Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins
- Autores
- Etulain, Julia; Lapponi, María José; Patrucchi, S.J.; Romaniuk, María Albertina; Benzadón, R.; Klement, G. L.; Negrotto, Soledad; Schattner, Mirta Ana
- Año de publicación
- 2011
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Background: Hyperthermia is one of the main disturbances of homeostasis occurring during sepsis or hypermetabolic states such as cancer. Platelets are important mediators of the inflammation that accompanies these processes, but very little is known about the changes in platelet function that occur at different temperatures. Objectives: To explore the effect of higher temperatures on platelet physiology. Methods: Platelet responses including adhesion, spreading (fluorescence microscopy), α IIbβ 3 activation (flow cytometry), aggregation (turbidimetry), ATP release (luminescence), thromboxane A 2 generation, alpha-granule protein secretion (ELISA) and protein phosphorylation from different signaling pathways (immunoblotting) were studied. Results: Preincubation of platelets at temperatures higher than 37°C (38.5-42°C) inhibited thrombin-induced hemostasis, including platelet adhesion, aggregation, ATP release and thromboxane A 2 generation. The expression of P-selectin and CD63, as well as vascular endothelial growth factor (VEGF) release, was completely inhibited by hyperthermia, whereas von Willebrand factor (VWF) and endostatin levels remained substantially increased at high temperatures. This suggested that release of proteins from platelet granules is modulated not only by classical platelet agonists but also by microenvironmental factors. The observed gradation of response involved not only antiangiogenesis regulators, but also other cargo proteins. Some signaling pathways were more stable than others. While ERK1/2 and AKT phosphorylation were resistant to changes in temperature, Src, Syk, p38 phosphorylation and IkappaB degradation were decreased in a temperature-dependent fashion. Conclusions: Higher temperatures, such as those observed with fever or tissue invasion, inhibit the hemostatic functions of platelets and selectively regulate the release of alpha-granule proteins. © 2011 International Society on Thrombosis and Haemostasis.
Fil: Etulain, Julia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Lapponi, María José. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Patrucchi, S.J.. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Romaniuk, María Albertina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Benzadón, R.. Centro de Educación Médica e Investigaciones Clínicas “Norberto Quirno”; Argentina
Fil: Klement, G. L.. St Elizabeth’s Medical Center; Estados Unidos
Fil: Negrotto, Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Schattner, Mirta Ana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina - Materia
-
Alpha-Granule Secretion
Hyperthermia
Inflammation
Platelet Aggregation
Platelets
Temperature - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/52931
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Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteinsEtulain, JuliaLapponi, María JoséPatrucchi, S.J.Romaniuk, María AlbertinaBenzadón, R.Klement, G. L.Negrotto, SoledadSchattner, Mirta AnaAlpha-Granule SecretionHyperthermiaInflammationPlatelet AggregationPlateletsTemperaturehttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Background: Hyperthermia is one of the main disturbances of homeostasis occurring during sepsis or hypermetabolic states such as cancer. Platelets are important mediators of the inflammation that accompanies these processes, but very little is known about the changes in platelet function that occur at different temperatures. Objectives: To explore the effect of higher temperatures on platelet physiology. Methods: Platelet responses including adhesion, spreading (fluorescence microscopy), α IIbβ 3 activation (flow cytometry), aggregation (turbidimetry), ATP release (luminescence), thromboxane A 2 generation, alpha-granule protein secretion (ELISA) and protein phosphorylation from different signaling pathways (immunoblotting) were studied. Results: Preincubation of platelets at temperatures higher than 37°C (38.5-42°C) inhibited thrombin-induced hemostasis, including platelet adhesion, aggregation, ATP release and thromboxane A 2 generation. The expression of P-selectin and CD63, as well as vascular endothelial growth factor (VEGF) release, was completely inhibited by hyperthermia, whereas von Willebrand factor (VWF) and endostatin levels remained substantially increased at high temperatures. This suggested that release of proteins from platelet granules is modulated not only by classical platelet agonists but also by microenvironmental factors. The observed gradation of response involved not only antiangiogenesis regulators, but also other cargo proteins. Some signaling pathways were more stable than others. While ERK1/2 and AKT phosphorylation were resistant to changes in temperature, Src, Syk, p38 phosphorylation and IkappaB degradation were decreased in a temperature-dependent fashion. Conclusions: Higher temperatures, such as those observed with fever or tissue invasion, inhibit the hemostatic functions of platelets and selectively regulate the release of alpha-granule proteins. © 2011 International Society on Thrombosis and Haemostasis.Fil: Etulain, Julia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Lapponi, María José. