Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/20636
Title: Galectin-3 Knockdown Impairs Survival, Migration, and Immunomodulatory Actions of Mesenchymal Stromal Cells in a Mouse Model of Chagas Disease Cardiomyopathy
Authors: Souza, Bruno Solano de Freitas
Silva, Kátia Nunes da
Silva, Daniela Nascimento
Rocha, Vinícius Pinto Costa
Paredes, Bruno Diaz
Azevedo, Carine Machado
Nonaka, Carolina Kymie
Carvalho, Gisele Batista
Vasconcelos, Juliana Fraga
Santos, Ricardo Ribeiro dos
Soares, Milena Botelho Pereira
Affilliation: Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil
São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / São Rafael Hospital. Center for Biotechnology and Cell Therapy. Salvador, BA, Brazil
Abstract: Therapies based on transplantation of mesenchymal stromal cells (MSC) hold promise for the management of inflammatory disorders. In chronic Chagas disease cardiomyopathy (CCC), caused by chronic infection with Trypanosoma cruzi, the exacerbated immune response plays a critical pathophysiological role and can be modulated by MSC. Here, we investigated the role of galectin-3 (Gal-3), a beta-galactoside-binding lectin with several actions on immune responses and repair process, on the immunomodulatory potential of MSC. Gal-3 knockdown in MSC did not affect the immunophenotype or differentiation potential. However, Gal-3 knockdown MSC showed decreased proliferation, survival, and migration. Additionally, when injected intraperitoneally into mice with CCC, Gal-3 knockdown MSC showed impaired migration in vivo. Transplantation of control MSC into mice with CCC caused a suppression of cardiac inflammation and fibrosis, reducing expression levels of CD45, TNFα, IL-1β, IL-6, IFNγ, and type I collagen. In contrast, Gal-3 knockdown MSC were unable to suppress the immune response or collagen synthesis in the hearts of mice with CCC. Finally, infection with T. cruzi demonstrated parasite survival in wild-type but not in Gal-3 knockdown MSC. These findings demonstrate that Gal-3 plays a critical role in MSC survival, proliferation, migration, and therapeutic potential in CCC.
Keywords: Chagas disease
Chagasic cardiomyopathy
Cells Transplantation
Trypanosoma cruzi
Animals
Mice
keywords: Doença de Chagas
Cardiomiopatia chagasica
Transplante de celulas
Trypanosoma cruzi
Animais
Ratos
Issue Date: 2017
Publisher: Hindawi Publishing Corporation
Citation: SOUZA, B. S. F. et al. Galectin-3 Knockdown Impairs Survival, Migration, and Immunomodulatory Actions of Mesenchymal Stromal Cells in a Mouse Model of Chagas Disease Cardiomyopathy. Stem Cells International, 3282656, 2017.
DOI: 10.1155/2017/3282656
ISSN: 1687-966X
Copyright: open access
Appears in Collections:BA - IGM - Artigos de Periódicos

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