JULIANA DIAS LOURENCO
Projetos de Pesquisa
Unidades Organizacionais
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina
7 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 SantosconferenceObject 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.- The deleterious effects of smoking in bone mineralization and fibrillar matrix composition(2020) BARBOSA, Alexandre Povoa; LOURENCO, Juliana Dias; JUNQUEIRA, Jader Joel Machado; FRANCA, Silva Larissa Emidio de; MARTINS, Janaina S.; OLIVEIRA JUNIOR, Manoel Carneiro; BEGALLI, Isadora; VELOSA, Ana Paula Pereira; OLIVO, Clarice Rosa; BASTOS, Thiago Bernardes; JORGETTI, Vanda; PAULA, Vieira Rodolfo de; TEODORO, Walcy Rosolia; LOPES, Fernanda D. T. Q. S.Introduction: This study aimed to verify the effects of cigarette smoke exposure in bone mineralization and fibrillar matrix composition as well as in bone healing after tibial fracture induction. Methods: C57Bl/6 Mice were assigned according to exposure and surgery: C room air; F room air and tibia open osteotomy; CS cigarette smoke; FCS cigarette smoke and tibia open osteotomy. In order to study fracture healing we performed, under anesthesia, a bone injury through a tibial shaft osteotomy. Bone samples were obtained to evaluate bone histomorphometry, trabecular morphology and volume, trabecular collagen types composition and presence of inflammatory cytokines and growth factors. Results: CS exposure significantly reduced the thickness of bone trabeculae associated with decrease in mineralizing surface and mineral deposition rate, leading a lower bone formation rate and longer mineralization time. Resorption surface and osteoclastic surface were greater in the CS group, attesting increased resorptive action. There was a decrease in type I collagen deposition and genes expression in the CS and FCS groups compared to C group and in contrast there was an increase in type V collagen deposition and genes expression in the CS, FC and FSC groups compared to C group. Also, CS exposure induced a decrease in bone forming cytokines and an increase in inflammatory associated cytokines, and these changes were intensified under fracture conditions. Conclusion: Cigarette smoke exposure alters bone matrix composition and worsens bone mineralization, leading to bone fragility by increasing collagen V synthesis and deposition and impairing collagen I fibril forming and assembling. And these deleterious effects contributed to the worsening in fracture healing after tibia osteotomy.
conferenceObject A protease inhibitor from the tick rhipicephalus boophilus microplus attenuated parenchymal destruction in elastase-induced emphysema(2013) OLIVO, Clarice Rosa; LOURENCO, Juliana Dias; ALMEIDA, Francine M.; NEVES, Luana Paiva; ARANTES, Petra Mello; PRADO, Carla Maximo; TIBERIO, Iolanda; TANAKA, Aparecida S.; SASAKI, Sergio D.; MARTINS, Milton Arruda; LOPES, Fernanda D. T. Q. S.- A murine model of elastase and cigarette smoke induced emphysema(2017) RODRIGUES, Rubia; OLIVO, Clarice Rosa; LOURENCO, Juliana Dias; RIANE, Alyne; CERVILHA, Daniela Aparecida de Brito; LOPES, Fernanda Degobbi Tenrio Quirino dos SantosObjective: To describe a murine model of emphysema induced by a combination of exposure to cigarette smoke (CS) and instillation of porcine pancreatic elastase (PPE). Methods: A total of 38 C57BL/6 mice were randomly divided into four groups: control (one intranasal instillation of 0.9% saline solution); PPE (two intranasal instillations of PPE); CS (CS exposure for 60 days); and CS + PPE (two intranasal instillations of PPE + CS exposure for 60 days). At the end of the experimental protocol, all animals were anesthetized and tracheostomized for calculation of respiratory mechanics parameters. Subsequently, all animals were euthanized and their lungs were removed for measurement of the mean linear intercept (Lm) and determination of the numbers of cells that were immunoreactive to macrophage (MAC)-2 antigen, matrix metalloproteinase (MMP)-12, and glycosylated 91-kDa glycoprotein (gp91phox) in the distal lung parenchyma and peribronchial region. Results: Although there were no differences among the four groups regarding the respiratory mechanics parameters assessed, there was an increase in the Lm in the CS + PPE group. The numbers of MAC-2-positive cells in the peribronchial region and distal lung parenchyma were higher in the CS + PPE group than in the other groups, as were the numbers of cells that were positive for MMP-12 and gp91phox, although only in the distal lung parenchyma. Conclusions: Our model of emphysema induced by a combination of PPE instillation and CS exposure results in a significant degree of parenchymal destruction in a shorter time frame than that employed in other models of CS-induced emphysema, reinforcing the importance of protease-antiprotease imbalance and oxidant-antioxidant imbalance in the pathogenesis of emphysema.
