MARIANGELA MACCHIONE
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
49 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 49
- Expression patterns of peroxiredoxin genes in bronchial epithelial cells exposed to diesel exhaust particles(2021) SERIANI, Robson; PAULA, Carla Peres de; CUNHA, Anderson Ferreira da; OLIVEIRA, Marcos Antonio de; KREMPEL, Paloma Gava; FRIAS, Daniela Perroni; NEGRI, Elnara Marcia; MAUAD, Thais; MACCHIONE, MariangelaSeveral mechanisms have been suggested to explain the adverse effects of air pollutants on airway cells. One such explanation is the presence of high concentrations of oxidants and pro-oxidants in environmental pollutants. All animal and plant cells have developed several mechanisms to prevent damage by oxidative molecules. Among these, the peroxiredoxins (PRDXs) are of interest due to a high reactivity with reactive oxygen species (ROS) through the functioning of the thioredoxin/thioredoxin reductase system. This study aimed to verify the gene expression patterns of the PRDX family in bronchial epithelial airway cells (BEAS-2B) cells exposed to diesel exhaust particles (DEPs) at a concentration of 15 mu g/mL for 1 or 2 h because this it is a major component of particulate matter in the atmosphere. There was a significant decrease in mRNA fold changes of PRDX2 (0.43 +/- 0.34; *p = 0.0220), PRDX5 (0.43 +/- 0.34; *p = 0.0220), and PRDX6 (0.33 +/- 0.25; *p = 0.0069) after 1 h of exposure to DEPs. The reduction in mRNA levels may consequently lead to a decrease in the levels of PRDX proteins, increasing oxidative stress in bronchial epithelial cells BEAS-2B and thus, negatively affecting cellular functions.
- Influence of particles from atmospheric pollution in female hormonal receptors in bronchi cells.>(2020) SMELAN, Juliana; ALMEIDA, Juliane; FRIAS, Daniela; BRENTANI, Mitzi; MACCHIONE, Mariangela
- Smoking load reduction is insufficient to downregulate miR-301b, a lung cancer promoter(2020) ARCAS, Camila dos Santos; LIN-WANG, Hui Tzu; UMEDA, Iracema Ioco Kikuchi; SOUSA, Marcio Goncalves de; UTIYAMA, Daniela Mitiyo Odagiri; MANSUR, Antonio de Padua; MACCHIONE, Mariangela; HIRATA, Mario Hiroyuki; NAKAGAWA, Naomi KondoSeveral circulating miRNAs identified in the plasma of smokers have been implicated as promoters of nasopharyngeal and lung carcinoma. To investigate the plasma profile of miRNAs in subjects who reduces the number of smoked cigarettes and who quit after six months. We accompanied 28 individuals enrolled in a Smoking Cessation Program over 6 months. At Baseline, clinical characteristics, co-morbidities, and smoking history were similar among subjects. After 6 months, two groups were defined: who successfully quitted smoking (named ""quitters"", n=18, mean age 57 years, 11 male) and who reduced the number of cigarettes smoked (20-90%) but failed to quit smoking (named ""smokers"", n=10, mean age 52 years, 3 male). No significant clinical changes were observed between groups at baseline and after a 6-month period, however, quitters showed significant downregulations in seven miRNAs at baseline: miR-17 (-2.90 -fold, p=0.029), miR-20a (-3.80-fold, p=0.021); miR-20b (-4.71-fold, p=0.027); miR-30a (-3.95-fold, p=0.024); miR-93 (-3.63-fold, p=0.022); miR-125a(-1.70 -fold, p= 0.038); and miR-195 (-5.37-fold, p=0.002), and after a 6-month period in 6 miRNAs: miR-17 (-5.30-fold, p=0.012), miR-20a (-2.04-fold, p=0.017), miR-20b (-5.44-fold, p=0.017), miR-93 (-4.00-fold, p=0.041), miR-101 (-4.82-fold, p=0.047) and miR-125b (-3.65-fold, p=0.025). Using time comparisons, only quitters had significant downregulation in miR-301b (-2.29-fold, p=0.038) after 6-month. Reductions in the number of smoked cigarettes was insufficient to change the plasma profile of miRNA after 6 months. Only quitting smoking (100% reduction) significantly downregulated miR-301b related to hypoxic conditions, promotion of cell proliferation, decreases in apoptosis, cancer development, and progression as increases in radiotherapy and chemotherapy resistance.
