Login Register Cart 0
Generic placeholder image

Current Medicinal Chemistry

Editor-in-Chief

ISSN (Print): 0929-8673
ISSN (Online): 1875-533X

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe Translate in Chinese
Review Article

Chemical Mediators’ Expression Associated with the Modulation of Pain in Rheumatoid Arthritis

Author(s): José Luis Cortes-Altamirano, Abril Morraz-Varela, Samuel Reyes-Long, Marwin Gutierrez, Cindy Bandala, Denise Clavijo-Cornejo and Alfonso Alfaro-Rodriguez*

Volume 27, Issue 36, 2020

Page: [6208 - 6218] Pages: 11

DOI: 10.2174/0929867326666190816225348

Price: $65

Abstract

Background: The management of pain in patients with rheumatoid arthritis (RA) is a complex subject due to the autoimmune nature of the pathology. Studies have shown that chemical mediators play a fundamental role in the determination, susceptibility and modulation of pain at different levels of the central and peripheral nervous system, resulting in interesting novel molecular targets to mitigate pain in patients with RA. However, due to the complexity of pain physiology in RA cand the many chemical mediators, the results of several studies are controversial.

Objective: The aim of this study was to identify the chemical mediators that are able to modulate pain in RA.

Method: In this review, a search was conducted on PubMed, ProQuest, EBSCO, and the Science Citation index for studies that evaluated the expression of chemical mediators on the modulation of pain in RA.

Results: Few studies have highlighted the importance of the expression of some chemical mediators that modulate pain in patients with rheumatoid arthritis. The expression of TRPV1, ASIC-3, and TDV8 encode ionic channels in RA and modulates pain, likewise, the transcription factors in RA, such as TNFα, TGF-β1, IL-6, IL-10, IFN-γ, IL-1b, mTOR, p21, caspase 3, EDNRB, CGRPCALCB, CGRP-CALCA, and TAC1 are also directly involved in pain perception.

Conclusion: The expression of all chemical mediators is directly related to RA and the modulation of pain by a complex intra and extracellular signaling pathway, however, transcription factors are involved in modulating acute pain, while the ionic channels are involved in chronic pain in RA.

Keywords: Rheumatoid arthritis, pain, transcription factors, ionic channels, chemical mediators, nociception.

