Florencia M. Barbé-Tuana
Universidade Federal do Rio Grande do Sul
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Publication
Featured researches published by Florencia M. Barbé-Tuana.
Obesity | 2015
Eduardo Mundstock; Edgar E. Sarria; Helen Zatti; Fernanda Mattos Louzada; Lucas Kich Grun; Marcus H. Jones; Fátima Theresinha Costa Rodrigues Guma; João Mário Mazzola; Matias Epifanio; Renato T. Stein; Florencia M. Barbé-Tuana; Rita Mattiello
The main objective of this systematic review is to assess the effects of obesity on telomere length.
Schizophrenia Research | 2016
Letícia Sanguinetti Czepielewski; Raffael Massuda; Bruna Schilling Panizzutti; Eduarda Dias da Rosa; Danielle Silveira Macêdo; Lucas Kich Grun; Florencia M. Barbé-Tuana; Clarissa Severino Gama
Schizophrenia (SZ) is associated with broad burden. The clinical manifestations of SZ are related to pathophysiological alterations similar to what is seen in normal aging. Our aim was to evaluate the differences in telomere length (TL), a biomarker of cellular aging, in subjects with SZ (n=36), unaffected siblings (SB, n=36) and healthy controls (HC, n=47). SZ had shorter TL compared to HC, but no difference was found in SB comparing to SZ. These findings indicate that a pathological accelerated aging profile could be present in the course of SZ and further studies are needed to confirm TL as potential endophenotype, especially in at risk populations.
Revista Brasileira de Psiquiatria | 2016
Florencia M. Barbé-Tuana; Mariana Migliorini Parisi; Bruna Schilling Panizzutti; Gabriel Rodrigo Fries; Lucas Kich Grun; Fátima Theresinha Costa Rodrigues Guma; Flávio Kapczinski; Michael Berk; Clarissa Severino Gama; Adriane Ribeiro Rosa
Objective: Bipolar disorder (BD) has been associated with increased rates of age-related diseases, such as type II diabetes, metabolic syndrome, osteoporosis, and cardiovascular disorders. Several biological findings have been associated with age-related disorders, including increased oxidative stress, inflammation, and telomere shortening. The objective of this study was to compare telomere length among participants with BD at early and late stages and age- and gender-matched healthy controls. Methods: Twenty-six euthymic subjects with BD and 34 healthy controls were recruited. Genomic DNA was extracted from peripheral blood and mean telomere length was measured using real-time quantitative polymerase chain reaction. Results: Telomere length was significantly shorter in both the early and late subgroups of BD subjects when compared to the respective controls (p = 0.002 and p = 0.005, respectively). The sample size prevented additional subgroup analyses, including potential effects of medication, smoking status, and lifestyle. Conclusion: This study is concordant with previous evidence of telomere shortening in BD, in both early and late stages of the disorder, and supports the notion of accelerated aging in BD.
Biochimica et Biophysica Acta | 2016
Paula Pierozan; Helena Biasibetti; Felipe Schmitz; Helena Ávila; Mariana Migliorini Parisi; Florencia M. Barbé-Tuana; Angela Terezinha de Souza Wyse; Regina Pessoa-Pureur
QUIN is a glutamate agonist playing a role in the misregulation of the cytoskeleton, which is associated with neurodegeneration in rats. In this study, we focused on microglial activation, FGF2/Erk signaling, gap junctions (GJs), inflammatory parameters and redox imbalance acting on cytoskeletal dynamics of the in QUIN-treated neural cells of rat striatum. FGF-2/Erk signaling was not altered in QUIN-treated primary astrocytes or neurons, however cytoskeleton was disrupted. In co-cultured astrocytes and neurons, QUIN-activated FGF2/Erk signaling prevented the cytoskeleton from remodeling. In mixed cultures (astrocyte, neuron, microglia), QUIN-induced FGF-2 increased level failed to activate Erk and promoted cytoskeletal destabilization. The effects of QUIN in mixed cultures involved redox imbalance upstream of Erk activation. Decreased connexin 43 (Cx43) immunocontent and functional GJs, was also coincident with disruption of the cytoskeleton in primary astrocytes and mixed cultures. We postulate that in interacting astrocytes and neurons the cytoskeleton is preserved against the insult of QUIN by activation of FGF-2/Erk signaling and proper cell-cell interaction through GJs. In mixed cultures, the FGF-2/Erk signaling is blocked by the redox imbalance associated with microglial activation and disturbed cell communication, disrupting the cytoskeleton. Thus, QUIN signal activates differential mechanisms that could stabilize or destabilize the cytoskeleton of striatal astrocytes and neurons in culture, and glial cells play a pivotal role in these responses preserving or disrupting a combination of signaling pathways and cell-cell interactions. Taken together, our findings shed light into the complex role of the active interaction of astrocytes, neurons and microglia in the neurotoxicity of QUIN.