- Physicochemical properties and toxicological assessment of modified CdS nanoparticles(2014) SILVA, Andrea R. da; AUCELIO, Ricardo Q.; RODRIGUEZ-COTTO, Rosa I.; ORTIZ-MARTINEZ, Mario G.; RIVERA-RAMIREZ, Evasomary; FRIAS, Daniela Perroni; MACCHIONE, Mariangela; JIMENEZ-VELEZ, Braulio; GIODA, AdrianaCadmium sulfite (CdS) nanoparticles (NPs) modified with different stabilizing agents (2-mercaptopropionic acid or 2MPA, 3-mercaptopropionic acid or 3MPA, and L-cysteine or cys) were designed to be used as luminescent probes. The toxicity and inflammatory response of luminescent CdS NPs (average diameter between 2 and 3 nm) was evaluated ""in vitro"" using human lung epithelial cells (BEAS-2B). Also, mucociliary function changes or injuries were assessed by mucociliary transport (MCT) and ciliary beat frequency (CBF) measurements using frog palates. Toxicity assays showed that Cd concentrations above 1.0 mg L-1 were toxic to BEAS-2B, while Cd associated to NPs was not toxic at the concentrations tested (fivefolds that of Cd toxicity). Cadmium at toxic levels of 2.5 mg L-1 significantly induced the release of both cytokines, IL-6 and IL-8, conversely none toxic levels (2.5 mg L-1) of 2MPA-CdS nanoparticles showed similar effects. However, cys-CdS and 3MPA-CdS NPs did not induce the secretions of either IL-6 or IL-8 by lung epithelial cells at the same Cd concentration of 2.5 mg L-1. Conversely, significant reduction in the secretion of these two pro-inflammatory cytokines was observed. The MCT and CBF results revealed no impairment on mucociliary behavior except a very slight change in mucus viscosity by 3MPA-CdS NPs. These findings highlight the potential of 3MPA-CdS and cys-CdS NPs for future biomedical research, and encourage further histopathological and metabolic studies in order to strengthen that possibility.
- Human bronchial epithelial cells exposed in vitro to diesel exhaust particles exhibit alterations in cell rheology and cytotoxicity associated with decrease in antioxidant defenses and imbalance in pro- and anti-apoptotic gene expression(2016) SERIANI, Robson; SOUZA, Claudia Emanuele Carvalho de; KREMPEL, Paloma Gava; FRIAS, Daniela Perroni; MATSUDA, Monique; CORREIA, Aristides Tadeu; FERREIRA, Marcia Zotti Justo; ALENCAR, Adriano Mesquita; NEGRI, Elnara Marcia; SALDIVA, Paulo Hilario Nascimento; MAUAD, Thais; MACCHIONE, MariangelaDiesel exhaust particles (DEPs) from diesel engines produce adverse alterations in cells of the airways by activating intracellular signaling pathways and apoptotic gene overexpression, and also by influencing metabolism and cytoskeleton changes. This study used human bronchial epithelium cells (BEAS-2B) in culture and evaluates their exposure to DEPs (15ug/mL for 1 and 2 h) in order to determine changes to cell rheology (viscoelasticity) and gene expression of the enzymes involved in oxidative stress, apoptosis, and cytotoxicity. BEAS-2B cells exposed to DEPs were found to have a significant loss in stiffness, membrane stability, and mitochondrial activity. The genes involved in apoptosis [B cell lymphoma 2 (BCL-2 and caspase-3)] presented inversely proportional expressions (p=0.05, p=0.01, respectively), low expression of the genes involved in antioxidant responses [SOD1 (superoxide dismutase 1); SOD2 (superoxide dismutase 2), and GPx (glutathione peroxidase) (p=0.01)], along with an increase in cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) (p=0.01). These results suggest that alterations in cell rheology and cytotoxicity could be associated with oxidative stress and imbalance between pro-and antiapoptotic genes.
