MONIQUE MATSUDA

(Fonte: Lattes)
Índice h a partir de 2011
14
Projetos de Pesquisa
Unidades Organizacionais
LIM/33 - Laboratório de Oftalmologia, Hospital das Clínicas, Faculdade de Medicina

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Agora exibindo 1 - 10 de 33
  • article 60 Citação(ões) na Scopus
    Diesel Exhaust Particles Selectively Induce Both Proinflammatory Cytokines and Mucin Production in Cornea and Conjunctiva Human Cell Lines
    (2013) TAU, Julia; NOVAES, Priscila; MATSUDA, Monique; TASAT, Deborah R.; SALDIVA, Paulo H.; BERRA, Alejandro
    PURPOSE. To evaluate the effect of diesel exhaust particles (DEP) on the viability, proliferation, apoptosis, secretion of cytokines (IL-6, IL-8, and TNF-alpha), and mucin gene transcription (MUC1, MUC5AC, and MUC16) in human epithelial cells of the cornea (HCLE) and conjunctiva (IOBA-NHC). METHODS. HCLE and IOBA-NHC cells were incubated with DEP (10-500 mu g/mL) for 24 hours. Cell proliferation was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Apoptotic cells were measured by an annexin V-FITC and propidium iodide kit for flow cytometry. Proinflammatory cytokines were determined by an ELISA kit. Mucin gene transcription was quantified by real-time PCR. RESULTS. DEP significantly decreased the viability, proliferation, and secretion of IL-8, but increased the secretion of IL-6 on both HCLE and IOBA-NHC cell lines in a dose-dependent manner. Neither cornea nor conjunctiva cells incubated with DEP released TNF-alpha. DEP induced a significant increase in the percentage of apoptotic cells in IOBA-NHC, whereas no changes were observed in HCLE. Finally, DEP significantly decreased the transcription levels of MUC1 and MUC16 in HCLE, but increased the transcription levels of MUC1, MUC5AC, and MUC16 in IOBA-NHC. CONCLUSIONS. These findings suggest that human corneal and conjunctival epithelial cells incubated with DEP showed cytotoxicity and an inflammatory response mediated by IL-6, not by TNF-alpha or IL-8. Also, the decrease in mucin expression in the cornea cells might leave exposed areas in the cornea for contact with DEP. Finally, the increase in mucin expression in the conjunctiva cells might be involved at least in the clearance of DEP to protect the ocular epithelium.
  • article 0 Citação(ões) na Scopus
    Basiliximab Does Not Impair Airway Mucociliary Clearance of Rats
    (2022) CORREIA, Aristides Tadeu; ALMEIDA, Francine Maria de; AUGUSTO-COTTET, Marcia Cristina; NOLASCO, Patricia; BENTO, Afonso Silva Alves; HIRANO, Hugo Kenji Matsushima; SOUZA, Maria Cecilia Ribeiro de; SANTOS, Elizabete Silva dos; CASTRO, Julia Helena Rodrigues de; MATSUDA, Monique; PEGO-FERNANDES, Paulo Manuel; PAZETTI, Rogerio
    Previous studies have shown that immunosuppressive drugs impair the airway mucociliary clearance of rats. However, considering the high specificity of basiliximab (BSX) and the absence of studies reporting its side effects, our aim was to investigate whether BSX, associated or not with triple therapy, impairs the mucociliary system. Forty rats were divided into 4 groups: Control, BSX, Triple, and BSX + Triple. After 15 days of treatment, animals were euthanized and the ciliary beating frequency (CBF), mucociliary transport velocity (MCTV), neutral and acid mucin production, Muc5ac and Muc5b gene expression, inflammatory cell number, and interleukin (IL)-6 concentration were analyzed. CBF and MCTV were lower in Triple and BSX + Triple groups (p < 0.05). Neutral mucin percentage was higher in Triple group (p < 0.05), and acid mucin percentage was higher in Triple and BSX + Triple groups (p < 0.05). The Muc5ac and Muc5b gene expression was higher in Triple and BSX + Triple groups (p < 0.05). Animals from Triple and BSX + Triple groups presented fewer mononuclear cells (p < 0.05). The number of polymorphonuclear cells was higher in the Triple group (p < 0.05). In the analysis of inflammatory cells in the blood, there was a decrease in lymphocytes and an increase in neutrophils in the Triple and BSX + Triple groups (p < 0.05). The concentration of IL-6 significantly increased in the animals of the Triple and BSX + Triple groups (p < 0.05). BSX did not change the mucociliary apparatus of rats.
