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
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/52931
Acceder
id CONICETDig_57a999a2b64c2829f5328cca9ee72715
oai_identifier_str oai:ri.conicet.gov.ar:11336/52931
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling 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 Técnicas2025-10-15T14:27:04Zoai: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:34982025-10-15 14:27:04.662CONICET 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/
dc.format.none.fl_str_mv 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
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str 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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score 13.22299

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