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<title lang=en>Calcium signaling and β2-adrenergic receptors regulate 1-nitropyrene induced CXCL8 responses in BEAS-2B cells.</title>
<creator>Mayati, Abdullah</creator>
<creator>Le Ferrec, Eric</creator>
<creator>Holme, Jørn A</creator>
<creator>Fardel, Olivier</creator>
<creator>Lagadic-Gossmann, Dominique</creator>
<creator>Ovrevik, Johan</creator>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Norwegian Institute of Public Health ; Division of Environmental Medicine</contributor>
<contributor>The work was supported by the Research Council of Norway, through the Environmental Exposures and Health Outcomes-program (Grants nos. 185620 and 228143).</contributor>
<description>International audience</description>
<source>ISSN: 0887-2333</source>
<source>Toxicology in Vitro</source>
<publisher>Elsevier</publisher>
<identifier>hal-01058607</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01058607</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01058607/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01058607/file/Calcium_Signaling_and_I_2-Adrenergic_Receptors-final.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01058607</source>
<source>Toxicology in Vitro, Elsevier, 2014, 28 (6), pp.1153-7. 〈10.1016/j.tiv.2014.05.012〉</source>
<identifier>DOI : 10.1016/j.tiv.2014.05.012</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.tiv.2014.05.012</relation>
<identifier>PUBMED : 24904980</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/24904980</relation>
<language>en</language>
<subject lang=en>Lung</subject>
<subject lang=en>Inflammation</subject>
<subject lang=en>Chemokines</subject>
<subject lang=en>Polycyclic aromatic hydrocarbons</subject>
<subject lang=en>Calcium</subject>
<subject lang=en>Adrenergic receptors</subject>
<subject>[SDV.BC] Life Sciences [q-bio]/Cellular Biology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Nitro-polycyclic aromatic hydrocarbons (nitro-PAHs) are widespread environmental pollutants, generated from reactions between PAHs and nitrogen oxides during combustion processes. In the present study we have investigated the mechanisms of CXCL8 (IL-8) responses induced by 1-nitropyrene (1-NP) in human bronchial epithelial BEAS-2B cells, with focus on the possible importance of Ca(2+)-signaling and activation of β2-adrenergic receptors (β2AR). Ca(2+)-chelator treatment obliterated 1-NP-induced CXCL8 (IL-8) responses. 1-NP at 10μM (but not 1μM) induced a rapid and sustained increase in intracellular Ca(2+)-levels ([Ca(2+)]i). The early but not the later, sustained phase of 1-NP-induced [Ca(2+)]i was suppressed by beta-blocker treatment (carazolol). Moreover, inhibition of β2AR by blocking-antibody, beta-blocker treatment (ICI 118551) or siRNA transfection attenuated CXCL8 responses induced by 1-NP. The results confirm that PAHs may induce Ca(2+)-signaling also in BEAS-2B cells, at least partly through activation of β2AR, and suggest that both β2AR- and Ca(2+)-signaling may be involved in 1-NP-induced CXCL8 responses in bronchial epithelial cells.</description>
<date>2014-09</date>
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