  • article 95 Citação(ões) na Scopus
    Correlation Between Signs and Symptoms of Ocular Surface Dysfunction and Tear Osmolarity With Ambient Levels of Air Pollution in a Large Metropolitan Area
    (2013) TORRICELLI, Andre A. M.; NOVAES, Priscila; MATSUDA, Monique; BRAGA, Alfesio; SALDIVA, Paulo H. N.; ALVES, Milton R.; MONTEIRO, Mario L. R.
    Purpose: To evaluate the effect of high levels of environmental air pollution on tear osmolarity and its possible correlation with clinical signs and symptoms. Methods: This was a panel study involving 71 taxi drivers and traffic controllers from Sao Paulo, Brazil. Mean individual levels of 24-hour exposure to nitrogen dioxide (NO2) and particulate matter smaller than 2.5 mu m (PM2.5) were assessed on 4 different occasions. On the first and third visits, subjects were submitted to clinical evaluations including the administration of the Ocular Surface Disease Index questionnaire, slit-lamp examination, estimation of tear breakup time (BUT), the Schirmer test, and vital staining of the cornea and conjunctiva. On the second and fourth visits, tear samples were collected for osmolarity assays. Statistical analysis was performed using generalized estimating equations. Results: Although the taxi drivers and traffic controllers in our sample were exposed to high levels of NO2 and PM2.5, few symptoms were reported on the Ocular Surface Disease Index questionnaire. BUT values were reduced, whereas vital staining and Schirmer test mean results were within normal limits, despite considerable variability. A significant and negative correlation was found between PM2.5 levels and tear film osmolarity levels (P < 0.05). An increase of 10 mu g/m(3) in PM2.5 was associated with a 10.9 mOsm/kg decrease in tear osmolarity. There also was a negative correlation, although not statistically significant, between NO2 and tear osmolarity. Conclusions: Exposure to air pollution reduces tear film stability and influences tear film osmolarity. Combining clinical examination with the assessment of tear osmolarity may help understand ocular surface response to high levels of air pollution.
  • article 17 Citação(ões) na Scopus
    Cellular components of the idiopathic epiretinal membrane
    (2022) SILVA, Rafael Andre da; RODA, Vinicius Moraes de Paiva; MATSUDA, Monique; SIQUEIRA, Paula Veloso; LUSTOZA-COSTA, Gabriela Jesus; WU, Davi Chen; HAMASSAKI, Dania Emi
    Idiopathic epiretinal membrane (iERM) is a fibrocellular proliferation on the inner surface of the retina, which leads to decreased visual acuity and even central visual loss. As iERM is associated to advanced age and posterior vitreous detachment, a higher prevalence is expected with increasing life expectancy and aging of the global population. Although various cell types of retinal and extra-retinal origin have been described in iERMs (Muller glial cells, astrocytes, hyalocytes, retinal pigment epithelium cells, myofibroblasts, and fibroblasts), myofibroblasts have a central role in collagen production and contractile activity. Thus, myofibroblast differentiation is considered a key event for the iERM formation and progression, and fibroblasts, Muller glial cells, hyalocytes, and retinal pigment epithelium have been identified as myofibroblast precursors. On the other side, the different cell types synthesize growth factors, cytokines, and extracellular matrix, which have a crucial role in ERM pathogenesis. In the present review, the major cellular components and their functions are summarized, and their possible roles in the iERM formation are discussed. By exploring in detail the cellular and molecular aspects of iERM, we seek to contribute for better understanding of this fibrotic disease and the origin of myofibroblasts, which may eventually drive to more targeted therapeutic approaches.
