Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/27763
Title: Bradykinin B-1 receptor expression induced by tissue damage in the rat portal vein - A critical role for mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways
Authors: Medeiros, R.
Cabrini, D. A.
Ferreira, J.
Fernandes, E. S.
Mori, Marcelo Alves da Silva [UNIFESP]
Pesquero, João Bosco [UNIFESP]
Bader, Michael [UNIFESP]
Avellar, Maria Christina Werneck [UNIFESP]
Campos, M. M.
Calixto, J. B.
Universidade Federal de Santa Catarina (UFSC)
Universidade Federal de São Paulo (UNIFESP)
Max Delbruck Ctr Mol Med
Keywords: receptor, bradykinin B-1
tissue damage
mitogen-activated protein kinases
portal vein
rats
Issue Date: 28-May-2004
Publisher: Lippincott Williams & Wilkins
Citation: Circulation Research. Philadelphia: Lippincott Williams & Wilkins, v. 94, n. 10, p. 1375-1382, 2004.
Abstract: The bradykinin B-1 receptor (B1R) is normally absent under physiological conditions, but is highly inducible during inflammatory conditions or following tissue damage. the present study attempted to determine some of the mechanisms underlying B1R upregulation following tissue injury in rat portal vein. Damage induced by tissue isolation and in vitro incubation caused a significant and time-dependent increase in des-Arg(9)-bradykinin (des-Arg(9)-BK) responsiveness that paralleled the B1R mRNA expression, as confirmed by real-time quantitative PCR. in vitro incubation of rat portal vein also induced the activation of some members of the mitogen activated protein kinase ( MAPK) family, namely, extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and p38 MAPK, an effect accompanied by degradation of the inhibitory protein IkappaBalpha and translocation of nuclear transcription factor-kappaB (NF-kappaB) to the nucleus. the blockade of p38 MAPK, JNK or NF-kappaB, but not ERK pathways with selective inhibitors, resulted in a significant reduction of the upregulated contractile response caused by the selective B1R agonist des-Arg(9)-BK, and largely prevented the induction of B1R mRNA expression in the rat portal vein. Together, these results demonstrate that in vitro tissue damage induces activation of several intracellular signaling pathways that have a key role in the control of B1R expression. B1R could exert a pivotal role in the development of the cardiovascular response associated with vascular damage.
URI: http://repositorio.unifesp.br/handle/11600/27763
ISSN: 0009-7330
Other Identifiers: http://dx.doi.org/10.1161/01.RES.0000128404.65887.08
Appears in Collections:Em verificação - Geral

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