MARIANA MATERA VERAS
Projetos de Pesquisa
Unidades Organizacionais
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina - Líder
9 resultados
Resultados de Busca
Agora exibindo 1 - 9 de 9
conferenceObject Influence of exposure to concentrated urban air particles on the respiratory system of (LDLr-/-) mice(2014) MAUAD, Thais; ALEMANY, Adair; VERAS, Mariana; JUNIOR, Gabriel Ribeiro; COSTA, Natalia; CATANOZI, Sergio; ABDALLA, Dulcineia; SALDIVA, PauloconferenceObject Particulate air pollution affects alveolization in a juvenile mice model of asthma(2014) VERAS, Mariana; TELES, Aila; COSTA, Natalia; RIBEIRO-JUNIOR, Gabriel; SALDIVA, Paulo; MAUAD, Thais- Stereological approach to the pathology of lung aging in humans(2020) SANTOS, Fabricio; FROIO, Francisca Lucas; RIBEIRO JUNIOR, Gabriel; VERAS, Mariana Matera; JUSTO, Lisie; SALDIVA, Paulo; COSTA, Natalia De Souza Xavier; MAUAD, Thais
conferenceObject SIRT1, SIRT2, SIRT6 and P21 gene expression in the lungs of mice chronically exposed to ambient particulate matter(2014) MAUAD, Thais; RIBEIRO, Gabriel; VERAS, Mariana; COSTA, Natalia; SHIMADA, Ana; ALEMANY, Adair; MENDES, Thais; SALDIVA, Paulo; FARSKY, SandraconferenceObject Differentially expressed genes in the lungs of fetuses mice exposed to ambient air pollution(2014) MENDES-LOPES, Thais; VERAS, Mariana; COSTA, Natalia; MAZZOTTI, Tatiane; BRITO, Glauber; CHAMMAS, Roger; SALDIVA, Paulo; MAUAD, Thais- Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice(2022) COSTA, Natalia de Souza Xavier; TELES, Aila Mirtes; BRITO, Jose Mara de; LOPES, Thais de Barros Mendes; ROSSI, Renata Calciolari; MAGALHAES, Fernanda; COSTA, Arantes; SARAIVA-ROMANHOLO, Beatriz Mangueira; PERINI, Adenir; FURUYA, Tatiane Katsue; CARRASCO, Alexis German Murillo; VERAS, Mariana Matera; SALDIVA, Paulo Hilaroi Nascimento; CHAMMAS, Roger; MAUAD, ThaisThe perinatal period and early infancy are considered critical periods for lung development. During this period, adversities such as environmental exposures, allergic sensitization, and asthma are believed to impact lung health in adulthood. Therefore, we hypothesized that concomitant exposure to allergic sensitization and urban -derived fine particulate matter (PM2.5) in the early postnatal period of mice would cause more profound alter-ations in lung alveolarization and growth and differently modulate lung inflammation and gene expression than either insult alone in adult life. BALB/c mice were sensitized with ovalbumin (OVA) and exposed to PM2.5 from the fifth day of life. Then, we assessed lung responsiveness, inflammation in BALF, lung tissue, and alveolari-zation by stereology. In addition, we performed a transcriptomic analysis of lung tissue on the 40th day of life. Our results showed that young adult mice submitted to allergic sensitization and exposure to ambient PM2.5 since early life presented decreased lung growth with impaired alveolarization, a mixed neutrophilic-eosinophilic pattern of lung inflammation, increased airway responsiveness, and increased expression of genes linked to neutrophil recruitment when compared to animals that were OVA-sensitized or PM(2.5 )exposed only. Both, early life allergic sensitization and PM2.5 exposure, induced inflammation and impaired lung growth, but concomitant exposure was associated with worsened inflammation parameters and caused alveolar enlargement. Our experimental data provide pathological support for the hypothesis that allergic or environmental insults in early life have permanent adverse consequences for lung growth. In addition, combined insults were associated with the development of a COPD-like phenotype in young adult mice. Together with our data, current evidence points to the urgent need for healthier environments with fewer childhood disadvantage factors during the critical windows of lung development and growth.