« Previous Next »
[1]
Loeser, J.D.; Treede, R.D. The Kyoto protocol of IASP basic pain terminology. Pain, 2008, 137(3), 473-477.
[http://dx.doi.org/10.1016/j.pain.2008.04.025] [PMID: 18583048]
[2]
Buskila, D. Genetics of chronic pain states. Best Pract. Res. Clin. Rheumatol., 2007, 21(3), 535-547.
[http://dx.doi.org/10.1016/j.berh.2007.02.011] [PMID: 17602998]
[3]
Fillingim, R.B.; Wallace, M.R.; Herbstman, D.M.; Ribeiro-Dasilva, M.; Staud, R. Genetic contributions to pain: a review of findings in humans. Oral Dis., 2008, 14(8), 673-682.
[http://dx.doi.org/10.1111/j.1601-0825.2008.01458.x] [PMID: 19193196]
[4]
Cortes-Altamirano, J.L.; Olmos-Hernandez, A.; Jaime, H.B.; Carrillo-Mora, P.; Bandala, C.; Reyes-Long, S.; Alfaro-Rodríguez, A. 5-HT1, 5-HT2, 5-HT3 and 5-HT7 receptors and their role in the modulation of pain response in the central nervous system. Curr. Neuropharmacol., 2018, 16(2), 210-221.
[http://dx.doi.org/10.2174/1570159X15666170911121027] [PMID: 28901281]
[5]
WHO Scientific Group on the Burden of Musculoskeletal Conditions at the Start of the New Millennium The burden of musculoskeletal conditions at the start of the new millennium. World Health Organ. Tech. Rep. Ser. 2003. 919(i-x), 1-218.
[PMID: 14679827]
[6]
McDougall, J.J. Arthritis and pain. Neurogenic origin of joint pain. Arthritis Res. Ther., 2006, 8(6), 220.
[http://dx.doi.org/10.1186/ar2069] [PMID: 17118212]
[7]
Phillips, K.; Clauw, D.J. Central pain mechanisms in the rheumatic diseases: future directions. Arthritis Rheum., 2013, 65(2), 291-302.
[http://dx.doi.org/10.1002/art.37739] [PMID: 23045168]
[8]
Fitzcharles, M.A.; Lussier, D.; Shir, Y. Management of chronic arthritis pain in the elderly. Drugs Aging, 2010, 27(6), 471-490.
[http://dx.doi.org/10.2165/11536530-000000000-00000] [PMID: 20524707]
[9]
May, S. Self-management of chronic low back pain and osteoarthritis. Nat. Rev. Rheumatol., 2010, 6(4), 199-209.
[http://dx.doi.org/10.1038/nrrheum.2010.26] [PMID: 20357789]
[10]
Edwards, R.R.; Cahalan, C.; Mensing, G.; Smith, M.; Haythornthwaite, J.A. Pain, catastrophizing and depression in the rheumatic diseases. Nat. Rev. Rheumatol., 2011, 7(4), 216-224.
[http://dx.doi.org/10.1038/nrrheum.2011.2] [PMID: 21283147]
[11]
Heiberg, T.; Kvien, T.K. Preferences for improved health examined in 1,024 patients with rheumatoid arthritis: pain has highest priority. Arthritis Rheum., 2002, 47(4), 391-397.
[http://dx.doi.org/10.1002/art.10515] [PMID: 12209485]
[12]
Hess, A.; Axmann, R.; Rech, J.; Finzel, S.; Heindl, C.; Kreitz, S.; Sergeeva, M.; Saake, M.; Garcia, M.; Kollias, G.; Straub, R.H.; Sporns, O.; Doerfler, A.; Brune, K.; Schett, G. Blockade of TNF-α rapidly inhibits pain responses in the central nervous system. Proc. Natl. Acad. Sci. USA, 2011, 108(9), 3731-3736.
[http://dx.doi.org/10.1073/pnas.1011774108] [PMID: 21245297]
[13]
Borenstein, D.G.; Hassett, A.L.; Pisetsky, D. Pain management in rheumatology research, training and practice. Clin. Exp. Rheumatol., 2017, 35(5)(Suppl. 107), 2-7.
[PMID: 28967362]
[14]
James, S. Human pain and genetics: some basics. Br. J. Pain, 2013, 7(4), 171-178.
[http://dx.doi.org/10.1177/2049463713506408] [PMID: 26516521]
