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Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis

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Resumo:Rationale Stressful life events are suggested to contribute to the development of various pathologies, such as cardiovascular disorders, whose etiopathogenesis is highly associated with elevated levels of serum amyloid A (SAA) proteins. SAA synthesis inthe liver isregulated bya complex network ofcytokines actingindependently orinconcert withvarious hormones/stimulants including the stress-activated sympathetic nervous system. Objective This study aims to investigate the underlying mechanisms that regulate the stress-induced hepatic synthesis of SAA, with particular focus on adrenoceptors (AR), major components of the sympathoadrenal response to stress. Methods and results We demonstrated that repeated stress elevates IL-1β, IL-6, and TNFα serum levels in mice, accompanied by increased synthesis and secretion of hepatic SAA1/2 and SAA3, an effect that was blocked by AR antagonists. Moreover, stimulation ofα1- andβ1/2-ARsmimics thestress effectonSAA1/2 regulation, whereas α2-AR stimulation exhibitsa relatively weakimpactonSAA.InsupportoftheessentialcytokinecontributionintheAR-agonistinducedSAAproductionisthefactthat theanti-inflammatorydrug,sodiumsalicylate,preventedtheAR-stimulatedhepaticSAA1/2synthesisbyreducingIL-1βlevels, whereasIL-1βinhibitionwithAnakinramimicsthissodiumsalicylatepreventiveeffect,thusindicatingacrucial rolefor IL-1β. Interestingly, the AR-driven SAA3 synthesis was elevated by sodium salicylate in a TNFα-dependent way, supporting diverse and complex regulatory roles of cytokines in SAA production. In contrast to α1/α2-AR, the β1/2-AR-mediated SAA1/2 and SAA3 upregulation cannot be reversed by fenofibrate, a hypolipidemic drug with anti-inflammatory properties. Conclusion Taken together, these findings strongly support a critical role of the AR-stimulated inflammatory response in the hepatic SAA production under stressful conditions, highlighting distinct AR type-specific mechanisms that regulate the hepatic synthesis of SAA1/2 and SAA3.
Autores principais:Konstandi, Maria
Outros Autores:Sotiropoulos, I.; Matsubara, Tsutomu; Malliou, Foteini; Katsogridaki, Alexandra; Andriopoulou, Christina E.; Gonzalez, Frank J.
Assunto:Adrenoceptors IL-1β IL-6 SAA1/2 SAA3 Stress TNFα SAA1 2 IL-1 beta Ciências Médicas::Medicina Básica
Ano:2019
País:Portugal
Tipo de documento:artigo
Tipo de acesso:acesso aberto
Instituição associada:Universidade do Minho
Idioma:inglês
Origem:RepositóriUM - Universidade do Minho
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author Konstandi, Maria
author2 Sotiropoulos, I.
Matsubara, Tsutomu
Malliou, Foteini
Katsogridaki, Alexandra
Andriopoulou, Christina E.
Gonzalez, Frank J.
author2_role author
author
author
author
author
author
author_facet Konstandi, Maria
Sotiropoulos, I.
Matsubara, Tsutomu
Malliou, Foteini
Katsogridaki, Alexandra
Andriopoulou, Christina E.
Gonzalez, Frank J.
author_role author
contributor_name_str_mv RepositóriUM - Universidade do Minho
country_str PT
creators_json_txt [{\"Person.name\":\"Konstandi, Maria\"},{\"Person.name\":\"Sotiropoulos, I.\"},{\"Person.name\":\"Matsubara, Tsutomu\"},{\"Person.name\":\"Malliou, Foteini\"},{\"Person.name\":\"Katsogridaki, Alexandra\"},{\"Person.name\":\"Andriopoulou, Christina E.\"},{\"Person.name\":\"Gonzalez, Frank J.\"}]
datacite.contributors.contributor.contributorName.fl_str_mv RepositóriUM - Universidade do Minho
datacite.creators.creator.creatorName.fl_str_mv Konstandi, Maria
Sotiropoulos, I.
Matsubara, Tsutomu
Malliou, Foteini
Katsogridaki, Alexandra
Andriopoulou, Christina E.