conferenceObject Effects of early life exposure to concentrated ambient particle on lung function of mice(2013) MENDES-LOPES, Thais; VERAS, Mariana; ALMEIDA, Francine; COSTA, Natalia; LOPES, Fernanda; SALDIVA, Paulo; MAUAD, Thais- Pre- and postnatal exposure of mice to concentrated urban PM2.5 decreases the number of alveoli and leads to altered lung function at an early stage of life(2018) LOPES, Thais de Barros Mendes; GROTH, Espen E.; VERAS, Mariana; FURUYA, Tatiane K.; COSTA, Natalia de Souza Xavier; RIBEIRO JUNIOR, Gabriel; LOPES, Fernanda Degobbi; ALMEIDA, Francine M. de; CARDOSO, Wellington V.; SALDIVA, Paulo Hilario Nascimento; CHAMMAS, Roger; MAUAD, ThaisGestational exposure to air pollution is associated with negative outcomes in newborns and children. In a previous study, we demonstrated a synergistic negative effect of pre- and postnatal exposure to PM2.5 on lung development in mice. However, the means by which air pollution affects development of the lung have not yet been identified. In this study, we exposed pregnant BALB/c mice and their offspring to concentrated urban PM2.5 (from Sao Paulo, Brazil; target dose 600 mu g/m(3) for 1 h daily). Exposure was started on embryonic day 5.5 (E5.5, time of placental implantation). Lung tissue of fetuses and offspring was submitted to stereological and transcriptomic analyses at E14.5 (pseudoglandular stage of lung development), E18.5 (saccular stage) and P40 (postnatal day 40, alveolarized lung). Additionally, lung function and cellularity of bronchoalveolar lavage (BAL) fluid were studied in offspring animals at P40. Compared to control animals that were exposed to filtered air throughout gestation and postnatal life, PM-exposed mice exhibited higher lung elastance and a lower alveolar number at P40 whilst the total lung volume and cellularity of BAL fluid were not affected. Glandular and saccular structures of fetal lungs were not altered upon gestational exposure; transcriptomic signatures, however, showed changes related to DNA damage and its regulation, inflammation and regulation of cell proliferation. A differential expression was validated at E14.5 for the candidates Sox8, Angptl4 and Gas1. Our data substantiate the in utero biomolecular effect of gestational exposure to air pollution and provide first-time stereological evidence that pre- and early life-postnatal exposure compromise lung development, leading to a reduced number of alveoli and an impairment of lung function in the adult mouse.
- Diesel exhaust exposure intensifies inflammatory and structural changes associated with lung aging in mice(2019) RIBEIRO JUNIOR, Gabriel; COSTA, Natalia de Souza Xavier; BELOTTI, Luciano; ALEMANY, Adair Aparecida dos Santos; AMATO-LOURENCO, Luis Fernando; CUNHA, Paula Gabriela da; DURO, Stephanie de Oliveira; RIBEIRO, Susan Pereira; VERAS, Mariana Matera; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; MARCOURAKIS, Tania; SALDIVA, Paulo Hilario Nascimento; FARSKY, Sandra Helena Poliselli; MAUAD, ThaisLife expectancy is increasing worldwide. Lung aging is a process marked by changes in multiple morphological, physiological and age-related biomarkers (e.g., sirtuins) and is influenced by external factors, such as air pollution. Hence, the elderly are considered more vulnerable to the air pollution hazards. We hypothesized that diesel exhaust (DE) exposure intensifies changes in lung inflammatory and structural parameters in aging subjects. Two- and fifteen-month-old mice were exposed to DE for 30 days. Lung function was measured using the forced oscillation method. The inflammatory profile was evaluated in the bronchoalveolar lavage fluid (BALF) and blood, and lung volumes were estimated by stereology. Antioxidant enzyme activity was evaluated by spectrophotometry, sirtuin 1 (SIRT1), sirtuin 2 (SIRT2) and sirtuin 6 (SIRT6) expression was assessed by reverse transcription polymerase chain reaction (RT-PCR), and levels of the sirtuin proteins were evaluated by immunohistochemical staining in lung tissues. Older mice presented decreased pulmonary resistance and elastance, increased macrophage infiltration and decreased tumor necrosis factor (TNF) and interleukin 10 (IL-10) levels in the BALF, reduced activities of the antioxidant enzymes glutathione peroxidase (GPx) and glutathione reductase (GR), and increased activity glutathione S-transferase (GST); increased lung volumes with decreased elastic fiber and increased airway collagen content. SIRT1 gene expression was decreased in older animals, but protein levels were increased. DE exposure increased macrophage infiltration and oxidative stress in the lungs of animals of both ages. SIRT6 gene expression was decreased by DE exposure, with increased protein levels. In older animals, DE affected lung structure and collagen content. Lung aging features, such as decreased antioxidant reserves, lower IL-10 expression, and decreased SIRT1 levels may predispose subjects to exacerbated responses after DE exposure. Our data support the hypothesis that strategies designed to reduce ambient air pollution are an important step towards healthy aging.