Australian and New Zealand Journal of Psychiatry | 2016
Bruna Maria Ascoli; Luíza Paul Géa; Rafael Colombo; Florencia M. Barbé-Tuana; Flávio Kapczinski; Adriane Ribeiro Rosa
Objective: Bipolar disorder is a chronic, severe and disabling disease; however, its pathophysiology remains poorly understood. Recent evidence has suggested that inflammation and immune dysregulation play a significant role in the pathophysiology of bipolar disorder. This review is aimed to highlight the importance of systemic inflammation in modulating the inflammatory response of microglia and hence its potential involvement with bipolar disorder. We also discuss novel therapeutic strategies that emerge from this new research. Method: This article presents a theoretical synthesis of the effects of systemic inflammation on the immune response of the central nervous system in bipolar disorder. The complex relationship between stress, pro-inflammatory cytokines and microglial dysfunction is summarized, emphasizing the role of the kynurenine pathway in this process and, consequently, their effects on neuronal plasticity. Results: Bipolar patients demonstrate increased serum levels of pro-inflammatory cytokines (interleukin-1β, interleukin-6 and tumor necrosis factor-α) and lower hypothalamic–pituitary–adrenal axis sensitivity. This imbalance in the immune system promotes a change in blood–brain barrier permeability, leading to an inflammatory signal spread in the central nervous system from the periphery, through macrophages activation (M1 polarization). Chronic microglial activation can result in neuronal apoptosis, neurogenesis inhibition, hippocampal volume reduction, lower neurotransmitters synthesis and cytotoxicity, by increasing glutamate production and kynurenine metabolism. Conclusions: This review provides an overview of the mechanisms involved in the immune system imbalance and its potential involvement in the pathophysiology of bipolar disorder. Consequently, new strategies that normalize the immune-inflammatory pathways may provide a valuable therapeutic target for the treatment of these disorders.
Journal of Cellular Biochemistry | 2015
Izabel Cristina Custodio de Souza; Leo Anderson Meira Martins; Mariana de Vasconcelos; Cleverson Moraes de Oliveira; Florencia M. Barbé-Tuana; Claudia Marlise Balbinotti Andrade; Letícia Ferreira Pettenuzzo; Radovan Borojevic; Rogério Margis; Regina Maria Vieira da Costa Guaragna; Fátima Theresinha Costa Rodrigues Guma
The activation of hepatic stellate cell (HSC), from a quiescent cell featuring cytoplasmic lipid droplets to a proliferative myofibroblast, plays an important role in liver fibrosis development. The GRX line is an activated HSC model that can be induced by all‐trans‐retinol to accumulate lipid droplets. Resveratrol is known for activating Sirtuin1 (SIRT1), a NAD+‐dependent deacetylase that suppresses the activity of peroxisome proliferator‐activated receptor gamma (PPARγ), an important adipogenic transcription factor involved in the quiescence maintenance of HSC. We evaluated the effects of 0.1 μM of resveratrol in retinol‐induced GRX quiescence by investigating the interference of SIRT1 and PPARγ on cell lipogenesis. GRX lipid accumulation was evaluated through Oil‐red O staining, triacylglycerides quantification, and [14C] acetate incorporation into lipids. mRNA expression and protein content of SIRT1 and PPARγ were measured by RT‐PCR and immunoblotting, respectively. Resveratrol‐mediated SIRT1 stimuli did not induce lipogenesis and reduced the retinol‐mediated fat‐storing capacity in GRX. In order to support our results, we established a cell culture model of transgenic super expression of PPARγ in GRX cells (GRXPγ). Resveratrol reduced lipid droplets accumulation in GRXPγ cells. These results suggest that the PPARγ/SIRT1 ratio plays an important role in the fate of HSC. Thus, whenever the PPARγ activity is greater than SIRT1 activity the lipogenesis is enabled. J. Cell. Biochem. 116: 2304–2312, 2015.
The Prostate | 2015
Gabriela Elisa Hirsch; Mariana Migliorini Parisi; Leo Anderson Meira Martins; Cláudia M. B. Andrade; Florencia M. Barbé-Tuana; Fátima Theresinha Costa Rodrigues Guma
Prostate cancer is a leading cause of death among men due to the limited number of treatment strategies available for advanced disease. γ‐oryzanol is a component of rice bran, rich in phytosterols, known for its antioxidant, anti‐carcinogenic and endocrinological effects. It is known that γ‐oryzanol may affect prostate cancer cells through the down regulation of the antioxidant genes and that phytosterols have anti‐proliferative and apoptotic effects. There are evidences showing that some of the components of γ‐oryzanol can modulate genes involved in the development and progression of prostate cancer, as caveolin‐1 (Cav‐1) and prostate specific androgen‐regulated gene (PCGEM1).