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Patrucchi, S.J.. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Romaniuk, María Albertina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Benzadón, R.. Centro de Educación Médica e Investigaciones Clínicas “Norberto Quirno”; ArgentinaFil: Klement, G. L.. St Elizabeth’s Medical Center; Estados UnidosFil: Negrotto, Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Schattner, Mirta Ana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaWiley Blackwell Publishing, Inc2011-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/52931Etulain, Julia; Lapponi, María José; Patrucchi, S.J.; Romaniuk, María Albertina; Benzadón, R.; et al.; Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins; Wiley Blackwell Publishing, Inc; Journal of Thrombosis and Haemostasis; 9; 8; 8-2011; 1562-15711538-7933CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1111/j.1538-7836.2011.04394.xinfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1538-7836.2011.04394.xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:37:59Zoai:ri.conicet.gov.ar:11336/52931instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:38:00.022CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins |
title |
Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins |
spellingShingle |
Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins Etulain, Julia Alpha-Granule Secretion Hyperthermia Inflammation Platelet Aggregation Platelets Temperature |
title_short |
Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins |
title_full |
Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins |
title_fullStr |
Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins |
title_full_unstemmed |
Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins |
title_sort |
Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins |
dc.creator.none.fl_str_mv |
Etulain, Julia Lapponi, María José Patrucchi, S.J. Romaniuk, María Albertina Benzadón, R. Klement, G. L. Negrotto, Soledad Schattner, Mirta Ana |
author |
Etulain, Julia |
author_facet |
Etulain, Julia Lapponi, María José Patrucchi, S.J. Romaniuk, María Albertina Benzadón, R. Klement, G. L. Negrotto, Soledad Schattner, Mirta Ana |
author_role |
author |
author2 |
Lapponi, María José Patrucchi, S.J. Romaniuk, María Albertina Benzadón, R. Klement, G. L. Negrotto, Soledad Schattner, Mirta Ana |
author2_role |
author author author author author author author |
dc.subject.none.fl_str_mv |
Alpha-Granule Secretion Hyperthermia Inflammation Platelet Aggregation Platelets Temperature |
topic |
Alpha-Granule Secretion Hyperthermia Inflammation Platelet Aggregation Platelets Temperature |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
dc.description.none.fl_txt_mv |
Background: Hyperthermia is one of the main disturbances of homeostasis occurring during sepsis or hypermetabolic states such as cancer. Platelets are important mediators of the inflammation that accompanies these processes, but very little is known about the changes in platelet function that occur at different temperatures. Objectives: To explore the effect of higher temperatures on platelet physiology. Methods: Platelet responses including adhesion, spreading (fluorescence microscopy), α IIbβ 3 activation (flow cytometry), aggregation (turbidimetry), ATP release (luminescence), thromboxane A 2 generation, alpha-granule protein secretion (ELISA) and protein phosphorylation from different signaling pathways (immunoblotting) were studied. Results: Preincubation of platelets at temperatures higher than 37°C (38.5-42°C) inhibited thrombin-induced hemostasis, including platelet adhesion, aggregation, ATP release and thromboxane A 2 generation. The expression of P-selectin and CD63, as well as vascular endothelial growth factor (VEGF) release, was completely inhibited by hyperthermia, whereas von Willebrand factor (VWF) and endostatin levels remained substantially increased at high temperatures. This suggested that release of proteins from platelet granules is modulated not only by classical