12 results on '"Marcotti, Aida"'
Search Results
2. Supplementary data for TRPA1 modulation by Sigma-1 receptor prevents oxaliplatin-induced painful peripheral neuropathy
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Marcotti, Aida, Fernández-Trillo, Jorge, González, Alejandro, Vizcaíno-Escoto, Marta, Ros-Arlanzón, Pablo, Romero, Luz, Vela, José Miguel, Gomis, Ana, Viana, Félix, Peña, Elvira de la, Marcotti, Aida, Fernández-Trillo, Jorge, González, Alejandro, Vizcaíno-Escoto, Marta, Ros-Arlanzón, Pablo, Romero, Luz, Vela, José Miguel, Gomis, Ana, Viana, Félix, and Peña, Elvira de la
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- 2023
3. TRPA1 modulation by Sigma-1 receptor prevents oxaliplatin-induced painful peripheral neuropathy
- Author
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Generalitat Valenciana, Ministerio de Educación (España), Esteve, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Marcotti, Aida, Fernández-Trillo, Jorge, González, Alejandro, Vizcaíno-Escoto, Marta, Ros-Arlanzón, Pablo, Romero, Luz, Vela, José Miguel, Gomis, Ana, Viana, Félix, Peña, Elvira de la, Generalitat Valenciana, Ministerio de Educación (España), Esteve, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Marcotti, Aida, Fernández-Trillo, Jorge, González, Alejandro, Vizcaíno-Escoto, Marta, Ros-Arlanzón, Pablo, Romero, Luz, Vela, José Miguel, Gomis, Ana, Viana, Félix, and Peña, Elvira de la
- Abstract
Chemotherapy-induced peripheral neuropathy is a frequent, disabling side effect of anticancer drugs. Oxaliplatin, a platinum compound used in the treatment of advanced colorectal cancer, often leads to a form of chemotherapy-induced peripheral neuropathy characterized by mechanical and cold hypersensitivity. Current therapies for chemotherapy-induced peripheral neuropathy are ineffective, often leading to the cessation of treatment. Transient receptor potential ankyrin 1 (TRPA1) is a polymodal, non-selective cation-permeable channel expressed in nociceptors, activated by physical stimuli and cellular stress products. TRPA1 has been linked to the establishment of chemotherapy-induced peripheral neuropathy and other painful neuropathic conditions. Sigma-1 receptor is an endoplasmic reticulum chaperone known to modulate the function of many ion channels and receptors. Sigma-1 receptor antagonist, a highly selective antagonist of Sigma-1 receptor, has shown effectiveness in a phase II clinical trial for oxaliplatin chemotherapy-induced peripheral neuropathy. However, the mechanisms involved in the beneficial effects of Sigma-1 receptor antagonist are little understood. We combined biochemical and biophysical (i.e. intermolecular Förster resonance energy transfer) techniques to demonstrate the interaction between Sigma-1 receptor and human TRPA1. Pharmacological antagonism of Sigma-1R impaired the formation of this molecular complex and the trafficking of functional TRPA1 to the plasma membrane. Using patch-clamp electrophysiological recordings we found that antagonists of Sigma-1 receptor, including Sigma-1 receptor antagonist, exert a marked inhibition on plasma membrane expression and function of human TRPA1 channels. In TRPA1-expressing mouse sensory neurons, Sigma-1 receptor antagonists reduced inward currents and the firing of actions potentials in response to TRPA1 agonists. Finally, in a mouse experimental model of oxaliplatin neuropathy, systemic treatment with
- Published
- 2023
4. TRPA1 modulation by Sigma-1 receptor prevents oxaliplatin-induced painful peripheral neuropathy
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Marcotti, Aida, primary, Fernández-Trillo, Jorge, additional, González, Alejandro, additional, Vizcaíno-Escoto, Marta, additional, Ros-Arlanzón, Pablo, additional, Romero, Luz, additional, Vela, José Miguel, additional, Gomis, Ana, additional, Viana, Félix, additional, and de la Peña, Elvira, additional
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- 2022
- Full Text
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5. TRPA1 modulation by Sigma-1 receptor prevents oxaliplatin-induced painful peripheral neuropathy.