[15]
Harth, M.; Nielson, W.R. Pain and affective distress in arthritis: relationship to immunity and inflammation. Expert Rev. Clin. Immunol., 2019, 15(5), 541-552.
[http://dx.doi.org/10.1080/1744666x.2019.1573675] [PMID: 30669892]
[16]
Actor, J.K.; Smith, K.C. Translational Inflammation; Perspectives in Translational Cell Biology, 2019, pp. 1-22.
[http://dx.doi.org/10.1016/B978-0-12-813832-8.00001-7]
[17]
Kim, H.; Clark, D.; Dionne, R.A. Genetic contributions to clinical pain and analgesia: avoiding pitfalls in genetic research. J. Pain, 2009, 10(7), 663-693.
[http://dx.doi.org/10.1016/j.jpain.2009.04.001] [PMID: 19559388]
[18]
Fillingim, R.B. Individual differences in pain: understanding the mosaic that makes pain personal. Pain, 2017, 158(1)(Suppl. 1), S11-S18.
[http://dx.doi.org/10.1097/j.pain.0000000000000775] [PMID: 27902569]
[19]
Waxman, S.G.; Zamponi, G.W. Regulating excitability of peripheral afferents: emerging ion channel targets. Nat. Neurosci., 2014, 17(2), 153-163.
[http://dx.doi.org/10.1038/nn.3602] [PMID: 24473263]
[20]
Ahern, G.P.; Brooks, I.M.; Miyares, R.L.; Wang, X.B. Extracellular cations sensitize and gate capsaicin receptor TRPV1 modulating pain signaling. J. Neurosci., 2005, 25(21), 5109-5116.
[http://dx.doi.org/10.1523/JNEUROSCI.0237-05.2005] [PMID: 15917451]
[21]
Kargbo, R.B. TRPV1 Modulators for the treatment of pain and inflammation. ACS Med. Chem. Lett., 2019, 10(2), 143-144.
[http://dx.doi.org/10.1021/acsmedchemlett.8b00618] [PMID: 30783490]
[22]
Caterina, M.J.; Schumacher, M.A.; Tominaga, M.; Rosen, T.A.; Levine, J.D.; Julius, D. The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature, 1997, 389(6653), 816-824.
[http://dx.doi.org/10.1038/39807] [PMID: 9349813]
[23]
Caterina, M.J.; Julius, D. The vanilloid receptor: a molecular gateway to the pain pathway. Annu. Rev. Neurosci., 2001, 24, 487-517.
[http://dx.doi.org/10.1146/annurev.neuro.24.1.487] [PMID: 11283319]
[24]
Velisetty, P.; Stein, R.A.; Valdez, S.F.J.; Vásquez, V.; Cordero-Morales, J.F. Expression and purification of the pain receptor TRPV1 for spectroscopic analysis. Biophys. J., 2018, 114(3), 482a.
[http://dx.doi.org/10.1016/j.bpj.2017.11.2649]
[25]
Arribas-Blázquez, M.; Olivos-Oré, L.A.; Barahona, M.V.; Sánchez de la Muela, M.; Solar, V.; Jiménez, E.; Gualix, J.; McIntosh, J.M.; Ferrer-Montiel, A.; Miras-Portugal, M.T.; Artalejo, A.R. Overexpression of P2X3 and P2X7 receptors and TRPV1 channels in adrenomedullary chromaffin cells in a rat model of neuropathic pain. Int. J. Mol. Sci., 2019, 20(1), 155.
[http://dx.doi.org/10.3390/ijms20010155] [PMID: 30609840]
[26]
Engler, A.; Aeschlimann, A.; Simmen, B.R.; Michel, B.A.; Gay, R.E.; Gay, S.; Sprott, H. Expression of transient receptor potential vanilloid 1 (TRPV1) in synovial fibroblasts from patients with osteoarthritis and rheumatoid arthritis. Biochem. Biophys. Res. Commun., 2007, 359(4), 884-888.
[http://dx.doi.org/10.1016/j.bbrc.2007.05.178] [PMID: 17560936]
[27]
Fan, C.; Chu, X.; Wang, L.; Shi, H.; Li, T. Botulinum toxin type A reduces TRPV1 expression in the dorsal root ganglion in rats with adjuvant-arthritis pain. Toxicon, 2017, 133, 116-122.
