Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/7909
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dc.contributor.authorCastro-Caldas, M.-
dc.contributor.authorDuarte, C. B.-
dc.contributor.authorCarvalho, A. P.-
dc.contributor.authorLopes, M. C. Fernandes-
dc.date.accessioned2009-02-17T10:35:56Z-
dc.date.available2009-02-17T10:35:56Z-
dc.date.issued2002en_US
dc.identifier.citationMolecular and Cellular Biochemistry. 237:1 (2002) 31-38en_US
dc.identifier.urihttp://hdl.handle.net/10316/7909-
dc.description.abstractThe mechanisms by which glucocorticoids (GC) regulate annexin I (ANXA1) secretion in different cells are still a matter of debate. The aims of this study were to evaluate the ability of dexamethasone (Dex) to induce ANXA1 secretion and to investigate the roles of the intracellular free Ca2+ concentration ([Ca2+]i), and of the GC receptor, on that process. For this purpose, the human immature lymphoblastic CCRF-CEM cell line was used. Treatment of the cells with Dex, for up to 4 h, significantly reduced the intracellular content of ANXA1 and increased the amount of this protein bound to the outer surface of the plasma membrane, whereas exposure of cells to Dex, for 12 h, induced the synthesis of ANXA1. At the same short time periods, Dex also induced a significant increase in the [Ca2+]i. Incubation of the cells with BAPTA-AM (10 µM), a cell-permeant high affinity Ca2+ chelator, completely inhibited Dex-induced ANXA1 secretion. Furthermore, the Ca2+ ionophore, ionomycin, alone induced ANXA1 cleavage, but not its secretion. Additionally, we used brefeldin A to investigate the involvement of the classical endoplasmic reticulum (ER)-Golgi pathway of protein secretion in the release of ANXA1. The GC receptor antagonist, RU486, neither reverted the Dex-dependent ANXA1 secretion nor inhibited the increase of the [Ca2+]i induced by Dex. Together, our results indicate that Dex induces ANXA1 synthesis and secretion in CCRF-CEM cells. ANXA1 secretion in this cell type show the following characteristics: (i) is unlikely to involve the classical ER-Golgi pathway; (ii) requires a Ca2+-dependent cleavage of ANXA1; (iii) involves both Ca2+-dependent and independent mechanisms; and (iv) is apparently independent of the GC receptor alpha isoform.en_US
dc.language.isoengeng
dc.rightsopenAccesseng
dc.titleDexamethasone induces the secretion of annexin I in immature lymphoblastic cells by a calcium-dependent mechanismen_US
dc.typearticleen_US
dc.identifier.doi10.1023/A:1016502120139en_US
uc.controloAutoridadeSim-
item.grantfulltextopen-
item.fulltextCom Texto completo-
item.openairetypearticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0002-1474-0208-
Appears in Collections:FCTUC Ciências da Vida - Artigos em Revistas Internacionais
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