- Author
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Marcotti, Aida, Fernández-Trillo, Jorge, González, Alejandro, Vizcaíno-Escoto, Marta, Ros-Arlanzón, Pablo, Romero, Luz, Vela, José Miguel, Gomis, Ana, Viana, Félix, and Peña, Elvira de la
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PERIPHERAL neuropathy , *FLUORESCENCE resonance energy transfer , *VINCRISTINE , *NEURALGIA , *CELL membranes , *SENSORY neurons - Abstract
Chemotherapy-induced peripheral neuropathy is a frequent, disabling side effect of anticancer drugs. Oxaliplatin, a platinum compound used in the treatment of advanced colorectal cancer, often leads to a form of chemotherapy-induced peripheral neuropathy characterized by mechanical and cold hypersensitivity. Current therapies for chemotherapy-induced peripheral neuropathy are ineffective, often leading to the cessation of treatment. Transient receptor potential ankyrin 1 (TRPA1) is a polymodal, non-selective cation-permeable channel expressed in nociceptors, activated by physical stimuli and cellular stress products. TRPA1 has been linked to the establishment of chemotherapy-induced peripheral neuropathy and other painful neuropathic conditions. Sigma-1 receptor is an endoplasmic reticulum chaperone known to modulate the function of many ion channels and receptors. Sigma-1 receptor antagonist, a highly selective antagonist of Sigma-1 receptor, has shown effectiveness in a phase II clinical trial for oxaliplatin chemotherapy-induced peripheral neuropathy. However, the mechanisms involved in the beneficial effects of Sigma-1 receptor antagonist are little understood. We combined biochemical and biophysical (i.e. intermolecular Förster resonance energy transfer) techniques to demonstrate the interaction between Sigma-1 receptor and human TRPA1. Pharmacological antagonism of Sigma-1R impaired the formation of this molecular complex and the trafficking of functional TRPA1 to the plasma membrane. Using patch-clamp electrophysiological recordings we found that antagonists of Sigma-1 receptor, including Sigma-1 receptor antagonist, exert a marked inhibition on plasma membrane expression and function of human TRPA1 channels. In TRPA1-expressing mouse sensory neurons, Sigma-1 receptor antagonists reduced inward currents and the firing of actions potentials in response to TRPA1 agonists. Finally, in a mouse experimental model of oxaliplatin neuropathy, systemic treatment with a Sigma-1 receptor antagonists prevented the development of painful symptoms by a mechanism involving TRPA1. In summary, the modulation of TRPA1 channels by Sigma-1 receptor antagonists suggests a new strategy for the prevention and treatment of chemotherapy-induced peripheral neuropathy and could inform the development of novel therapeutics for neuropathic pain. [ABSTRACT FROM AUTHOR]
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- 2023
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6. TRPA1 ion channel modulation by the Sigma-1 receptor
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Fernández-Trillo, Jorge, Marcotti, Aida, González, Alejandro, Vizcaíno, Marta, Sala, Salvador, Gomis, Ana, Viana, Félix, Peña, Elvira de la, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Ministerio de Economía y Competitividad (España), and European Commission
- Abstract
Resumen del póster presentado al 4th International TRP Meeting, celebrado virtualmente del 15 al 17 de septiembre de 2021., TRPA1 channels play a fundamental role in chemonociception, as molecular transducers of reactive irritants, stress and tissue damage. Their role in cold and mechanical nociception has also being described. Sigma-1 receptor (σ-1R) is a molecular chaperone that modulates both trafficking and function of various ion channels. In mice, the σ-1R antagonist, S1RA, is able to reduce the symptoms of neuropathic pain. Since the molecular determinants of this antinociceptive effect remain unknown, we studied a possible modulation