegenerative diseases: The roles of purinergic signaling and the P2Y-like receptor GPR17". Neuropharmacology. 104: 82–93. doi:10.1016/j.neuropharm.2015.10.005. hdl:2434/349470. PMID 26453964. S2CID 26235050.
  10. ^ Ye RD, Boulay F, Wang JM, Dahlgren C, Gerard C, Parmentier M, Serhan CN, Murphy PM (2009). "International Union of Basic and Clinical Pharmacology. LXXIII. Nomenclature for the formyl peptide receptor (FPR) family". Pharmacological Reviews. 61 (2): 119–61. doi:10.1124/pr.109.001578. PMC 2745437. PMID 19498085.
  11. ^ Lim JY, Park CK, Hwang SW (2015). "Biological Roles of Resolvins and Related Substances in the Resolution of Pain". BioMed Research International. 2015: 830930. doi:10.1155/2015/830930. PMC 4538417. PMID 26339646.
  12. ^ a b Serhan CN, Chiang N, Dalli J, Levy BD (2014). "Lipid mediators in the resolution of inflammation". Cold Spring Harbor Perspectives in Biology. 7 (2): a016311. doi:10.1101/cshperspect.a016311. PMC 4315926. PMID 25359497.
  13. ^ Qu Q, Xuan W, Fan GH (2015). "Roles of resolvins in the resolution of acute inflammation". Cell Biology International. 39 (1): 3–22. doi:10.1002/cbin.10345. PMID 25052386. S2CID 10160642.
  14. ^ Mariani F, Roncucci L (2015). "Chemerin/chemR23 axis in inflammation onset and resolution". Inflammation Research. 64 (2): 85–95. doi:10.1007/s00011-014-0792-7. PMID 25548799. S2CID 18957311.
  15. ^ Brink C, Dahlén SE, Drazen J, Evans JF, Hay DW, Rovati GE, Serhan CN, Shimizu T, Yokomizo T (2004). "International Union of Pharmacology XLIV. Nomenclature for the oxoeicosanoid receptor". Pharmacol. Rev. 56 (1): 149–57. doi:10.1124/pr.56.1.4. PMID 15001665. S2CID 7229884.
  16. ^ Powell WS, Rokach J (2015). "Biosynthesis, biological effects, and receptors of hydroxyeicosatetraenoic acids (HETEs) and oxoeicosatetraenoic acids (oxo-ETEs) derived from arachidonic acid". Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids. 1851 (4): 340–55. doi:10.1016/j.bbalip.2014.10.008. PMC 5710736. PMID 25449650.
  17. ^ a b c d e f Matsuoka T, Narumiya S (2007). "Prostaglandin receptor signaling in disease". TheScientificWorldJournal. 7: 1329–47. doi:10.1100/tsw.2007.182. PMC 5901339. PMID 17767353.
  18. ^ a b c d Ricciotti E, FitzGerald GA (2011). "Prostaglandins and inflammation". Arteriosclerosis, Thrombosis, and Vascular Biology. 31 (5): 986–1000. doi:10.1161/ATVBAHA.110.207449. PMC 3081099. PMID 21508345.
  19. ^ Hohjoh H, Inazumi T, Tsuchiya S, Sugimoto Y (2014). "Prostanoid receptors and acute inflammation in skin". Biochimie. 107 Pt A: 78–81. doi:10.1016/j.biochi.2014.08.010. PMID 25179301.
  20. ^ a b Claar D, Hartert TV, Peebles RS (2015). "The role of prostaglandins in allergic lung inflammation and asthma". Expert Review of Respiratory Medicine. 9 (1): 55–72. doi:10.1586/17476348.2015.992783. PMC 4380345. PMID 25541289.
  21. ^ a b Bauer J, Ripperger A, Frantz S, Ergün S, Schwedhelm E, Benndorf RA (2014). "Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane-mediated thromboxane A2 receptor activation". British Journal of Pharmacology. 171 (13): 3115–31. doi:10.1111/bph.12677. PMC 4080968. PMID 24646155.
  22. ^ Lüscher TF, Steffel J (2016). "Individualized antithrombotic therapy". Hamostaseologie. 36 (1): 26–32. doi:10.5482/HAMO-14-12-0080. PMID 25597592. S2CID 11677603.
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