[http://dx.doi.org/10.1016/j.toxicon.2017.05.001] [PMID: 28478059]
[28]
Marrone, M.C.; Morabito, A.; Giustizieri, M.; Chiurchiù, V.; Leuti, A.; Mattioli, M.; Marinelli, S.; Riganti, L.; Lombardi, M.; Murana, E.; Totaro, A.; Piomelli, D.; Ragozzino, D.; Oddi, S.; Maccarrone, M.; Verderio, C.; Marinelli, S. TRPV1 channels are critical brain inflammation detectors and neuropathic pain biomarkers in mice. Nat. Commun., 2017, 8, 15292.
[http://dx.doi.org/10.1038/ncomms15292] [PMID: 28489079]
[29]
Szabó, A.; Helyes, Z.; Sándor, K.; Bite, A.; Pintér, E.; Németh, J.; Bánvölgyi, A.; Bölcskei, K.; Elekes, K.; Szolcsányi, J. Role of transient receptor potential vanilloid 1 receptors in adjuvant-induced chronic arthritis: in vivo study using gene-deficient mice. J. Pharmacol. Exp. Ther., 2005, 314(1), 111-119.
[http://dx.doi.org/10.1124/jpet.104.082487] [PMID: 15831443]
[30]
Hsieh, W.S.; Kung, C.C.; Huang, S.L.; Lin, S.C.; Sun, W.H. TDAG8, TRPV1 and ASIC3 involved in establishing hyperalgesic priming in experimental rheumatoid arthritis. Sci. Rep., 2017, 7(1), 8870.
[http://dx.doi.org/10.1038/s41598-017-09200-6] [PMID: 28827659]
[31]
Ji, R.R.; Samad, T.A.; Jin, S.X.; Schmoll, R.; Woolf, C.J. p38 MAPK activation by NGF in primary sensory neurons after inflammation increases TRPV1 levels and maintains heat hyperalgesia. Neuron, 2002, 36(1), 57-68.
[http://dx.doi.org/10.1016/S0896-6273(02)00908-X] [PMID: 12367506]
[32]
Duo, L.; Hu, L.; Tian, N.; Cheng, G.; Wang, H.; Lin, Z.; Wang, Y.; Yang, Y. TRPV1 gain-of-function mutation impairs pain and itch sensations in mice. Mol. Pain, 2018, 141744806918762031
[http://dx.doi.org/10.1177/1744806918762031] [PMID: 29424270]
[33]
(a) Fernandes, E.S.; Russel, F.A.; Alawi, M.K.; Sand, C.; Liang, L.; Salomon, R.; Bodkin, J.V.; Aubdool, A.A.; Arno, M.; Gentry, C.; Smillie, S.J.; Bevan, S.; Keeble, J.E.; Malcangio, M.; Brain, S.D. Environmental cold exposure increases blood flow and affects pain sensitivity in the knee joints of CFA-induced arthritic mice in a TRPA1-dependent manner. Arthritis Res. Ther., 2014, 18(7)
[http://dx.doi.org/10.1186/s13075-015-0905-x] [PMID: 26754745]
(b) Engler, A.; Aeschlimann, A.; Simmen, B.R.; Michel, B.A.; Gay, R.E.; Gay, S.; Sprott, H. Expression of transient receptor potential vanilloid 1 (TRPV1) in synovial fibroblasts from patients with osteoarthritis and rheumatoid arthritis. Biochem. Biophys. Res. Commun., 2007, 359(4), 884-888.
[http://dx.doi.org/10.1016/j.bbrc.2007.05.178]] [PMID: 17560936]
[34]
Izumi, M.; Ikeuchi, M.; Ji, Q.; Tani, T. Local ASIC3 modulates pain and disease progression in a rat model of osteoarthritis. J. Biomed. Sci., 2012, 19(1), 77.
[http://dx.doi.org/10.1186/1423-0127-19-77] [PMID: 22909215]
[35]
Yen, L.T.; Hsu, Y.C.; Lin, J.G.; Hsieh, C.L.; Lin, Y.W. Role of ASIC3, Nav1.7 and Nav1.8 in electroacupuncture-induced analgesia in a mouse model of fibromyalgia pain. Acupunct. Med., 2018, 36(2), 110-116.
[http://dx.doi.org/10.1136/acupmed-2016-011244] [PMID: 29343477]
[36]
Sluka, K.A.; Price, M.P.; Breese, N.M.; Stucky, C.L.; Wemmie, J.A.; Welsh, M.J. Chronic hyperalgesia induced by repeated acid injections in muscle is abolished by the loss of ASIC3, but not ASIC1. Pain, 2003, 106(3), 229-239.
