H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway
Nitroxyl (HNO) is a redox sibling of nitric oxide (NO) that targets distinct signalling pathways with pharmacological endpoints of high significance in the treatment of heart failure. Beneficial HNO effects depend, in part, on its ability to release calcitonin gene-related peptide (CGRP) through an...
Guardado en:
| Autores principales: | , , , , , , , , , , , , , , , , , , , , , , , , |
|---|---|
| Formato: | JOUR |
| Materias: | |
| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_20411723_v5_n_p_Eberhardt |
| Aporte de: |
| id |
todo:paper_20411723_v5_n_p_Eberhardt |
|---|---|
| record_format |
dspace |
| spelling |
todo:paper_20411723_v5_n_p_Eberhardt2023-10-03T16:37:51Z H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway Eberhardt, M. Dux, M. Namer, B. Miljkovic, J. Cordasic, N. Will, C. Kichko, T.I. De La Roche, J. Fischer, M. Suárez, S.A. Bikiel, D. Dorsch, K. Leffler, A. Babes, A. Lampert, A. Lennerz, J.K. Jacobi, J. Martí, M.A. Doctorovich, F. Högestätt, E.D. Zygmunt, P.M. Ivanovic-Burmazovic, I. Messlinger, K. Reeh, P. Filipovic, M.R. calcitonin gene related peptide hydrogen sulfide nitric oxide nitroxyl transient receptor potential channel A1 unclassified drug calcitonin gene related peptide hydrogen sulfide nitric oxide nitrogen oxide nitroxyl transient receptor potential channel Trpa1 protein, mouse amino terminal sequence animal cell article blood pressure blood vessel tone calcium transport cerebrospinal fluid controlled study disulfide bond electrophilicity female human immunoprecipitation immunoreactivity male mast cell degranulation matrix assisted laser desorption ionization time of flight mass spectrometry mean arterial pressure mouse nonhuman regulatory mechanism sensory nerve cell signal transduction spinal ganglion vasodilatation animal aorta brain stem drug effects genetics immunohistochemistry in vitro study knockout mouse mass spectrometry metabolism signal transduction trigeminus ganglion Animals Aorta Brain Stem Calcitonin Gene-Related Peptide Humans Hydrogen Sulfide Immunohistochemistry In Vitro Techniques Mice Mice, Knockout Nitric Oxide Nitrogen Oxides Signal Transduction Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Transient Receptor Potential Channels Trigeminal Ganglion Nitroxyl (HNO) is a redox sibling of nitric oxide (NO) that targets distinct signalling pathways with pharmacological endpoints of high significance in the treatment of heart failure. Beneficial HNO effects depend, in part, on its ability to release calcitonin gene-related peptide (CGRP) through an unidentified mechanism. Here we propose that HNO is generated as a result of the reaction of the two gasotransmitters NO and H 2 S. We show that H 2 S and NO production colocalizes with transient receptor potential channel A1 (TRPA1), and that HNO activates the sensory chemoreceptor channel TRPA1 via formation of amino-terminal disulphide bonds, which results in sustained calcium influx. As a consequence, CGRP is released, which induces local and systemic vasodilation. H 2 S-evoked vasodilatatory effects largely depend on NO production and activation of HNO-TRPA1-CGRP pathway. We propose that this neuroendocrine HNO-TRPA1-CGRP signalling pathway constitutes an essential element for the control of vascular tone throughout the cardiovascular system. © 2014 Macmillan Publishers Limited. All rights reserved. Fil:Suárez, S.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Bikiel, D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Martí, M.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Doctorovich, F. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_20411723_v5_n_p_Eberhardt |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
calcitonin gene related peptide hydrogen sulfide nitric oxide nitroxyl transient receptor potential channel A1 unclassified drug calcitonin gene related peptide hydrogen sulfide nitric oxide nitrogen oxide nitroxyl transient receptor potential channel Trpa1 protein, mouse amino terminal sequence animal cell article blood pressure blood vessel tone calcium transport cerebrospinal fluid controlled study disulfide bond electrophilicity female human immunoprecipitation immunoreactivity male mast cell degranulation matrix assisted laser desorption ionization time of flight mass spectrometry mean arterial pressure mouse nonhuman regulatory mechanism sensory nerve cell signal transduction spinal ganglion vasodilatation animal aorta brain stem drug effects genetics immunohistochemistry in vitro study knockout mouse mass spectrometry metabolism signal transduction trigeminus ganglion Animals Aorta Brain Stem Calcitonin Gene-Related Peptide Humans Hydrogen Sulfide Immunohistochemistry In Vitro Techniques Mice Mice, Knockout Nitric Oxide Nitrogen Oxides Signal Transduction Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Transient Receptor Potential Channels Trigeminal Ganglion |
| spellingShingle |
calcitonin gene related peptide hydrogen sulfide nitric oxide nitroxyl transient receptor potential channel A1 unclassified drug calcitonin gene related peptide hydrogen sulfide nitric oxide nitrogen oxide nitroxyl transient receptor potential channel Trpa1 protein, mouse amino terminal sequence animal cell article blood pressure blood vessel tone calcium transport cerebrospinal fluid controlled study disulfide bond electrophilicity female human immunoprecipitation immunoreactivity male mast cell degranulation matrix assisted laser desorption ionization time of flight mass spectrometry mean arterial pressure mouse nonhuman regulatory mechanism sensory nerve cell signal transduction spinal ganglion vasodilatation animal aorta brain stem drug effects genetics immunohistochemistry in vitro study knockout mouse mass spectrometry metabolism signal transduction trigeminus ganglion Animals Aorta Brain Stem Calcitonin Gene-Related Peptide Humans Hydrogen Sulfide Immunohistochemistry In Vitro Techniques Mice Mice, Knockout Nitric Oxide Nitrogen Oxides Signal Transduction Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Transient Receptor Potential Channels Trigeminal Ganglion Eberhardt, M. Dux, M. Namer, B. Miljkovic, J. Cordasic, N. Will, C. Kichko, T.I. De La Roche, J. Fischer, M. Suárez, S.A. Bikiel, D. Dorsch, K. Leffler, A. Babes, A. Lampert, A. Lennerz, J.K. Jacobi, J. Martí, M.A. Doctorovich, F. Högestätt, E.D. Zygmunt, P.M. Ivanovic-Burmazovic, I. Messlinger, K. Reeh, P. Filipovic, M.R. H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway |
| topic_facet |
calcitonin gene related peptide hydrogen sulfide nitric oxide nitroxyl transient receptor potential channel A1 unclassified drug calcitonin gene related peptide hydrogen sulfide nitric oxide nitrogen oxide nitroxyl transient receptor potential channel Trpa1 protein, mouse amino terminal sequence animal cell article blood pressure blood vessel tone calcium transport cerebrospinal fluid controlled study disulfide bond electrophilicity female human immunoprecipitation immunoreactivity male mast cell degranulation matrix assisted laser desorption ionization time of flight mass spectrometry mean arterial pressure mouse nonhuman regulatory mechanism sensory nerve cell signal transduction spinal ganglion vasodilatation animal aorta brain stem drug effects genetics immunohistochemistry in vitro study knockout mouse mass spectrometry metabolism signal transduction trigeminus ganglion Animals Aorta Brain Stem Calcitonin Gene-Related Peptide Humans Hydrogen Sulfide Immunohistochemistry In Vitro Techniques Mice Mice, Knockout Nitric Oxide Nitrogen Oxides Signal Transduction Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Transient Receptor Potential Channels Trigeminal Ganglion |
| description |
Nitroxyl (HNO) is a redox sibling of nitric oxide (NO) that targets distinct signalling pathways with pharmacological endpoints of high significance in the treatment of heart failure. Beneficial HNO effects depend, in part, on its ability to release calcitonin gene-related peptide (CGRP) through an unidentified mechanism. Here we propose that HNO is generated as a result of the reaction of the two gasotransmitters NO and H 2 S. We show that H 2 S and NO production colocalizes with transient receptor potential channel A1 (TRPA1), and that HNO activates the sensory chemoreceptor channel TRPA1 via formation of amino-terminal disulphide bonds, which results in sustained calcium influx. As a consequence, CGRP is released, which induces local and systemic vasodilation. H 2 S-evoked vasodilatatory effects largely depend on NO production and activation of HNO-TRPA1-CGRP pathway. We propose that this neuroendocrine HNO-TRPA1-CGRP signalling pathway constitutes an essential element for the control of vascular tone throughout the cardiovascular system. © 2014 Macmillan Publishers Limited. All rights reserved. |
| format |
JOUR |
| author |
Eberhardt, M. Dux, M. Namer, B. Miljkovic, J. Cordasic, N. Will, C. Kichko, T.I. De La Roche, J. Fischer, M. Suárez, S.A. Bikiel, D. Dorsch, K. Leffler, A. Babes, A. Lampert, A. Lennerz, J.K. Jacobi, J. Martí, M.A. Doctorovich, F. Högestätt, E.D. Zygmunt, P.M. Ivanovic-Burmazovic, I. Messlinger, K. Reeh, P. Filipovic, M.R. |
| author_facet |
Eberhardt, M. Dux, M. Namer, B. Miljkovic, J. Cordasic, N. Will, C. Kichko, T.I. De La Roche, J. Fischer, M. Suárez, S.A. Bikiel, D. Dorsch, K. Leffler, A. Babes, A. Lampert, A. Lennerz, J.K. Jacobi, J. Martí, M.A. Doctorovich, F. Högestätt, E.D. Zygmunt, P.M. Ivanovic-Burmazovic, I. Messlinger, K. Reeh, P. Filipovic, M.R. |
| author_sort |
Eberhardt, M. |
| title |
H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway |
| title_short |
H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway |
| title_full |
H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway |
| title_fullStr |
H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway |
| title_full_unstemmed |
H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway |
| title_sort |
h2s and no cooperatively regulate vascular tone by activating a neuroendocrine hno-trpa1-cgrp signalling pathway |
| url |
http://hdl.handle.net/20.500.12110/paper_20411723_v5_n_p_Eberhardt |
| work_keys_str_mv |
AT eberhardtm h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT duxm h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT namerb h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT miljkovicj h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT cordasicn h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT willc h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT kichkoti h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT delarochej h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT fischerm h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT suarezsa h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT bikield h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT dorschk h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT lefflera h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT babesa h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT lamperta h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT lennerzjk h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT jacobij h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT martima h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT doctorovichf h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT hogestatted h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT zygmuntpm h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT ivanovicburmazovici h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT messlingerk h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT reehp h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway AT filipovicmr h2sandnocooperativelyregulatevasculartonebyactivatinganeuroendocrinehnotrpa1cgrpsignallingpathway |
| _version_ |
1807316231543324672 |