  • article 6 Citação(ões) na Scopus
    Increased expression of Filaggrin and Claudin-1 in the ocular surface of patients with atopic dermatitis
    (2022) CALLOU, T. M. P.; ORFALI, R. L.; SOTTO, M. N.; V, N. Pereira; ZANIBONI, M. C.; AOKI, V; BRITO, M. P.; MATSUDA, M.; SANTO, R. M.
    Background Atopic dermatitis (AD) is an itchy, chronic and inflammatory skin condition, with dysfunctional immune response and skin barrier defects. Reduction of filaggrin (FLG) and tight junctions (TJ) proteins, such as claudin-1 (CLDN-1), expression in cutaneous epithelial barrier is remarkable in AD pathogenesis. Ocular involvement occurs in approximately 40% of AD patients leading to changes in the structure of the conjunctiva. Objectives We aimed to evaluate the expression of FLG and CLDN-1 in the ocular surface of adults with AD, analysing bulbar conjunctival cells collected by a novel non-invasive cellular imprint. Methods Bulbar conjunctival epithelial cells were collected by cellular imprint technique, and FLG and CLDN-1 expression were assessed by immunofluorescence (IF) and real-time polymerase chain reaction (RT-PCR). Results We detected increased expression of FLG and CLDN-1, as well as their transcript levels in AD patients compared with healthy controls (HC). There was a positive correlation between tear film break-up time (TBUT) and FLG expression. Fluorescein staining was inversely associated with FLG expression. Conclusions Our results may reflect a reactive response of the ocular surface to AD-related ocular inflammation and associated dry eye disease. Further investigations focusing on the role of FLG and TJ expression in the ocular surface of AD patients may increment the understanding of the pathophysiology of extracutaneous AD and developing future targeted therapies.
  • article 22 Citação(ões) na Scopus
    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, Mariangela
    Diesel 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.
  • conferenceObject
    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
  • article 10 Citação(ões) na Scopus
    The genetics of human running: ACTN3 polymorphism as an evolutionary tool improving the energy economy during locomotion
    (2016) PASQUA, Leonardo A.; BUENO, Salomao; MATSUDA, Monique; MARQUEZINI, Monica V.; LIMA-SILVA, Adriano E.; SALDIVA, Paulo H. N.; BERTUZZI, Romulo
    Background: Covering long distances was an important trait to human evolution and continues to be highlighted for health and athletic status. This ability is benefitted by a low cost of locomotion (CoL), meaning that the individuals who are able to expend less energy would be able to cover longer distances. The CoL has been shown to be influenced by distinct and even 'opposite' factors, such as physiological and muscular characteristics, which are genetically inherited. In this way, DNA alterations could be important determinants of the characteristics associated with the CoL. A polymorphism in the ACTN3 gene (R577X) has been related to physical performance, associating the X allele with endurance and the R allele with strength/power abilities. Aim: To investigate the influence of ACTN3 genotypes on the CoL. Subjects and methods: One hundred and fifty healthy male individuals performed two constant speed tests (at 10 and 12 km/h) to determine the CoL. Results: Interestingly, the results showed that heterozygous individuals (RX genotype) presented significantly lower CoL compared to RR and XX individuals. Conclusions: It is argued that RX genotype might generate an intermediate strength-to-endurance phenotype, leading to a better phenotypic profile for energy economy during running and, consequently, for long-term locomotion.