[http://dx.doi.org/10.1016/S0304-3959(03)00269-0] [PMID: 14659506]
[37]
Sluka, K.A.; Radhakrishnan, R.; Benson, C.J.; Eshcol, J.O.; Price, M.P.; Babinski, K. Katherine, Audettee, M.; Yeomans D.C.; Wilson, S.P. ASIC3 in muscle mediates mechanical, but not heat, hyperalgesia associated with muscle inflammation. Pain, 2007, 129, 102-112.
[http://dx.doi.org/10.1016/j.pain.2006.09.038] [PMID: 17134831]
[38]
Stephan, G.; Huang, L.; Tang, Y.; Vilotti, S.; Fabbretti, E.; Yu, Y.; Nörenberg, W.; Franke, H.; Gölöncsér, F.; Sperlágh, B.; Dopychai, A.; Hausmann, R.; Schmalzing, G.; Rubini, P.; Illes, P. The ASIC3/P2X3 cognate receptor is a pain-relevant and ligand-gated cationic channel. Nat. Commun., 2018, 9(1), 1354.
[http://dx.doi.org/10.1038/s41467-018-03728-5] [PMID: 29636447]
[39]
Wu, W.L.; Cheng, C.F.; Sun, W.H.; Wong, C.W.; Chen, C.C. Targeting ASIC3 for pain, anxiety, and insulin resistance. Pharmacol. Ther., 2012, 134(2), 127-138.
[http://dx.doi.org/10.1016/j.pharmthera.2011.12.009] [PMID: 22233754]
[40]
Deval, E.; Noël, J.; Lay, N.; Alloui, A.; Diochot, S.; Friend, V.; Jodar, M.; Lazdunski, M.; Lingueglia, E. ASIC3, a sensor of acidic and primary inflammatory pain. EMBO J., 2008, 27(22), 3047-3055.
[http://dx.doi.org/10.1038/emboj.2008.213] [PMID: 18923424]
[41]
Sluka, K.A.; Rasmussen, L.A.; Edgar, M.M.; O’Donnell, J.M.; Walder, R.Y.; Kolker, S.J.; Boyle, D.L.; Firestein, G.S. Acid-sensing ion channel 3 deficiency increases inflammation but decreases pain behavior in murine arthritis. Arthritis Rheum., 2013, 65(5), 1194-1202.
[http://dx.doi.org/10.1002/art.37862] [PMID: 23335302]
[42]
Weng, H.J.; Patel, K.N.; Jeske, N.A.; Bierbower, S.M.; Zou, W.; Tiwari, V.; Zheng, Q.; Tang, Z.; Mo, G.C.; Wang, Y.; Geng, Y.; Zhang, J.; Guan, Y.; Akopian, A.N.; Dong, X. Tmem100 is a regulator of TRPA1-TRPV1 complex and contributes to persistent pain. Neuron, 2015, 85(4), 833-846.
[http://dx.doi.org/10.1016/j.neuron.2014.12.065] [PMID: 25640077]
[43]
Li, C.; Deng, T.; Shang, Z.; Wang, D.; Xiao, Y. Blocking TRPA1 and TNF-α signal improves bortezomib-induced neuropathic pain. Cell. Physiol. Biochem., 2018, 51(5), 2098-2110.
[http://dx.doi.org/10.1159/000495828] [PMID: 30522101]
[44]
Firestein, G.S.; Manning, A.M. Signal transduction and transcription factors in rheumatic disease. Arthritis Rheum., 1999, 42(4), 609-621.
[http://dx.doi.org/10.1002/1529-0131(199904)42:4<609: AID-ANR3>3.0.CO;2-I] [PMID: 10211874]
[45]
McMahon, S.B.; Cafferty, W.B.; Marchand, F. Immune and glial cell factors as pain mediators and modulators. Exp. Neurol., 2005, 192(2), 444-462.
[http://dx.doi.org/10.1016/j.expneurol.2004.11.001] [PMID: 15755561]
[46]
Marchand, F.; Perretti, M.; McMahon, S.B. Role of the immune system in chronic pain. Nat. Rev. Neurosci., 2005, 6(7), 521-532.
[http://dx.doi.org/10.1038/nrn1700] [PMID: 15995723]
[47]
Moalem, G.; Tracey, D.J. Immune and inflammatory mechanisms in neuropathic pain. Brain Res. Brain Res. Rev., 2006, 51(2), 240-264.
[http://dx.doi.org/10.1016/j.brainresrev.2005.11.004] [PMID: 16388853]
[48]
