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Resolvin D1 and D2 Inhibit Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Ion Channel Activation on Sensory Neurons via Lipid Raft Modification.
Int J Mol Sci. 2020 Jul 16; 21(14)IJ

Abstract

Transient Receptor Potential Vanilloid 1 and Ankyrin 1 (TRPV1, TRPA1) cation channels are expressed in nociceptive primary sensory neurons and regulate nociceptor and inflammatory functions. Resolvins are endogenous lipid mediators. Resolvin D1 (RvD1) is described as a selective inhibitor of TRPA1-related postoperative and inflammatory pain in mice acting on the G protein-coupled receptor DRV1/GPR32. Resolvin D2 (RvD2) is a very potent TRPV1 and TRPA1 inhibitor in DRG neurons, and decreases inflammatory pain in mice acting on the GPR18 receptor, via TRPV1/TRPA1-independent mechanisms. We provided evidence that resolvins inhibited neuropeptide release from the stimulated sensory nerve terminals by TRPV1 and TRPA1 activators capsaicin (CAPS) and allyl-isothiocyanate (AITC), respectively. We showed that RvD1 and RvD2 in nanomolar concentrations significantly decreased TRPV1 and TRPA1 activation on sensory neurons by fluorescent calcium imaging and inhibited the CAPS- and AITC-evoked [45]Ca-uptake on TRPV1- and TRPA1-expressing CHO cells. Since CHO cells are unlikely to express resolvin receptors, resolvins are suggested to inhibit channel opening through surrounding lipid raft disruption. Here, we proved the ability of resolvins to alter the membrane polarity related to cholesterol composition by fluorescence spectroscopy. It is concluded that targeting lipid raft integrity can open novel peripheral analgesic opportunities by decreasing the activation of nociceptors.

Authors+Show Affiliations

Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary. János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary.Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary. János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary.Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary. János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary.János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary. Department of Experimental Physics, Faculty of Sciences, University of Pécs, Ifjúság str. 6, H-7624 Pécs, Hungary.János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary. Department of Experimental Physics, Faculty of Sciences, University of Pécs, Ifjúság str. 6, H-7624 Pécs, Hungary.Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary. János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary. Department of Pharmacology and Pharmacotherapy, Semmelweis University, Nagyvárad sq. 4, H-1089 Budapest, Hungary.Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary. János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary. Department of Pharmacology, Faculty of Pharmacy, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary.Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary. János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary.János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary. Institute of Physiology, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary.Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary.Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary. János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary.Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624 Pécs, Hungary. János Szentágothai Research Centre and Centre for Neuroscience, University of Pécs, Ifjúság str. 20, H-7624 Pécs, Hungary.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32708653

Citation

Payrits, Maja, et al. "Resolvin D1 and D2 Inhibit Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Ion Channel Activation On Sensory Neurons Via Lipid Raft Modification." International Journal of Molecular Sciences, vol. 21, no. 14, 2020.
Payrits M, Horváth Á, Biró-Sütő T, et al. Resolvin D1 and D2 Inhibit Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Ion Channel Activation on Sensory Neurons via Lipid Raft Modification. Int J Mol Sci. 2020;21(14).
Payrits, M., Horváth, Á., Biró-Sütő, T., Erostyák, J., Makkai, G., Sághy, É., Pohóczky, K., Kecskés, A., Kecskés, M., Szolcsányi, J., Helyes, Z., & Szőke, É. (2020). Resolvin D1 and D2 Inhibit Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Ion Channel Activation on Sensory Neurons via Lipid Raft Modification. International Journal of Molecular Sciences, 21(14). https://doi.org/10.3390/ijms21145019
Payrits M, et al. Resolvin D1 and D2 Inhibit Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Ion Channel Activation On Sensory Neurons Via Lipid Raft Modification. Int J Mol Sci. 2020 Jul 16;21(14) PubMed PMID: 32708653.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Resolvin D1 and D2 Inhibit Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Ion Channel Activation on Sensory Neurons via Lipid Raft Modification. AU - Payrits,Maja, AU - Horváth,Ádám, AU - Biró-Sütő,Tünde, AU - Erostyák,János, AU - Makkai,Géza, AU - Sághy,Éva, AU - Pohóczky,Krisztina, AU - Kecskés,Angéla, AU - Kecskés,Miklós, AU - Szolcsányi,János, AU - Helyes,Zsuzsanna, AU - Szőke,Éva, Y1 - 2020/07/16/ PY - 2020/04/29/received PY - 2020/07/12/revised PY - 2020/07/13/accepted PY - 2020/7/26/entrez PY - 2020/7/28/pubmed PY - 2021/2/23/medline KW - Resolvin D1 KW - Resolvin D2 KW - lipid rafts KW - nerve terminal KW - sensory neuron KW - transient receptor potential channel JF - International journal of molecular sciences JO - Int J Mol Sci VL - 21 IS - 14 N2 - Transient Receptor Potential Vanilloid 1 and Ankyrin 1 (TRPV1, TRPA1) cation channels are expressed in nociceptive primary sensory neurons and regulate nociceptor and inflammatory functions. Resolvins are endogenous lipid mediators. Resolvin D1 (RvD1) is described as a selective inhibitor of TRPA1-related postoperative and inflammatory pain in mice acting on the G protein-coupled receptor DRV1/GPR32. Resolvin D2 (RvD2) is a very potent TRPV1 and TRPA1 inhibitor in DRG neurons, and decreases inflammatory pain in mice acting on the GPR18 receptor, via TRPV1/TRPA1-independent mechanisms. We provided evidence that resolvins inhibited neuropeptide release from the stimulated sensory nerve terminals by TRPV1 and TRPA1 activators capsaicin (CAPS) and allyl-isothiocyanate (AITC), respectively. We showed that RvD1 and RvD2 in nanomolar concentrations significantly decreased TRPV1 and TRPA1 activation on sensory neurons by fluorescent calcium imaging and inhibited the CAPS- and AITC-evoked [45]Ca-uptake on TRPV1- and TRPA1-expressing CHO cells. Since CHO cells are unlikely to express resolvin receptors, resolvins are suggested to inhibit channel opening through surrounding lipid raft disruption. Here, we proved the ability of resolvins to alter the membrane polarity related to cholesterol composition by fluorescence spectroscopy. It is concluded that targeting lipid raft integrity can open novel peripheral analgesic opportunities by decreasing the activation of nociceptors. SN - 1422-0067 UR - https://www.unboundmedicine.com/medline/citation/32708653/Resolvin_D1_and_D2_Inhibit_Transient_Receptor_Potential_Vanilloid_1_and_Ankyrin_1_Ion_Channel_Activation_on_Sensory_Neurons_via_Lipid_Raft_Modification_ DB - PRIME DP - Unbound Medicine ER -