- Chronic exposure to diesel particles worsened emphysema and increased M2-like phenotype macrophages in a PPE-induced model(2020) MOREIRA, Alyne Riani; CASTRO, Thamyres Barros Pereira de; KOHLER, Julia Benini; ITO, Juliana Tiyaki; SILVA, Larissa Emidio de Franca; LOURENCO, Juliana Dias; ALMEIDA, Rafael Ribeiro; SANTANA, Fernanda Roncon; BRITO, Jose Mara; RIVERO, Dolores Helena Rodriguez Ferreira; VALE, Maria Isabel Cardoso Alonso; PRADO, Carla Maximo; CAMARA, Niels Olsen Saraiva; SALDIVA, Paulo Hilario Nascimento; OLIVO, Clarice Rosa; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosChronic exposure to ambient levels of air pollution induces respiratory illness exacerbation by increasing inflammatory responses and apoptotic cells in pulmonary tissues. The ineffective phagocytosis of these apoptotic cells (efferocytosis) by macrophages has been considered an important factor in these pathological mechanisms. Depending on microenvironmental stimuli, macrophages can assume different phenotypes with different functional actions. M1 macrophages are recognized by their proinflammatory activity, whereas M2 macrophages play pivotal roles in responding to microorganisms and in efferocytosis to avoid the progression of inflammatory conditions. To verify how exposure to air pollutants interferes with macrophage polarization in emphysema development, we evaluated the different macrophage phenotypes in a PPE-induced model with the exposure to diesel exhaust particles. C57BL/6 mice received intranasal instillation of porcine pancreatic elastase (PPE) to induce emphysema, and the control groups received saline. Both groups were exposed to diesel exhaust particles or filtered air for 60 days according to the groups. We observed that both the diesel and PPE groups had an increase in alveolar enlargement, collagen and elastic fibers in the parenchyma and the number of macrophages, lymphocytes and epithelial cells in BAL, and these responses were exacerbated in animals that received PPE instillation prior to exposure to diesel exhaust particles. The same response pattern was found inCaspase-3 positive cell analysis, attesting to an increase in cell apoptosis, which is in agreement with the increase in M2 phenotype markers, measured by RT-PCR and flow cytometry analysis. We did not verify differences among the groups for the M1 phenotype. In conclusion, our results showed that both chronic exposure to diesel exhaust particles and PPE instillation induced inflammatory conditions, cell apoptosis and emphysema development, as well as an increase in M2 phenotype macrophages, and the combination of these two factors exacerbated these responses. The predominance of the M2-like phenotype likely occurred due to the increased demand for efferocytosis. However, M2 macrophage activity was ineffective, resulting in emphysema development and worsening of symptoms.
conferenceObject Effects of moderate aerobic exercise trainning in acute and late phase of lung infection induced by streptococcus pneumoniae(2013) OLIVO, Clarice Rosa; MIYAJI, Eliane; OLIVEIRA, Maria Leonor; LOURENCO, Juliana Dias; ALMEIDA, Francine Maria; ARANTES, Petra M.; LOPES, Fernanda D. T. Q. S.; MARTINS, Milton A.