Leung, L.; Cahill, C.M. TNF-α and neuropathic pain-a review. J. Neuroinflammation, 2010, 7(1), 27.
[http://dx.doi.org/10.1186/1742-2094-7-27] [PMID: 20398373]
[49]
DeLeo, J.A.; Colburn, R.W.; Rickman, A.J. Cytokine and growth factor immunohistochemical spinal profiles in two animal models of mononeuropathy. Brain Res., 1997, 759(1), 50-57.
[http://dx.doi.org/10.1016/S0006-8993(97)00209-6] [PMID: 9219862]
[50]
Park, C.K.; Lü, N.; Xu, Z.Z.; Liu, T.; Serhan, C.N.; Ji, R.R. Resolving TRPV1- and TNF-α-mediated spinal cord synaptic plasticity and inflammatory pain with neuroprotectin D1. J. Neurosci., 2011, 31(42), 15072-15085.
[http://dx.doi.org/10.1523/JNEUROSCI.2443-11.2011] [PMID: 22016541]
[51]
Gu, Y.; Yang, D.K.; Spinas, E.; Kritas, S.K.; Saggini, A.; Caraffa, A.; Antinolfi, P.; Saggini, R.; Conti, P. Role of TNF in mast cell neuroinflammation and pain. J. Biol. Regul. Homeost. Agents, 2015, 29(4), 787-791.
[PMID: 26753638]
[52]
Cunha, F.Q.; Poole, S.; Lorenzetti, B.B.; Ferreira, S.H. The pivotal role of tumour necrosis factor alpha in the development of inflammatory hyperalgesia. Br. J. Pharmacol., 1992, 107(3), 660-664.
[http://dx.doi.org/10.1111/j.1476-5381.1992.tb14503.x] [PMID: 1472964]
[53]
Schäfers, M.; Sorkin, L.S.; Sommer, C. Intramuscular injection of tumor necrosis factor-alpha induces muscle hyperalgesia in rats. Pain, 2003, 104(3), 579-588.
[http://dx.doi.org/10.1016/S0304-3959(03)00115-5] [PMID: 12927630]
[54]
Wagner, R.; Myers, R.R. Endoneurial injection of TNF-alpha produces neuropathic pain behaviors. Neuroreport, 1996, 7(18), 2897-2901.
[http://dx.doi.org/10.1097/00001756-199611250-00018] [PMID: 9116205]
[55]
Woolf, C.J.; Allchorne, A.; Safieh-Garabedian, B.; Poole, S. Cytokines, nerve growth factor and inflammatory hyperalgesia: the contribution of tumour necrosis factor alpha. Br. J. Pharmacol., 1997, 121(3), 417-424.
[http://dx.doi.org/10.1038/sj.bjp.0701148] [PMID: 9179382]
[56]
Zelenka, M.; Schäfers, M.; Sommer, C. Intraneural injection of interleukin-1beta and tumor necrosis factor-alpha into rat sciatic nerve at physiological doses induces signs of neuropathic pain. Pain, 2005, 116(3), 257-263.
[http://dx.doi.org/10.1016/j.pain.2005.04.018] [PMID: 15964142]
[57]
Huang, P.C.; Tsai, K.L.; Chen, Y.W.; Lin, H.T.; Hung, C.H. Exercise combined with ultrasound attenuates neuropathic pain in rats associated with downregulation of IL-6 and TNF-α, but with upregulation of IL-10. Anesth. Analg., 2017, 124(6), 2038-2044.
[http://dx.doi.org/10.1213/ANE.0000000000001600] [PMID: 28319508]
[58]
Zhang, Q.; Yu, J.; Wang, J.; Ding, C.P.; Han, S.P.; Zeng, X.Y.; Wang, J.Y. The red nucleus TNF-α participates in the initiation and maintenance of neuropathic pain through different signaling pathways. Neurochem. Res., 2015, 40(7), 1360-1371.
[http://dx.doi.org/10.1007/s11064-015-1599-9] [PMID: 25952358]
[59]
Xu, J.T.; Xin, W.J.; Zang, Y.; Wu, C.Y.; Liu, X.G. The role of tumor necrosis factor-alpha in the neuropathic pain induced by Lumbar 5 ventral root transection in rat. Pain, 2006, 123(3), 306-321.
[http://dx.doi.org/10.1016/j.pain.2006.03.011] [PMID: 16675114]
[60]
Hao, S.; Mata, M.; Glorioso, J.C.; Fink, D.J. Gene transfer to interfere with TNF alpha signaling in neuropathic pain. Gene Ther., 2007, 14(13), 1010-1016.
