NATALIA GOMES GONCALVES
Projetos de Pesquisa
Unidades Organizacionais
LIM/22 - Laboratório de Patolologia Cardiovascular, Hospital das Clínicas, Faculdade de Medicina
4 resultados
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conferenceObject Metalloproteases gene expression and remodeling of lung parenchyma fibers during the progression of elastase induced emphysema(2014) ROBERTONI, Fabiola Santos Zambon; OLIVO, Clarice Rosa; LOURENCO, Juliana Dias; GONCALVES, Natalia Comes; VELOSA, Ana Paula Pereira; TEODORO, Walcy Rosolia; LIN, Chin Jia; MARTINS, Milton De Arruda; LOPES, Fernanda D. T. Q. dos Santos- Collagenase mRNA Overexpression and Decreased Extracellular Matrix Components Are Early Events in the Pathogenesis of Emphysema(2015) ROBERTONI, Fabola S. Z.; OLIVO, Clarice R.; LOURENCO, Juliana D.; GONCALVES, Natalia G.; VELOSA, Ana Paula P.; LIN, Chin J.; FLO, Claudia M.; SARAIVA-ROMANHOLO, Beatriz M.; SASAKI, Sergio D.; MARTINS, Milton A.; TEODORO, Walcy R.; LOPES, Fernanda Degobbi T. Q. S.To describe the progression of parenchymal remodeling and metalloproteinases gene expression in earlier stages of emphysema, mice received porcine pancreatic elastase (PPE) instillation and Control groups received saline solution. After PPE instillation (1, 3, 6 hours, 3 and 21 days) we measured the mean linear intercept, the volume proportion of types I and III collagen, elastin, fibrillin and the MMP-1, -8, -12 and -13 gene expression. We observed an initial decrease in type I (at the 3rd day) and type III collagen (from the 6th hour until the 3rd day), in posterior time points in which we detected increased gene expression for MMP-8 and -13 in PPE groups. After 21 days, the type III collagen fibers increased and the type I collagen values returned to similar values compared to control groups. The MMP-12 gene expression was increased in earlier times (3 and 6 hours) to which we detected a reduced proportion of elastin (3 days) in PPE groups, reinforcing the already established importance of MMP-12 in the breakdown of ECM. Such findings will be useful to better elucidate the alterations in ECM components and the importance of not only metalloelastase but also collagenases in earlier emphysema stages, providing new clues to novel therapeutic targets.
conferenceObject Temporal profile of metaloproteases gene expression in elastase-induced emphysema(2013) ROBERTONI, Fabiola Santos Zambon; OLIVO, Clarice Rosa; LOURENCO, Juliana Dias; GANCALVES, Natalia Gomes; VELOSA, Ana Paula Pereira; TEODORO, Walcy Rosolia; LIN, Chin Jia; MARTINS, Milton de Arruda; LOPES, Fernanda Degobbi Tenorio Q. S.- Th17/Treg imbalance in COPD progression: A temporal analysis using a CS-induced model(2019) ITO, Juliana Tiyaki; CERVILHA, Daniela Aparecida de Brito; LOURENCO, Juliana Dias; GONCALVES, Natalia Gomes; VOLPINI, Rildo Aparecido; CALDINI, Elia Garcia; LANDMAN, Gilles; LIN, Chin Jia; VELOSA, Ana Paula Pereira; TEODORO, Walcy Paganelli Rosolia; TIBERIO, Iolanda de Fatima Lopes Calvo; MAUAD, Thais; MARTINS, Milton de Arruda; MACCHIONE, Mariangela; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosBackground The imbalance between pro- and anti-inflammatory immune responses plays a pivotal role in chronic obstructive pulmonary disease (COPD) development and progression. To clarify the pathophysiological mechanisms of this disease, we performed a temporal analysis of immune response-mediated inflammatory progression in a cigarette smoke (CS)-induced mouse model with a focus on the balance between Th17 and Treg responses. Methods C57BL/6 mice were exposed to CS for 1, 3 or 6 months to induce COPD, and the control groups were maintained under filtered air conditions for the same time intervals. We then performed functional (respiratory mechanics) and structural (alveolar enlargement) analyses. We also quantified the NF-kappa B, TNF-alpha, CD4, CD8, CD20, IL-17, IL-6, FOXP3, IL-10, or TGF-beta positive cells in peribronchovascular areas and assessed FOXP3 and IL-10 expression through double-label immunofluorescence. Additionally, we evaluated the gene expression of NF-kappa B and TNF in bronchiolar epithelial cells. Results Our CS-induced COPD model exhibited an increased proinflammatory immune response (increased expression of the NF-kappa B, TNF-alpha, CD4, CD8, CD20, IL-17, and IL-6 markers) with a concomitantly decreased anti-inflammatory immune response (FOXP3, IL-10, and TGF-beta markers) compared with the control mice. These changes in the immune responses were associated with increased alveolar enlargement and impaired lung function starting on the first month and third month of CS exposure, respectively, compared with the control mice. Conclusion Our results showed that the microenvironmental stimuli produced by the release of cyto-kines during COPD progression lead to a Th17/Treg imbalance.