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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Balance between the two kinin receptors in the progression of experimental focal and segmental glomerulosclerosis in mice

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Pereira, Rafael Luiz [1, 2] ; Ferreira Felizardo, Raphael Jose [1] ; Cenedeze, Marcos Antoino [1] ; Hiyane, Meire Ioshie [2] ; Bassi, Enio Jose [1] ; Amano, Mariane Tami [1] ; Taemi Origassa, Clarice Sylvia [1] ; Silva, Reinaldo Correia [3] ; Aguiar, Cristhiane Favero [2] ; Carneiro, Sylvia Mendes [4] ; Pesquero, Joao Bosco [5] ; Araujo, Ronaldo Carvalho [5] ; Keller, Alexandre de Castro [6] ; Monteiro, Renato C. [7] ; Moura, Ivan Cruz [7] ; Pacheco-Silva, Alvaro [1, 8] ; Saraiva Camara, Niels Olsen [1, 2]
Total Authors: 17
Affiliation:
[1] Univ Fed Sao Paulo, Clin & Expt Immunol Lab, Div Nephrol, BR-04023900 Sao Paulo - Brazil
[2] Univ Sao Paulo, Inst Biomed Sci 4, Dept Immunol, Lab Transplantat Immunobiol, BR-05508000 Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Translat Med Div, Clin & Expt Immunol Lab, BR-04039002 Sao Paulo - Brazil
[4] Inst Butantan, Lab Cellular Biol, BR-05503900 Sao Paulo - Brazil
[5] Fed Univ Sao Paulo UNIFESP, Dept Biophys, BR-04023062 Sao Paulo - Brazil
[6] Fed Univ Sao Paulo UNIFESP, Dept Microbiol Immunol & Parasitol, BR-04023062 Sao Paulo - Brazil
[7] INSERM, Unite Mixte Rech 699, F-75870 Paris - France
[8] Albert Einstein Hosp, Inst Israelita Ensino & Pesquisa Albert Einst, Renal Transplantat Unit, BR-05521000 Sao Paulo - Brazil
Total Affiliations: 8
Document type: Journal article
Source: Disease Models & Mechanisms; v. 7, n. 6, p. 701-710, JUN 2014.
Web of Science Citations: 6
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. (AU)

FAPESP's process: 12/05605-5 - Modulation of mTOR signaling pathway in macrophages in the progression of focal and segmental glomerulosclerosis
Grantee:Rafael Luiz Pereira
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 07/07139-3 - The role of heme oxygenase 1 in different renal inflammatory process in experimental animal models
Grantee:Niels Olsen Saraiva Câmara
Support type: Research Projects - Thematic Grants
FAPESP's process: 12/02270-2 - New cellular, molecular and immunological mechanisms involved in acute and chronic renal injury: the search for new therapeutical approaches
Grantee:Niels Olsen Saraiva Câmara
Support type: Research Projects - Thematic Grants