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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney Injury

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Autor(es):
Correa-Costa, Matheus [1] ; Braga, Tarcio Teodoro [1] ; Felizardo, Raphael Jose Ferreira [2] ; Andrade-Oliveira, Vinicius [1] ; Regina Perez, Katia [3] ; Midea Cuccovia, Iolanda [4] ; Ioshie Hiyane, Meire [1] ; Santana da Silva, Joao [5] ; Saraiva Camara, Niels Olsen [1, 2]
Número total de Autores: 9
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, Lab Transplantat Immunobiol, BR-05508900 Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Div Nephrol, Lab Clin & Expt Immunol, BR-04023900 Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Biophys, BR-04023062 Sao Paulo - Brazil
[4] Univ Sao Paulo, Inst Chem, Dept Biochem, BR-05508000 Sao Paulo - Brazil
[5] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Biochem & Immunol, BR-14049900 Ribeirao Preto, SP - Brazil
Número total de Afiliações: 5
Tipo de documento: Artigo Científico
Fonte: Mediators of Inflammation; 2014.
Citações Web of Science: 14
Resumo

Macrophages play a special role in the onset of several diseases, including acute and chronic kidney injuries. In this sense, tubule interstitial nephritis (TIN) represents an underestimated insult, which can be triggered by different stimuli and, in the absence of a proper regulation, can lead to fibrosis deposition. Based on this perception, we evaluated the participation of macrophage recruitment in the development of TIN. Initially, we provided adenine-enriched food to WT and searched for macrophage presence and action in the kidney. Also, a group of animals were depleted of macrophages with the clodronate liposome while receiving adenine-enriched diet. We collected blood and renal tissue from these animals and renal function, inflammation, and fibrosis were evaluated. We observed higher expression of chemokines in the kidneys of adenine-fed mice and a substantial protection when macrophages were depleted. Then, we specifically investigated the role of some key chemokines, CCR5 and CCL3, in this TIN experimental model. Interestingly, CCR5 KO and CCL3 KO animals showed less renal dysfunction and a decreased proinflammatory profile. Furthermore, in those animals, there was less profibrotic signaling. In conclusion, we can suggest that macrophage infiltration is important for the onset of renal injury in the adenine-induced TIN. (AU)

Processo FAPESP: 09/54474-8 - Mecanismos celulares de resposta ao estresse em modelos experimentais de insultos renais
Beneficiário:Matheus Corrêa Costa
Linha de fomento: Bolsas no Brasil - Doutorado
Processo FAPESP: 12/02270-2 - Novos mecanismos celulares, moleculares e imunológicos das lesões renais agudas e crônicas: busca por novas estratégias terapêuticas
Beneficiário:Niels Olsen Saraiva Câmara
Linha de fomento: Auxílio à Pesquisa - Temático
Processo FAPESP: 13/25010-9 - Papel da heme oxigenase-1 na modulação da autofagia durante a lesão renal isquêmica
Beneficiário:Matheus Corrêa Costa
Linha de fomento: Bolsas no Brasil - Pós-Doutorado