Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/37806
Title: Balance between the two kinin receptors in the progression of experimental focal and segmental glomerulosclerosis in mice
Authors: Pereira, Rafael Luiz [UNIFESP]
Felizardo, Raphael Jose Ferreira [UNIFESP]
Cenedeze, Marcos Antonio [UNIFESP]
Hiyane, Meire Ioshie [UNIFESP]
Bassi, Enio Jose [UNIFESP]
Amano, Mariane Tami [UNIFESP]
Origassa, Clarice Sylvia Taemi [UNIFESP]
Silva, Reinaldo Correia [UNIFESP]
Aguiar, Cristhiane Favero
Carneiro, Sylvia Mendes
Pesquero, João Bosco [UNIFESP]
Araujo, Ronaldo Carvalho [UNIFESP]
Keller, Alexandre de Castro [UNIFESP]
Monteiro, Renato C.
Moura, Ivan Cruz
Pacheco-Silva, Alvaro [UNIFESP]
Camara, Niels Olsen Saraiva [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Inst Butantan
INSERM
Albert Einstein Hosp
Keywords: Focal and segmental glomerulosclerosis
Bradykinin receptors
Inflammation
Podocyte
Fibrosis
Issue Date: 1-Jun-2014
Publisher: Company of Biologists Ltd
Citation: Disease Models & Mechanisms. Cambridge: Company of Biologists Ltd, v. 7, n. 6, p. 701-710, 2014.
Abstract: Focal and segmental glomerulosclerosis (FSGS) is one of the most important renal diseases related to end-stage renal failure. Bradykinin has been implicated in the pathogenesis of renal inflammation, whereas the role of its receptor 2 (B2RBK; also known as BDKRB2) in FSGS has not been studied. FSGS was induced in wild-type and B2RBK-knockout mice by a single intravenous injection of Adriamycin (ADM). in order to further modulate the kinin receptors, the animals were also treated with the B2RBK antagonist HOE-140 and the B1RBK antagonist DALBK. Here, we show that the blockage of B2RBK with HOE-140 protects mice from the development of FSGS, including podocyte foot process effacement and the re-establishment of slit-diaphragm-related proteins. However, B2RBK-knockout mice were not protected from FSGS. These opposite results were due to B1RBK expression. B1RBK was upregulated after the injection of ADM and this upregulation was exacerbated in B2RBK-knockout animals. Furthermore, treatment with HOE-140 downregulated the B1RBK receptor. the blockage of B1RBK in B2RBK-knockout animals promoted FSGS regression, with a less-inflammatory phenotype. These results indicate a deleterious role of both kinin receptors in an FSGS model and suggest a possible cross-talk between them in the progression of disease.
URI: http://repositorio.unifesp.br/handle/11600/37806
ISSN: 1754-8403
Other Identifiers: http://dx.doi.org/10.1242/dmm.014548
Appears in Collections:Artigo
Artigo

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