Gonzalez, Frank J.
datacite.date.Accepted.fl_str_mv 2019-01-06T00:00:00Z
datacite.date.available.fl_str_mv 2020-01-06T07:00:21Z
datacite.date.embargoed.fl_str_mv 2020-01-06T07:00:21Z
datacite.rights.fl_str_mv http://purl.org/coar/access_right/c_abf2
datacite.subjects.subject.fl_str_mv Adrenoceptors
IL-1β
IL-6
SAA1/2
SAA3
Stress
TNFα
SAA1
2
IL-1 beta
Ciências Médicas::Medicina Básica
datacite.titles.title.fl_str_mv Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis
dc.contributor.none.fl_str_mv RepositóriUM - Universidade do Minho
dc.creator.none.fl_str_mv Konstandi, Maria
Sotiropoulos, I.
Matsubara, Tsutomu
Malliou, Foteini
Katsogridaki, Alexandra
Andriopoulou, Christina E.
Gonzalez, Frank J.
dc.date.Accepted.fl_str_mv 2019-01-06T00:00:00Z
dc.date.available.fl_str_mv 2020-01-06T07:00:21Z
dc.date.embargoed.fl_str_mv 2020-01-06T07:00:21Z
dc.format.none.fl_str_mv application/pdf
dc.identifier.none.fl_str_mv https://hdl.handle.net/1822/57992
dc.language.none.fl_str_mv eng
dc.publisher.none.fl_str_mv Springer Verlag
dc.rights.none.fl_str_mv http://purl.org/coar/access_right/c_abf2
dc.subject.none.fl_str_mv Adrenoceptors
IL-1β
IL-6
SAA1/2
SAA3
Stress
TNFα
SAA1
2
IL-1 beta
Ciências Médicas::Medicina Básica
dc.title.fl_str_mv Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis
dc.type.none.fl_str_mv http://purl.org/coar/resource_type/c_6501
description Rationale Stressful life events are suggested to contribute to the development of various pathologies, such as cardiovascular disorders, whose etiopathogenesis is highly associated with elevated levels of serum amyloid A (SAA) proteins. SAA synthesis inthe liver isregulated bya complex network ofcytokines actingindependently orinconcert withvarious hormones/stimulants including the stress-activated sympathetic nervous system. Objective This study aims to investigate the underlying mechanisms that regulate the stress-induced hepatic synthesis of SAA, with particular focus on adrenoceptors (AR), major components of the sympathoadrenal response to stress. Methods and results We demonstrated that repeated stress elevates IL-1β, IL-6, and TNFα serum levels in mice, accompanied by increased synthesis and secretion of hepatic SAA1/2 and SAA3, an effect that was blocked by AR antagonists. Moreover, stimulation ofα1- andβ1/2-ARsmimics thestress effectonSAA1/2 regulation, whereas α2-AR stimulation exhibitsa relatively weakimpactonSAA.InsupportoftheessentialcytokinecontributionintheAR-agonistinducedSAAproductionisthefactthat theanti-inflammatorydrug,sodiumsalicylate,preventedtheAR-stimulatedhepaticSAA1/2synthesisbyreducingIL-1βlevels, whereasIL-1βinhibitionwithAnakinramimicsthissodiumsalicylatepreventiveeffect,thusindicatingacrucial rolefor IL-1β. Interestingly, the AR-driven SAA3 synthesis was elevated by sodium salicylate in a TNFα-dependent way, supporting diverse and complex regulatory roles of cytokines in SAA production. In contrast to α1/α2-AR, the β1/2-AR-mediated SAA1/2 and SAA3 upregulation cannot be reversed by fenofibrate, a hypolipidemic drug with anti-inflammatory properties. Conclusion Taken together, these findings strongly support a critical role of the AR-stimulated inflammatory response in the hepatic SAA production under stressful conditions, highlighting distinct AR type-specific mechanisms that regulate the hepatic synthesis of SAA1/2 and SAA3.
dirty 0
eu_rights_str_mv openAccess
format article
fulltext.url.fl_str_mv https://repositorium.uminho.pt/bitstreams/4b4b6f5d-b09b-4508-96a7-74655ce49801/download
id rum_6de4fdfd4980020f2501b0ff92bf5f01
identifier.url.fl_str_mv https://hdl.handle.net/1822/57992
instacron_str repositorium
institution Universidade do Minho
instname_str Universidade do Minho
language eng
network_acronym_str rum
network_name_str RepositóriUM - Universidade do Minho
oai_identifier_str oai:repositorium.uminho.pt:1822/57992
organization_str_mv urn:organizationAcronym:repositorium
person_str_mv Konstandi, Maria
Sotiropoulos, I.
Matsubara, Tsutomu
Malliou, Foteini
Katsogridaki, Alexandra
Andriopoulou, Christina E.