of TRPA1 by σ-1R. We performed calcium imaging and patch-clamp experiments in HEK293 cells transfected with hTRPA1 tagged with tGFP (hTRPA1-tGFP). Incubation of these cells with S1RA decreased the amplitude of [Ca2+]i responses and of the membrane currents evoked by AITC. Similar results were obtained with BD1086, another σ-1R antagonist. FRET experiments in cells transfected with hTRPA1-tGFP and mCherry- σ-1R revealed that both proteins are localized at a distance compatible with a physical interaction that was supported by co-immunoprecipitation experiments. Treatment of these cells with S1RA decreased FRET levels, suggesting an impairment or conformational change of this putative interaction. Finally, TIRF-FRAP experiments indicate that S1RA reduces the trafficking of TRPA1 towards the plasma membrane, resulting in a reduction of TRPA1 expression at the plasma membrane which was confirmed by cell surface biotinylation assays. These results suggest a role TRPA1 in the anti-nociceptive effects of σ-1R antagonists., Funding source: SAF2016-77233-R, PID2019-108194RB-100, co-financed by ERDF, Severo Ochoa Program SEV-2017-0723 and GRISOLIA/2015/034.
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- 2021
7. Modulation of the TRPA1 ion channel by sigma-1 receptor
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Peña, Elvira de la, Marcotti, Aida, Fernández-Trillo, Jorge, González, Alejandro, Gomis, Ana, Viana, Félix, Esteve, Generalitat Valenciana, Ministerio de Economía y Competitividad (España), and European Commission
- Abstract
Resumen del póster presentado al 49th Annual Meeting of the Society for Neuroscience, celebrado en Chicago (USA) del 19 al 23 de octubre de 2019., TRPA1 channels expressed in mammalian nociceptor endings play a critical role in chemonociception as a molecular sensors of reactive irritants, stress and tissue damage. Additionally, TRPA1 has been implicated in noxious cold and mechanical pain sensation. Sigma-1 receptor (σ-1R) is a chaperone mainly located in endoplasmic reticulum membrane, acting as an interoganelle signaling modulator that regulates the trafficking and function of different ionic channels. In the context of pain, pharmacological treatment of mice with the σ-1R antagonist, E-52862 (provided by ESTEVE PHARMACEUTICALS SA), produces antinociceptive effects, and has been shown to reduce the symptoms of neuropathic pain but the molecular mechanism is still unresolved. We studied the possible role of σ-1R in the modulation of TRPA1 channels and the result of this modulation on pain in mice. Measurement of intracellular calcium changes [Ca2+]i (FURA-2), and patch-clamp recordings were carried out in HEK-293 cells transfected with human TRPA1 (HEK-hTRPA1), and in cultured mouse DRG sensory neurons responsive to 50 µM AITC, a TRPA1 agonist. In both systems, incubation (4-24h) with E-52862 decreased significantly, in a dose dependent manner, the amplitude of [Ca2+]i responses evoked by AITC. Whole-cell membrane currents in HEK-hTRPA1 cells in response to AITC were also reduced, following incubation with the drug. In DRG sensory neurons the firing of action potentials, recorded in cell-attached mode, the membrane depolarization and the number of action potentials recorded in whole-cell current-clamp configuration evoked by AITC, were also significantly reduced following incubation with E-52862. In mice, we found that pain behaviors (licking, lifting and flickering) associated with TRPA1 activation by intraplantar injection of 10 mM AITC, decreased following intraperitoneal injection 24 h before of (40mg/kg) E-52862. These results implicate TRPA1 channels in the anti-nociceptive effects of σ-1R antagonists. All experimental procedures were carried out according to Spanish Royal Decree 1201/2005 and the ECC directive 2010/63/EU., Esteve Pharmaceuticals SA; SAF2016-77233-R co-financed by the European Regional Development Fund (ERDF); SEV- 2013-0317; GRISOLIA/2015/034.
