Escherichia coli lipopolysaccharide impairs the calcium signaling pathway in mesangial cells: role of angiotensin II receptors

dc.contributor.authorMaquigussa, Edgar [UNIFESP]
dc.contributor.authorArnoni, Carine P. [UNIFESP]
dc.contributor.authorCristovam, Priscila C. [UNIFESP]
dc.contributor.authorOliveira, Andrea S. de [UNIFESP]
dc.contributor.authorHiga, Elisa M. S. [UNIFESP]
dc.contributor.authorBoim, Mirian A. [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T13:59:47Z
dc.date.available2016-01-24T13:59:47Z
dc.date.issued2010-06-01
dc.description.abstractSepsis causes impaired vascular reactivity, hypotension and acute renal failure. the ability of the Escherichia coli endotoxin (lipopolysaccharide [LPS]) to impair agonist-induced contractility in mesangial cells, which contributes to LPS-induced renal dysfunction, was evaluated. Agonist-induced intracellular calcium ([Ca(2+)]i) mobilization was analyzed using angiotensin II (AngII). the effect of LPS on the levels of the renin-angiotensin system (RAS) components and the roles of vasodilatation-inducing molecules including AT2 receptor (AT2R) and nitric oxide (NO) in the cell reactivity were also evaluated. Confluent human mesangial cells (HMCs) were stimulated with LPS (0111-B4, 100 mu g/mL). AngII-induced [Ca(2+)]i mobilization was measured by fluorometric analysis using Fura-2AM in the absence and presence of an AT2R antagonist (PD123319). the mRNA and protein levels for angiotensinogen, renin, angiotensin-converting enzyme, AT1R and AT2R were analyzed by realtime reverse transcriptase-polymerase chain reaction and Western blot, respectively. NO production was measured by the chemiluminescence method in the culture media after 24, 48 and 72 h of LPS incubation. After 24 h, LPS-stimulated HMCs displayed lower basal [Ca(2+)]i and an impaired response to AngII-induced rise in [Ca(2+)]i. LPS significantly increased AT2R levels, but did not cause significant alterations of RAS components. PD123319 restored both basal and AngII-induced [Ca(2+)]i peak, suggesting an involvement of AT2R in these responses. the expected increase in NO production was significant only after 72 h of LPS incubation and it was unaffected by PD123319. Results showed that LPS reduced the reactivity of HMCs to AngII and suggest that the vasodilatation induced by AT2R is a potential mediator of this response through a pathway independent of NO.en
dc.description.affiliationUniversidade Federal de São Paulo, Div Renal, Dept Med, BR-04023900 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Div Renal, Dept Med, BR-04023900 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipFundacao Oswaldo Ramos (FOR)
dc.description.sponsorshipFundo de Auxilio aos Docentes e Alunos (FADA)
dc.format.extent761-767
dc.identifierhttp://dx.doi.org/10.1258/ebm.2010.010006
dc.identifier.citationExperimental Biology and Medicine. Maywood: Soc Experimental Biology Medicine, v. 235, n. 6, p. 761-767, 2010.
dc.identifier.doi10.1258/ebm.2010.010006
dc.identifier.issn1535-3702
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/32617
dc.identifier.wosWOS:000278933200012
dc.language.isoeng
dc.publisherSoc Experimental Biology Medicine
dc.relation.ispartofExperimental Biology and Medicine
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectsepsisen
dc.subjectendotoxinen
dc.subjectmesangial cellen
dc.subjectintracellular calciumen
dc.subjectacute renal failureen
dc.subjectAT2 receptoren
dc.subjectnitric oxideen
dc.titleEscherichia coli lipopolysaccharide impairs the calcium signaling pathway in mesangial cells: role of angiotensin II receptorsen
dc.typeinfo:eu-repo/semantics/article
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