Gonzalez, Frank J.
publishDate 2019
publisher.none.fl_str_mv Springer Verlag
reponame_str RepositóriUM - Universidade do Minho
repository_id_str urn:repositoryAcronym:rum
service_str_mv urn:repositoryAcronym:rum
spelling engSpringer VerlagporRationale Stressful life events are suggested to contribute to the development of various pathologies, such as cardiovascular disorders, whose etiopathogenesis is highly associated with elevated levels of serum amyloid A (SAA) proteins. SAA synthesis inthe liver isregulated bya complex network ofcytokines actingindependently orinconcert withvarious hormones/stimulants including the stress-activated sympathetic nervous system. Objective This study aims to investigate the underlying mechanisms that regulate the stress-induced hepatic synthesis of SAA, with particular focus on adrenoceptors (AR), major components of the sympathoadrenal response to stress. Methods and results We demonstrated that repeated stress elevates IL-1β, IL-6, and TNFα serum levels in mice, accompanied by increased synthesis and secretion of hepatic SAA1/2 and SAA3, an effect that was blocked by AR antagonists. Moreover, stimulation ofα1- andβ1/2-ARsmimics thestress effectonSAA1/2 regulation, whereas α2-AR stimulation exhibitsa relatively weakimpactonSAA.InsupportoftheessentialcytokinecontributionintheAR-agonistinducedSAAproductionisthefactthat theanti-inflammatorydrug,sodiumsalicylate,preventedtheAR-stimulatedhepaticSAA1/2synthesisbyreducingIL-1βlevels, whereasIL-1βinhibitionwithAnakinramimicsthissodiumsalicylatepreventiveeffect,thusindicatingacrucial rolefor IL-1β. Interestingly, the AR-driven SAA3 synthesis was elevated by sodium salicylate in a TNFα-dependent way, supporting diverse and complex regulatory roles of cytokines in SAA production. In contrast to α1/α2-AR, the β1/2-AR-mediated SAA1/2 and SAA3 upregulation cannot be reversed by fenofibrate, a hypolipidemic drug with anti-inflammatory properties. Conclusion Taken together, these findings strongly support a critical role of the AR-stimulated inflammatory response in the hepatic SAA production under stressful conditions, highlighting distinct AR type-specific mechanisms that regulate the hepatic synthesis of SAA1/2 and SAA3.application/pdfporAdrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesisKonstandi, MariaSotiropoulos, I.Matsubara, TsutomuMalliou, FoteiniKatsogridaki, AlexandraAndriopoulou, Christina E.Gonzalez, Frank J.HostingInstitutionOrganizationalRepositóriUM - Universidade do Minhoe-mailmailto:repositorium@usdb.uminho.ptrepositorium@usdb.uminho.ptPMID30612190ISSNIsPartOf0033-3158EISSNIsPartOf1432-2072DOIIsPartOf10.1007/s00213-018-5149-42020-01-06T07:00:21Z2019-01-062019-01-06T00:00:00ZHandlehttps://hdl.handle.net/1822/57992http://purl.org/coar/access_right/c_abf2open accessAdrenoceptorsIL-1βIL-6SAA1/2SAA3StressTNFαSAA12IL-1 betahttp://www.oecd.org/science/inno/38235147.pdfFields of Science and Technology (FOS)Ciências Médicas::Medicina Básica1251909 bytesliteraturehttp://purl.org/coar/resource_type/c_6501journal articlehttp://purl.org/coar/access_right/c_abf2application/pdffulltexthttps://repositorium.uminho.pt/bitstreams/4b4b6f5d-b09b-4508-96a7-74655ce49801/download
spellingShingle Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis
Konstandi, Maria
Adrenoceptors
IL-1β
IL-6
SAA1/2
SAA3
Stress
TNFα
SAA1
2
IL-1 beta
Ciências Médicas::Medicina Básica
status SINGLETON
subject.fl_str_mv Adrenoceptors
IL-1β
IL-6
SAA1/2
SAA3
Stress
TNFα
SAA1
2
IL-1 beta
subject.other.fl_str_mv Ciências Médicas::Medicina Básica
title Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis
title_full Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis
title_fullStr Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis
title_full_unstemmed Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis
title_short Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis
title_sort Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis
topic Adrenoceptors
IL-1β
IL-6
SAA1/2
SAA3
Stress
TNFα
SAA1
2
IL-1 beta
Ciências Médicas::Medicina Básica
topic_facet Adrenoceptors
IL-1β
IL-6
SAA1/2
SAA3
Stress
TNFα
SAA1
2
IL-1 beta
Ciências Médicas::Medicina Básica
url https://hdl.handle.net/1822/57992
visible 1