- Relationship between Nrf2-Keap1 system and cell death in BEAS-2B exposed to Diesel Exhaust Particles(2017) FRIAS, Daniela; NUNES, Raquel; MATSUDA, Monique; YOSHIZAKI, Kelly; CARVALHO-OLIVEIRA, Regiani; PEREIRA, Daniela; VASCONCELLOS, Perola; MAUAD, Thais; MACCHIONE, Mariangela
- Effects of Intrauterine Exposure to Concentrated Ambient Particles on Mice Offspring Sensitized with House Dust Mite(2017) BRITO, Jose; ARANTES-COSTA, Fernanda Magalhaes; GUIMARAES, Eliane Tigre; VIEIRA, Rodolfo de Paula; MACCHIONE, Mariangela; MAUAD, Thais
- Nasal Mucociliary Clearance in Subjects With COPD After Smoking Cessation(2015) ITO, Juliana T.; RAMOS, Dionei; LIMA, Fabiano F.; RODRIGUES, Fernanda M. M.; GOMES, Paulo R.; MOREIRA, Graciane L.; MACCHIONE, Mariangela; TOLEDO, Alessandra C.; RAMOS, Ercy M. C.BACKGROUND: Exposure to cigarette smoke causes significant impairment in mucociliary clearance (MCC), which predisposes patients to secretion retention and recurrent airway infections that play a role in exacerbations of COPD. To determine whether smoking cessation may influence MCC and frequency of exacerbations, the following groups were evaluated: ex-smokers with COPD, smokers with COPD, current smokers with normal lung function, and nonsmokers with normal lung function. METHODS: Ninety-three subjects were divided into 4 groups: ex-smokers with COPD (n = 23, 62.4 +/- 8.0 y, 13 males), smokers with COPD (n = 17, 58.2 +/- 8.0 y, 6 males), current smokers (n = 27, 61.5 +/- 6.4 y, 17 males), and nonsmokers (n = 26, 60.8 +/- 11.3 y, 7 males). MCC was evaluated using the saccharin transit time (STT) test, and the frequency of exacerbations in the last year was assessed by questionnaire. The Kruskal-Wallis test followed by Dunn's test were used to compare STT among groups, and the Goodman test was used to compare the frequency of exacerbations. RESULTS: STT of smokers with COPD (16.5 [11-28] min; median [interquartile range 25-75%]) and current smokers (15.9 110-271 min) was longer compared with ex-smokers with COPD (9.7 [6-12] min) and nonsmokers (8 [6-16] min) (P < .001). There was no difference in STT values between smokers with COPD and current smokers, and these values in ex-smokers with COPD were similar to the control group (P > .05). The frequency of exacerbations was lower in ex-smokers with COPD compared with smokers with COPD. CONCLUSIONS: One year after smoking cessation, subjects with COPD had improved mucociliary clearance.
- Effects of air pollution on inflammation of respiratory system: Differences between male and female(2015) YOSHIZAKI, Kelly; LINO-DOS-SANTOS-FRANCO, Adriana; BRITO, Jose Mara; SANTOS, Thais Moraes Nascimento; VASCONCELOS, Perola; MAUAD, Thais; SALDIVA, Paulo Hilario Nascimento; MACCHIONE, Mariangela
- Low-dose chlorine exposure impairs lung function, inflammation and oxidative stress in mice(2021) GENARO, Isabella Santos de; ALMEIDA, Francine Maria de; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; KUNZLER, Deborah De Camargo Hizume; TRIPODE, Bruna Gabryela Busoletto; KURDEJAK, Adriana; CORDEIRO, Bruna Nakamura; PANDOLPHO, Renata; MACCHIONE, Mariangela; BRUGGEMANN, Thayse Regina; VIEIRA, Rodolfo Paula; MARTINS, Milton Arruda; TIBERIO, Iolanda de Fatima Lopes Calvo; SARAIVA-ROMANHOLO, Beatriz MangueiraAim: To explore the different consequences of acute and chronic exposure to chlorine gas (Cl-2) on the functional and histological parameters of health mice. Main methods: Firstly, male BALB/c mice were acute exposed to 3.3 or 33.3 or 70.5 mg/m(3) Cl-2. We analyzed the lung function, the inflammatory cells in the bronchoalveolar lavage, cell influx in the peribrochoalveolar space and mucus production. In a second phase, mice were chronic exposed to 70.5 mg/m(3) Cl-2. Besides the first phase analyses, we also evaluated the epithelial cells thickness, collagen deposition in the airways, immunohisto-chemistry stain for IL-1 beta, iNOS, IL-17 and ROCK-2 and the levels of IL-5, IL-13, IL-17, IL-1 beta and TNF-alpha in lung homogenate. Key findings: Acute exposure to chlorine impaired the lung function, increased the number of inflammatory cells in the BALF and in the airways, also increased the mucus production. Furthermore, when chlorine was exposed chronically, increased the airway remodeling with collagen deposition and epithelial cells thickness, positive cells for IL-1 beta, iNOS, IL-17 in the airways and in the alveolar walls and ROCK-2 in the alveolar walls, lung inflammation with increased levels of IL-5, IL-13, IL-1 beta and TNF-alpha in the lung homogenate, and also, induced the acid mucus production by the nasal epithelium. Significance: Acute and chronic exposure to low dose of chlorine gas worsens lung function, induces oxidative stress activation and mucus production and contributes to augmenting inflammation in health mice.