Schizophrenia Bulletin | 2018
Letícia Sanguinetti Czepielewski; Raffael Massuda; Bruna Schilling Panizzutti; Lucas Kich Grun; Florencia M. Barbé-Tuana; Antônio Lúcio Teixeira; Deanna M; Clarissa Severino Gama
Schizophrenia (SZ) is associated with increased somatic morbidity and mortality, in addition to cognitive impairments similar to those seen in normal aging, which may suggest that pathological accelerated aging occurs in SZ. Therefore, we aim to evaluate the relationships of age, telomere length (TL), and CCL11 (aging and inflammatory biomarkers, respectively), gray matter (GM) volume and episodic memory performance in individuals with SZ compared to healthy controls (HC). One hundred twelve participants (48 SZ and 64 HC) underwent clinical and memory assessments, structural MRI, and had their peripheral blood drawn for biomarkers analysis. Comparisons of group means and correlations were performed. Participants with SZ had decreased TL and GM volume, increased CCL11, and worse memory performance compared to HC. In SZ, shorter TL was related to increased CCL11, and both biomarkers were related to reduced GM volume, all of which were related to worse memory performance. Older age was only associated with reduced GM, but longer duration of illness was related with all the aforementioned variables. Younger age of disease onset was associated with increased CCL11 levels and worse memory performance. In HC, there were no significant correlations except between memory and GM. Our results are consistent with the hypothesis of accelerated aging in SZ. These results may indicate that it is not age itself, but the impact of the disease associated with a pathological accelerated aging that leads to impaired outcomes in SZ.
International Journal of Developmental Neuroscience | 2016
André Felipe Rodrigues; Helena Biasibetti; Bruna Stela Zanotto; Eduardo Farias Sanches; Paula Pierozan; Felipe Schmitz; Mariana Migliorini Parisi; Florencia M. Barbé-Tuana; Carlos Alexandre Netto; Angela Terezinha de Souza Wyse
Tissue accumulation of galactose is a hallmark in classical galactosemia. Cognitive deficit is a symptom of this disease which is poorly understood. The aim of this study was to investigate the effects of intracerebroventricular administration of galactose on memory (inhibitory avoidance and novel object recognition tasks) of adult rats. We also investigated the effects of galactose on acetylcholinesterase (AChE) activity, immunocontent and gene expression in hippocampus and cerebral cortex. Wistar rats received a single injection of galactose (4 mM) or saline (control). For behavioral parameters, galactose was injected 1 h or 24 h previously to the testing. For biochemical assessment, animals were decapitated 1 h, 3 h or 24 h after galactose or saline injection; hippocampus and cerebral cortex were dissected. Results showed that galactose impairs the memory formation process in aversive memory (inhibitory avoidance task) and recognition memory (novel object recognition task) in rats. The activity of AChE was increased, whereas the gene expression of this enzyme was decreased in hippocampus, but not in cerebral cortex. These findings suggest that these changes in AChE may, at least in part, to lead to memory impairment caused by galactose. Taken together, our results can help understand the etiopathology of classical galactosemia.
Clinical Psychopharmacology and Neuroscience | 2018
Pamela Ferrari; Mariana Migliorini Parisi; Rafael Colombo; Matheus Becker; Gabriel Rodrigo Fries; Bruna Maria Ascoli; Luíza Paul Géa; Marcia Kauer-Sant’Anna; Flávio Kapczinski; Fábio Klamt; Fátima Theresinha Costa Rodrigues Guma; Adriane Ribeiro Rosa; Florencia M. Barbé-Tuana
Objective Evidence has suggested that immune imbalance is involved with bipolar disorder (BD); however, its precise mechanism is poorly understood. This study investigated whether biochemical changes in the serum from BD patients could modulate the phenotype of cultured macrophages. Methods Eighteen subjects with BD and five healthy individuals were included in this study. The human monocyte cell line U-937 was activated with phorbol 12-myristate 13-acetate (PMA) and polarization was induced with RPMI-1640 media supplemented with 10% serum from each patient for 24 hours. Gene expression of selected M1 and M2 markers was assessed by quantitative PCR. Results Macrophages exposed to serum of manic and depressive BD patients displayed an increase of interleukin-1β (6.40±3.47 and 9.04±5.84 vs. 0.23±0.11; p<0.05) and tumor necrosis factor-α (2.23±0.91 and 2.03±0.45 vs. 0.62±0.24; p=0.002 and p=0.004, respectively) compared to euthymic group (there was no difference between euthymic and controls). In parallel, U-937 macrophages treated with serum of patients in acute episode displayed a down-regulation of CXCL9 (0.29±0.20 vs. 1.86±1.61; p=0.006) and CXCL10 expression (0.36±0.15 and 0.86±0.24 vs. 1.83±0.88; p<0.000 and p=0.04) compared to the euthymia group. Conclusion Our results are consistent with previous studies showing that changes in peripheral blood markers could modulate M1/M2 polarization in BD. The evidence of macrophages as source of inflammatory cytokines might be helpful to unravel how the mononuclear phagocyte system is involved in the etiology of BD.
Collaboration
Dive into the Florencia M. Barbé-Tuana's collaboration.
Fátima Theresinha Costa Rodrigues Guma
Universidade Federal do Rio Grande do Sul
View shared research outputsAngela Terezinha de Souza Wyse
Universidade Federal do Rio Grande do Sul
View shared research outputs