CHIN JIA LIN
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/22 - Laboratório de Patolologia Cardiovascular, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/22 - Laboratório de Patolologia Cardiovascular, Hospital das Clínicas, Faculdade de Medicina - Líder
8 resultados
Resultados de Busca
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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.conferenceObject Time course effects of exercise training on pulmonary injury induced by exposure to cigarette smoke in mice(2013) TOLEDO-ARRUDA, Alessandra C.; GUARNIER, Flavia; SUEHIRO, Camila L.; ALMEIDA, Francine; OLIVO, Clarice; LOPES, Fernanda; VIEIRA, Rodolfo; CAMARGO-FILHO, Jose Carlos Silva; CECCHINI, Rubens; LIN, Chin; MARTINS, Milton A.conferenceObject Aerobic Exercise Attenuates Skeletal Muscle Injury Induced By Cigarette Smoke Exposure In Mice(2014) TOLEDO-ARRUDA, A. C.; SUEHIRO, C. L.; GUARNIER, F. A.; VIEIRA, R. D. P.; ALMEIDA, F. M.; LOPES, F. D.; ARANTES, P. D. M. M.; CECCHINI, R.; LIN, C. J.; MARTINS, M. D. A.conferenceObject Time-Course Effects Of Aerobic Exercise On Lung Mechanics And Inflammation In Mice Exposed To Cigarette Smoke(2013) TOLEDO, A. C.; SUEHIRO, C.; ALMEIDA, F. M.; OLIVO, C.; LOPES, F. D.; VIEIRA, R. P.; LIN, C. J.; MARTINS, M. A.- Time-course effects of aerobic physical training in the prevention of cigarette smoke-induced COPD(2017) TOLEDO-ARRUDA, Alessandra C.; VIEIRA, Rodolfo P.; GUARNIER, Flavia A.; SUEHIRO, Camila L.; CALEMAN-NETO, Agostinho; OLIVO, Clarice R.; ARANTES, Petra M. M.; ALMEIDA, Francine M.; LOPES, Fernanda D. T. Q. S.; RAMOS, Ercy M. C.; CECCHINI, Rubens; LIN, Chin Jia; MARTINS, Milton ArrudaA previous study by our group showed that regular exercise training (ET) attenuated pulmonary injury in an experimental model of chronic exposure to cigarette smoke (CS) in mice, but the time-course effects of the mechanisms involved in this protection remain poorly understood. We evaluated the temporal effects of regular ET in an experimental model of chronic CS exposure. Male C57BL/6 mice were divided into four groups: Control (sedentary + air), Exercise (aerobic training + air), Smoke (sedentary + smoke), and Smoke + Exercise (aerobic training + smoke). Mice were exposed to CS and ET for 4, 8, or 12 wk. Exercise protected mice exposed to CS from emphysema and reductions in tissue damping and tissue elastance after 12 wk (P < 0.01). The total number of inflammatory cells in the bronchoalveolar lavage increased in the Smoke group, mainly due to the recruitment of macrophages after 4 wk, neutrophils and lymphocytes after 8 wk, and lymphocytes and macrophages after 12 wk (P < 0.01). Exercise attenuated this increase in mice exposed to CS. The protection conferred by exercise was mainly observed after exercise adaptation. Exercise increased IL-6 and IL-10 in the quadriceps and lungs (P < 0.05) after 12 wk. Total antioxidant capacity and SOD was increased and TNF-alpha and oxidants decreased in lungs of mice exposed to CS after 12 wk (P < 0.05). The protective effects of exercise against lung injury induced by cigarette smoke exposure suggests that anti-inflammatory mediators and antioxidant enzymes play important roles in chronic obstructive pulmonary disease development mainly after the exercise adaptation. NEW & NOTEWORTHY These experiments investigated for the first time the temporal effects of regular moderate exercise training in cigarette smoke-induced chronic obstructive pulmonary disease. We demonstrate that aerobic conditioning had a protective effect in emphysema development induced by cigarette smoke exposure. This effect was most likely secondary to an effect of exercise on oxidant-antioxidant balance and anti-inflammatory mediators.
- 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.