[http://dx.doi.org/10.1038/sj.gt.3302950] [PMID: 17443214]
[61]
Zhang, L.; Berta, T.; Xu, Z.Z.; Liu, T.; Park, J.Y.; Ji, R.R. TNF-α contributes to spinal cord synaptic plasticity and inflammatory pain: distinct role of TNF receptor subtypes 1 and 2. Pain, 2011, 152(2), 419-427.
[http://dx.doi.org/10.1016/j.pain.2010.11.014] [PMID: 21159431]
[62]
Tchetina, E.V.; Pivanova, A.N.; Markova, G.A.; Lukina, G.V.; Aleksandrova, E.N.; Aleksankin, A.P.; Makarov, S.A.; Kuzin, A.N. Rituximab downregulates gene expression associated with cell proliferation, survival, and proteolysis in the peripheral blood from rheumatoid arthritis patients: a link between high baseline autophagy-related ULK1 expression and improved pain control. Arthritis (Egypt), 2016, 2016,4963950.
[http://dx.doi.org/10.1155/2016/4963950] [PMID: 27057353]
[63]
Czeschik, J.C.; Hagenacker, T.; Schäfers, M.; Büsselberg, D. TNF-alpha differentially modulates ion channels of nociceptive neurons. Neurosci. Lett., 2008, 434(3), 293-298.
[http://dx.doi.org/10.1016/j.neulet.2008.01.070] [PMID: 18314270]
[64]
Jin, X.; Gereau, R.W. IV Acute p38-mediated modulation of tetrodotoxin-resistant sodium channels in mouse sensory neurons by tumor necrosis factor-alpha. J. Neurosci., 2006, 26(1), 246-255.
[http://dx.doi.org/10.1523/JNEUROSCI.3858-05.2006] [PMID: 16399694]
[65]
Liu, B.G.; Dobretsov, M.; Stimers, J.R.; Zhang, J.M. Tumor necrosis factor-α suppresses activation of sustained potassium currents in rat small diameter sensory neurons. Open Pain J., 2008, 1, 1.
[http://dx.doi.org/10.2174/1876386300902010001] [PMID: 20165558]
[66]
Oen, K.; Malleson, P.N.; Cabral, D.A.; Rosenberg, A.M.; Petty, R.E.; Nickerson, P.; Reed, M. Cytokine genotypes correlate with pain and radiologically defined joint damage in patients with juvenile rheumatoid arthritis. Rheumatology (Oxford), 2005, 44(9), 1115-1121.
[http://dx.doi.org/10.1093/rheumatology/keh689] [PMID: 15901906]
[67]
Marinova, K.; Toma, V.; Aeschlimann, A.; Gay, R.; Simmen, B.; Michel, B.; Gay, S.; Sprott, H. 227 differential “pain” gene expression and modulation exerted by ATP in synovial fibroblasts from patients with symptomatic osteoarthritis and rheumatoid arthritis. Eur. J. Pain, 2009, 13(S1), S73b-S73.
[http://dx.doi.org/10.1016/S1090-3801(09)60230-5]
[68]
Campbell, J.N.; Meyer, R.A. Mechanisms of neuropathic pain. Neuron, 2006, 52(1), 77-92.
[http://dx.doi.org/10.1016/j.neuron.2006.09.021] [PMID: 17015228]
[69]
Lechner, J.; Rudi, T.; von Baehr, V. Osteoimmunology of tumor necrosis factor-alpha, IL-6, and RANTES/CCL5: a review of known and poorly understood inflammatory patterns in osteonecrosis. Clin. Cosmet. Investig. Dent., 2018, 10, 251-262.
[http://dx.doi.org/10.2147/CCIDE.S184498] [PMID: 30519117]
[70]
Sisignano, M.; Lötsch, J.; Parnham, M.J.; Geisslinger, G. Potential biomarkers for persistent and neuropathic pain therapy. Pharmacol. Ther., 2019, 199, 16-29.
[http://dx.doi.org/10.1016/j.pharmthera.2019.02.004] [PMID: 30759376]

Rights & Permissions Print Cite
Article Metrics
14
© 2024 Bentham Science Publishers | Privacy Policy