Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS)
Introduction: Ischemic tolerance (IT) refers to a state where cells are resistant to the damaging effects caused by periods of ischemia. In a clinical scenario, the IT phenomenon would be activated by a recent transient ischemic attack (TIA) before an ischemic stroke (IS). The characterization of in...
| Autores: | , , , , , , , , , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2020 |
| País: | España |
| Institución: | Universitat Pompeu Fabra |
| Repositorio: | Repositorio Digital de la UPF |
| OAI Identifier: | oai:repositori.upf.edu:10230/48031 |
| Acceso en línea: | http://hdl.handle.net/10230/48031 http://dx.doi.org/10.3389/fneur.2020.552470 |
| Access Level: | acceso abierto |
| Palabra clave: | Biomarker (BM) Endogenous neuroprotection Ischemic preconditioning (IPC) Ischemic stroke Plasma Transient ischemic attack (TIA) Neuromuscular diseases care in the era of COVID-19 |
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Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS)Colàs-Campàs, LauraFarré, JoanMauri Capdevila, GerardMolina-Seguín, JessicaAymerich, NúriaOis Santiago, Angel JavierRoquer, JaumeTur, SilviaGarcía-Carreira, María Del CarmenMartí-Fàbregas, JoanCruz-Culebras, AntonioSegura, TomásArqué, GloriaPurroy, FranciscoBiomarker (BM)Endogenous neuroprotectionIschemic preconditioning (IPC)Ischemic strokePlasmaTransient ischemic attack (TIA)Neuromuscular diseases care in the era of COVID-19Introduction: Ischemic tolerance (IT) refers to a state where cells are resistant to the damaging effects caused by periods of ischemia. In a clinical scenario, the IT phenomenon would be activated by a recent transient ischemic attack (TIA) before an ischemic stroke (IS). The characterization of inflammatory protein expression patterns will contribute to improved understanding of IT. Methods: A total of 477 IS patients from nine hospitals, recruited between January 2011 and January 2016, were included in the current study and divided in three groups: 438 (91.9%) patients without previous TIA (group 1), 22 (4.6%) patients who suffered TIA 24 h before IS (group 2), and 17 (3.5%) patients who suffered TIA between 24 h and 7 days prior to IS (group 3). An inflammatory biomarker panel (IL-6, NT-proBNP, hsCRP, hs-Troponin, NSE, and S-100b) on plasma and a cytokine antibody array was performed to achieve the preconditioning signature potentially induced by TIA phenomena. Primary outcome was modified rankin scale (mRs) score at 90 days. Results: Recent previous TIA was associated with better clinical outcome at 90 days (median mRS of group 1: 2.0 [1.0-4.0]; group 2: 2.0 [0.0-3.0]; group 3: 1.0 [0-2.5]; p = 0.086) and smaller brain lesion (group 1: 3.7 [0.7-18.3]; group 2: 0.8 [0.3-8.9]; group 3: 0.6 [0.1-5.5] mL; p = 0.006). All inflammation biomarkers were down regulated in the groups of recent TIA prior to IS compared to those who did not suffer a TIA events. Moreover, a cytokine antibody array revealed 30 differentially expressed proteins between the three groups. Among them, HRG1-alpha (Fold change 74.4 between group 1 and 2; 74.2 between group 1 and 3) and MAC-1 (Fold change 0.05 between group 1 and 2; 0.06 between group 1 and 3) expression levels would better stratify patients with TIA 7 days before IS. These two proteins showed an earlier inflammation profile that was not detectable by the biomarker panel. Conclusion: Inflammatory pathways were activated by transient ischemic attack, however the period of time between this event and a further ischemic stroke could be determined by a protein signature that would contribute to define the role of ischemic tolerance induced by TIA.Frontiers202120212020info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttp://hdl.handle.net/10230/48031http://dx.doi.org/10.3389/fneur.2020.552470reponame:Repositorio Digital de la UPFinstname:Universitat Pompeu FabraInglésCopyright © 2020 Colàs-Campàs, Farre, Mauri-Capdevila, Molina-Seguín, Aymerich, Ois, Roquer, Tur, García-Carreira, Martí-Fàbregas, Cruz-Culebras, Segura, Arque and Purroy. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). http://creativecommons.org/licenses/by/4.0/. The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.http://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:repositori.upf.edu:10230/480312026-06-12T07:21:37Z |
| dc.title.none.fl_str_mv |
Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS) |
| title |
Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS) |
| spellingShingle |
Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS) Colàs-Campàs, Laura Biomarker (BM) Endogenous neuroprotection Ischemic preconditioning (IPC) Ischemic stroke Plasma Transient ischemic attack (TIA) Neuromuscular diseases care in the era of COVID-19 |
