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

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

Autor Medeiros, R. Google Scholar
Cabrini, D. A. Google Scholar
Ferreira, J. Google Scholar
Fernandes, E. S. Google Scholar
Mori, Marcelo Alves da Silva Autor UNIFESP Google Scholar
Pesquero, João Bosco Autor UNIFESP Google Scholar
Bader, Michael Autor UNIFESP Google Scholar
Avellar, Maria Christina Werneck Autor UNIFESP Google Scholar
Campos, M. M. Google Scholar
Calixto, J. B. Google Scholar
Instituição Universidade Federal de Santa Catarina (UFSC)
Universidade Federal de São Paulo (UNIFESP)
Max Delbruck Ctr Mol Med
Resumo 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.
Assunto receptor, bradykinin B-1
tissue damage
mitogen-activated protein kinases
portal vein
rats
Idioma Inglês
Data 2004-05-28
Publicado em Circulation Research. Philadelphia: Lippincott Williams & Wilkins, v. 94, n. 10, p. 1375-1382, 2004.
ISSN 0009-7330 (Sherpa/Romeo, fator de impacto)
Editor Lippincott Williams & Wilkins
Extensão 1375-1382
Fonte http://dx.doi.org/10.1161/01.RES.0000128404.65887.08
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000221677000014
URI http://repositorio.unifesp.br/handle/11600/27763

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