platelet agonists but also by microenvironmental factors. The observed gradation of response involved not only antiangiogenesis regulators, but also other cargo proteins. Some signaling pathways were more stable than others. While ERK1/2 and AKT phosphorylation were resistant to changes in temperature, Src, Syk, p38 phosphorylation and IkappaB degradation were decreased in a temperature-dependent fashion. Conclusions: Higher temperatures, such as those observed with fever or tissue invasion, inhibit the hemostatic functions of platelets and selectively regulate the release of alpha-granule proteins. © 2011 International Society on Thrombosis and Haemostasis. Fil: Etulain, Julia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina Fil: Lapponi, María José. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina Fil: Patrucchi, S.J.. Academia Nacional de Medicina de Buenos Aires; Argentina Fil: Romaniuk, María Albertina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina Fil: Benzadón, R.. Centro de Educación Médica e Investigaciones Clínicas “Norberto Quirno”; Argentina Fil: Klement, G. L.. St Elizabeth’s Medical Center; Estados Unidos Fil: Negrotto, Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina Fil: Schattner, Mirta Ana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina |
description |
Background: Hyperthermia is one of the main disturbances of homeostasis occurring during sepsis or hypermetabolic states such as cancer. Platelets are important mediators of the inflammation that accompanies these processes, but very little is known about the changes in platelet function that occur at different temperatures. Objectives: To explore the effect of higher temperatures on platelet physiology. Methods: Platelet responses including adhesion, spreading (fluorescence microscopy), α IIbβ 3 activation (flow cytometry), aggregation (turbidimetry), ATP release (luminescence), thromboxane A 2 generation, alpha-granule protein secretion (ELISA) and protein phosphorylation from different signaling pathways (immunoblotting) were studied. Results: Preincubation of platelets at temperatures higher than 37°C (38.5-42°C) inhibited thrombin-induced hemostasis, including platelet adhesion, aggregation, ATP release and thromboxane A 2 generation. The expression of P-selectin and CD63, as well as vascular endothelial growth factor (VEGF) release, was completely inhibited by hyperthermia, whereas von Willebrand factor (VWF) and endostatin levels remained substantially increased at high temperatures. This suggested that release of proteins from platelet granules is modulated not only by classical platelet agonists but also by microenvironmental factors. The observed gradation of response involved not only antiangiogenesis regulators, but also other cargo proteins. Some signaling pathways were more stable than others. While ERK1/2 and AKT phosphorylation were resistant to changes in temperature, Src, Syk, p38 phosphorylation and IkappaB degradation were decreased in a temperature-dependent fashion. Conclusions: Higher temperatures, such as those observed with fever or tissue invasion, inhibit the hemostatic functions of platelets and selectively regulate the release of alpha-granule proteins. © 2011 International Society on Thrombosis and Haemostasis. |
publishDate |
2011 |
dc.date.none.fl_str_mv |
2011-08 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/52931 Etulain, Julia; Lapponi, María José; Patrucchi, S.J.; Romaniuk, María Albertina; Benzadón, R.; et al.; Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins; Wiley Blackwell Publishing, Inc; Journal of Thrombosis and Haemostasis; 9; 8; 8-2011; 1562-1571 1538-7933 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/52931 |
identifier_str_mv |
Etulain, Julia; Lapponi, María José; Patrucchi, S.J.; Romaniuk, María Albertina; Benzadón, R.; et al.; Hyperthermia inhibits platelet hemostatic functions and selectively regulates the release of alpha-granule proteins; Wiley Blackwell Publishing, Inc; Journal of Thrombosis and Haemostasis; 9; 8; 8-2011; 1562-1571 1538-7933 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1111/j.1538-7836.2011.04394.x info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1538-7836.2011.04394.x |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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application/pdf application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Wiley Blackwell Publishing, Inc |
publisher.none.fl_str_mv |
Wiley Blackwell Publishing, Inc |
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reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.name.fl_str_mv |
CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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13.070432 |