- Published
- 2019
8. Joint nociceptor nerve activity and pain in an animal model of acute gout and its modulation by intra-articular hyaluronan
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Ministerio de Economía y Competitividad (España), European Commission, Generalitat Valenciana, Marcotti, Aida, Miralles, Ana, Domínguez-Sala, Eduardo, Pascual, Eliseo, Gomis, Ana, Belmonte, Carlos, Peña, Elvira de la, Ministerio de Economía y Competitividad (España), European Commission, Generalitat Valenciana, Marcotti, Aida, Miralles, Ana, Domínguez-Sala, Eduardo, Pascual, Eliseo, Gomis, Ana, Belmonte, Carlos, and Peña, Elvira de la
- Abstract
The mechanisms whereby deposition of monosodium urate (MSU) crystals in gout activates nociceptors to induce joint pain are incompletely understood. We tried to reproduce the signs of painful gouty arthritis, injecting into the knee joint of rats suspensions containing amorphous or triclinic, needle MSU crystals. The magnitude of MSU-induced inflammation and pain behavior signs were correlated with the changes in firing frequency of spontaneous and movement-evoked nerve impulse activity recorded in single knee joint nociceptor saphenous nerve fibers. Joint swelling, mechanical and cold allodynia, and hyperalgesia appeared 3 hours after joint injection of MSU crystals. In parallel, spontaneous and movement-evoked joint nociceptor impulse activity raised significantly. Solutions containing amorphous or needle-shaped MSU crystals had similar inflammatory and electrophysiological effects. Intra-articular injection of hyaluronan (HA, Synvisc), a high-MW glycosaminoglycan present in the synovial fluid with analgesic effects in osteoarthritis, significantly reduced MSU-induced behavioral signs of pain and decreased the enhanced joint nociceptor activity. Our results support the interpretation that pain and nociceptor activation are not triggered by direct mechanical stimulation of nociceptors by MSU crystals, but are primarily caused by the release of excitatory mediators by inflammatory cells activated by MSU crystals. Intra-articular HA decreased behavioral and electrophysiological signs of pain, possibly through its viscoelastic filtering effect on the mechanical forces acting over sensitized joint sensory endings and probably also by a direct interaction of HA molecules with the transducing channels expressed in joint nociceptor terminals.
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- 2018
9. Joint nociceptor nerve activity and pain in an animal model of acute gout and its modulation by intra-articular hyaluronan
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Marcotti, Aida, primary, Miralles, Ana, additional, Dominguez, Eduardo, additional, Pascual, Eliseo, additional, Gomis, Ana, additional, Belmonte, Carlos, additional, and de la Peña, Elvira, additional
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- 2018
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10. Cortical dynamics and subcortical signatures of motor-language coupling in Parkinson’s disease
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Melloni, Margherita, primary, Sedeño, Lucas, additional, Hesse, Eugenia, additional, García-Cordero, Indira, additional, Mikulan, Ezequiel, additional, Plastino, Angelo, additional, Marcotti, Aida, additional, López, José David, additional, Bustamante, Catalina, additional, Lopera, Francisco, additional, Pineda, David, additional, García, Adolfo M., additional, Manes, Facundo, additional, Trujillo, Natalia, additional, and Ibáñez, Agustín, additional
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- 2015
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11. En búsqueda de interfaces naturales para personas con discapacidad
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Beltramone, Diego Antonio, primary, Tula, Silvia Matilde, additional, Rivarola, Marcela Fabiana, additional, Hidalgo, Maria Belen, additional, Tancredi, Pablo Daniel, additional, Quinteros Quintana, Maria Luz, additional, Diaz, Juan Manuel, additional, Marcotti, Aida, additional, and Atea, Juan Javier, additional
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- 2014
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12. Non-Invasive Vein Detection Method using Infrared Light
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Marcotti, Aida, primary, Hidalgo, Maria Belen, additional, and Mathe, Ladislao, additional
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- 2013
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