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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.)

Connexin32 deficiency exacerbates carbon tetrachloride-induced hepatocellular injury and liver fibrosis in mice

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Cogliati, Bruno ; Yanguas, Sara Crespo ; Da Silva, Tereza Cristina ; Arrais Aloia, Thiago Pinheiro ; Nogueira, Marina Sayuri ; Real-Lima, Mirela Aline ; Chaible, Lucas Martins ; Sanches, Daniel Soares ; Willebrords, Joost ; Maes, Michael ; Alves Pereira, Isabel Veloso ; de Castro, Inar Alves ; Vinken, Mathieu ; Zaidan Dagli, Maria Lucia
Número total de Autores: 14
Tipo de documento: Artigo Científico
Fonte: TOXICOLOGY MECHANISMS AND METHODS; v. 26, n. 5, p. 362-370, JUN 2016.
Citações Web of Science: 4
Resumo

Objective: Liver fibrosis results from the perpetuation of the normal wound healing response to several types of injury. Despite the wealth of knowledge regarding the involvement of intracellular and extracellular signaling pathways in liver fibrogenesis, information about the role of intercellular communication mediated by gap junctions is scarce.Methods: In this study, liver fibrosis was chemically induced by carbon tetrachloride in mice lacking connexin32, the major liver gap junction constituent. The manifestation of liver fibrosis was evaluated based on a series of read-outs, including collagen morphometric and mRNA analysis, oxidative stress, apoptotic, proliferative and inflammatory markers.Results: More pronounced liver damage and enhanced collagen deposition were observed in connexin32 knockout mice compared to wild-type animals in experimentally triggered induced liver fibrosis. No differences between both groups were noticed in apoptotic signaling nor in inflammation markers. However, connexin32 deficient mice displayed decreased catalase activity and increased malondialdehyde levels.Conclusion: These findings could suggest that connexin32-based signaling mediates tissue resistance against liver damage by the modulation of the antioxidant capacity. In turn, this could point to a role for connexin32 signaling as a therapeutic target in the treatment of liver fibrosis. (AU)

Processo FAPESP: 05/59583-9 - Participação das conexinas 43 e 32 no desenvolvimento da fibrose hepática: estudo em camundongos geneticamente modificados
Beneficiário:Bruno Cogliati
Linha de fomento: Bolsas no Brasil - Doutorado Direto
Processo FAPESP: 06/56138-7 - Avaliação da importância das conexinas 32 e 43 na cirrose hepática induzida pela tioacetamida em camundongos
Beneficiário:Maria Lucia Zaidan Dagli
Linha de fomento: Auxílio à Pesquisa - Regular
Processo FAPESP: 13/50420-6 - Canais de conexina e panexina como alvos terapêuticos e biomarcadores nas doenças hepáticas aguda e crônica
Beneficiário:Mathieu Frederick Alexander Vinken
Linha de fomento: Auxílio à Pesquisa - Programa SPEC