| title_short |
Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS) |
| title_full |
Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS) |
| title_fullStr |
Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS) |
| title_full_unstemmed |
Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS) |
| title_sort |
Inflammatory response of ischemic tolerance in circulating plasma: preconditioning-induced by transient ischemic attack (TIA) phenomena in acute ischemia patients (AIS) |
| dc.creator.none.fl_str_mv |
Colàs-Campàs, Laura Farré, Joan Mauri Capdevila, Gerard Molina-Seguín, Jessica Aymerich, Núria Ois Santiago, Angel Javier Roquer, Jaume Tur, Silvia García-Carreira, María Del Carmen Martí-Fàbregas, Joan Cruz-Culebras, Antonio Segura, Tomás Arqué, Gloria Purroy, Francisco |
| author |
Colàs-Campàs, Laura |
| author_facet |
Colàs-Campàs, Laura Farré, Joan Mauri Capdevila, Gerard Molina-Seguín, Jessica Aymerich, Núria Ois Santiago, Angel Javier Roquer, Jaume Tur, Silvia García-Carreira, María Del Carmen Martí-Fàbregas, Joan Cruz-Culebras, Antonio Segura, Tomás Arqué, Gloria Purroy, Francisco |
| author_role |
author |
| author2 |
Farré, Joan Mauri Capdevila, Gerard Molina-Seguín, Jessica Aymerich, Núria Ois Santiago, Angel Javier Roquer, Jaume Tur, Silvia García-Carreira, María Del Carmen Martí-Fàbregas, Joan Cruz-Culebras, Antonio Segura, Tomás Arqué, Gloria Purroy, Francisco |
| author2_role |
author author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
Biomarker (BM) Endogenous neuroprotection Ischemic preconditioning (IPC) Ischemic stroke Plasma Transient ischemic attack (TIA) Neuromuscular diseases care in the era of COVID-19 |
| topic |
Biomarker (BM) Endogenous neuroprotection Ischemic preconditioning (IPC) Ischemic stroke Plasma Transient ischemic attack (TIA) Neuromuscular diseases care in the era of COVID-19 |
| description |
Introduction: Ischemic tolerance (IT) refers to a state where cells are resistant to the damaging effects caused by periods of ischemia. In a clinical scenario, the IT phenomenon would be activated by a recent transient ischemic attack (TIA) before an ischemic stroke (IS). The characterization of inflammatory protein expression patterns will contribute to improved understanding of IT. Methods: A total of 477 IS patients from nine hospitals, recruited between January 2011 and January 2016, were included in the current study and divided in three groups: 438 (91.9%) patients without previous TIA (group 1), 22 (4.6%) patients who suffered TIA 24 h before IS (group 2), and 17 (3.5%) patients who suffered TIA between 24 h and 7 days prior to IS (group 3). An inflammatory biomarker panel (IL-6, NT-proBNP, hsCRP, hs-Troponin, NSE, and S-100b) on plasma and a cytokine antibody array was performed to achieve the preconditioning signature potentially induced by TIA phenomena. Primary outcome was modified rankin scale (mRs) score at 90 days. Results: Recent previous TIA was associated with better clinical outcome at 90 days (median mRS of group 1: 2.0 [1.0-4.0]; group 2: 2.0 [0.0-3.0]; group 3: 1.0 [0-2.5]; p = 0.086) and smaller brain lesion (group 1: 3.7 [0.7-18.3]; group 2: 0.8 [0.3-8.9]; group 3: 0.6 [0.1-5.5] mL; p = 0.006). All inflammation biomarkers were down regulated in the groups of recent TIA prior to IS compared to those who did not suffer a TIA events. Moreover, a cytokine antibody array revealed 30 differentially expressed proteins between the three groups. Among them, HRG1-alpha (Fold change 74.4 between group 1 and 2; 74.2 between group 1 and 3) and MAC-1 (Fold change 0.05 between group 1 and 2; 0.06 between group 1 and 3) expression levels would better stratify patients with TIA 7 days before IS. These two proteins showed an earlier inflammation profile that was not detectable by the biomarker panel. Conclusion: Inflammatory pathways were activated by transient ischemic attack, however the period of time between this event and a further ischemic stroke could be determined by a protein signature that would contribute to define the role of ischemic tolerance induced by TIA. |
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2020 |
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2020 2021 2021 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
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article |
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http://hdl.handle.net/10230/48031 http://dx.doi.org/10.3389/fneur.2020.552470 |
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http://hdl.handle.net/10230/48031 http://dx.doi.org/10.3389/fneur.2020.552470 |
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Inglés |
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