  • article 6 Citação(ões) na Scopus
    Effects of air pollution exposure on inflammatory and endurance performance in recreationally trained cyclists adapted to traffic-related air pollution
    (2022) SILVEIRA, Andre C.; HASEGAWA, Julio S.; CRUZ, Ramon; MATSUDA, Monique; V, Monica Marquezini; LIMA-SILVA, Adriano Eduardo; V, Luisa Giles; SALDIVA, Paulo; KOEHLE, Michael S.; BERTUZZI, Romulo
    The aim of the present study was to analyze the effects of traffic-related air pollution (TRAP) on markers of inflammatory, neuroplasticity, and endurance performance-related parameters in recreationally trained cyclists who were adapted to TRAP during a 50-km cycling time trial (50-km cycling TT). Ten male cyclists performed a 50-km cycling TT inside an environmental chamber located in downtown Sao Paulo (Brazil), under TRAP or filtered air conditions. Blood samples were obtained before and after the 50-km cycling TT to measure markers of inflammatory [interleukin-6 (IL-6),C-reactive protein (CRP), interleukin-10 (IL-10), intercellular adhesion molecule-1 (ICAM-1)] and neuroplasticity [brain-derived neurotrophic factor (BDNF)]. Rating of perceived exertion (RPE), heart rate (HR), and power output (PO) were measured throughout the 50-km cycling TT. There were no significant differences between experimental conditions for responses of IL-6, CRP, and IL-10 (P > 0.05). When compared with exercise-induced changes in filtered air condition, TRAP provoked greater exercise-induced increase in BDNF levels (TRAP = 3.3 ?? 2.4-fold change; Filtered = 1.3 ?? 0.5-fold change; P = 0.04) and lower exercise-induced increase in ICAM-1 (Filtered = 1.1?? 0.1-fold change; TRAP = 1.0 ?? 0.1-fold change; P = 0.01). The endurance performance-related parameters (RPE, HR, PO, and time to complete the 50-km cycling TT) were not different between TRAP and filtered air conditions (P > 0.05). These findings suggest that the potential negative impacts of exposure to pollution on inflammatory, neuroplasticity, and performance-related parameters do not occur in recreationally trained cyclists who are adapted to TRAP.
  • article 10 Citação(ões) na Scopus
    Cellular stress response in human Milner cells (MIO-M1) after bevacizumab treatment
    (2017) MATSUDA, Monique; KREMPEL, Paloma Gava; MARQUEZINI, Monica Valeria; SHOLL-FRANCO, Alfred; LAMEU, Amanda; MONTEIRO, Mario Luiz R.; MIGUEL, Nadia Campos de Oliveira
    Bevacizumab, an anti-vascular endothelial growth factor (VEGF) agent, is widely used in the treatment of retinal vascular diseases. However, due to the essential role Muller cell derived VEGF plays in the maintenance of retinal neurons and glial cells, cell viability is likely to be affected by VEGF inhibition. We therefore evaluated the effect of bevacizumab-induced VEGF inhibition on Muller cells (MIO-M1) in vitro. MIO-M1 cells were cultured for 12 or 24 h in media containing bevacizumab at 0.25 or 0.5 mg/mL. Controls were cultured in medium only. Cell viability was determined with the trypan blue exclusion test and MTT assay. Caspase-3, beclin-1, glial fibrillary acidic protein (GFAP) and vimentin content were quantified by immunohistochemistry. Gene expression was evaluated by real-time quantitative PCR. Treatment with bevacizumab did not reduce MIO-M1 cell viability, but increased metabolic activity at 24 h (0.5 mg/mL) and induced apoptosis and autophagy, as shown by the increased caspase-3 levels at 12 h (0.25 and 0.5 mg/mL) and the increased beclin levels at 24 h (0.5 mg/mL). Caspase-3 mRNA was upregulated at 12 h and downregulated at 24 h in cells treated with bevacizumab at 0.25 mg/mL. Bevacizumab treatment was also associated with structural protein abnormalities, with decreased GFAP and vimentin content and upregulated GFAP and vimentin mRNA expression. Although bevacizumab did not significantly affect MIO-M1 cell viability, it led to metabolic and molecular changes (apoptosis, autophagy and structural abnormalities) suggestive of significant cellular toxicity.