Marina Guimarães Gobbo

Faculdade de Medicina de São José do Rio Preto

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Rejane M. Góes

Universidade Estadual Paulista (Unesp)

Sebastião Roberto Taboga

Universidade Estadual Paulista (Unesp)

Daniele Lisboa Ribeiro

Universidade Federal de Uberlândia

Eduardo Alves de Almeida

Universidade Regional de Blumenau

Guilherme Henrique Tamarindo

Universidade Estadual de Campinas (UNICAMP)

Maria Etelvina Pinto‐Fochi

Faculdade Ceres

R Carleo

Ospedale S.Gennaro

De Matteo A

Carolina Frandsen Pereira da Costa

AC Camargo Hospital

Eloísa Zanin Pytlowanciv

Universidade Estadual Paulista (Unesp)

Cooperative Institutions

Universidade Estadual Paulista (Unesp)

Universidade Estadual de Campinas (UNICAMP)

Faculdade de Medicina de São José do Rio Preto

Weatherford College

Sapienza University of Rome

Inserm

Harvard University

Istituti di Ricovero e Cura a Carattere Scientifico

UNSW Sydney

Exact Sciences (United States)

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

[Evaluation of the effect of picotamide on platelet function in diabetic subjects].

PubMed (1990)

R Carleo L Veno F Fuccio M. S. Bonavita De Matteo A

In this study the Authors verify the results of Picotamide on platelet aggregation in diabetic subjects. The results suggest that Picotamide has no influence on insulin or oral treatment of diabetic subjects. However, it is certain that platelet aggregation by ADP or collagen decreases due to the effect on thromboxane probably because of the limitation of platelet receptors.

Source

Cite

Citations (0)

A administração de melatonina durante a maturação sexual

Marina Guimarães Gobbo

epitelial, remodelação da

10.47749/t/unicamp.2015.960162

Cite

Citations (0)

Influence of Melatonin on the Proliferative and Apoptotic Responses of the Prostate under Normal and Hyperglycemic Conditions

Journal of Diabetes Research (2015)

Marina Guimarães Gobbo Nishtman Dizeyi Per‐Anders Abrahamsson Per-Anders Bertilsson Viviane Sanches Masitéli

The antitumor properties of melatonin (MLT) are known for prostate cancer cells. This study investigated whether MLT affects prostate maturation and interferes with tissue injuries induced by diabetes. MLT was administered to Wistar rats from 5 weeks of age in the drinking water (10 μ g/kg b.w.), and diabetes was induced at the 13th week by streptozotocin (4.5 mg/100g b.w., i.p.). The animals were euthanized in the 14th and 21st weeks. MLT reduced the immunostained cells for androgen receptor (AR) by 10% in younger rats. Diabetes decreased cell proliferation and increased apoptosis. MLT treatment impeded apoptosisp=0.02and augmented proliferationp=0.0008and PCNA content in prostate following long-term diabetes due to restoration of testosterone levels and expression of melatonin receptor type 1B. The effect of MLT (500 µ M, 5 mM, and 10 mM) on androgen-dependent (22Rv1) and androgen-independent (PC3) cancer cells and human prostate epithelial cells (PNTA1) under normal and hyperglycemic conditions (HG, 450 mg/dL) was analyzed. Contrary to PNTA1 and 22Rv1 cells, MLT improved the proliferation of PC3 cells in hyperglycemic medium. The combined data indicated that MLT had proliferative and antiapoptotic effects in prostate cells subjected to HG levels and it seems to involve specific MLT pathways rather than AR.

10.1155/2015/538529

Cite

Citations (19)

Prostate hyperplasia caused by long‐term obesity is characterized by high deposition of extracellular matrix and increased content of MMP‐9 and VEGF

International Journal of Experimental Pathology (2014)

Silas Amâncio Silva Marina Guimarães Gobbo Maria Etelvina Pinto‐Fochi Alex Rafacho Sebastião Roberto Taboga

Summary Recent studies have shown a positive association of cancer and obesity, but the morphological and molecular mechanisms involved in this relationship are still unknown. This study analysed the impact of long‐term obesity on rat prostate, focusing on stromal changes. Male adult Wistar rats were treated with high‐fat diet to induce obesity, while the control group received a balanced diet. After 30 weeks of feeding, the ventral prostate was analysed by immunohistochemistry for cell proliferation, smooth muscle α‐actin, vimentin, chondroitin sulphate and metalloproteinases (MMP‐2 and 9). The content of androgen receptor (AR), oestrogen receptors (ERs) and vascular endothelial growth factor (VEGF) was measured by Western blotting, and activity of catalase and Glutathione‐S‐Transferase (GST) were quantified by enzymatic assay. Long‐term obesity decreased testosterone plasma levels by 70% and resulted in stromal prostate hyperplasia, as evidenced by increased collagen fibres. Such stromal hyperplasia was associated with increased number of blood vessels and raised VEGF content, and increased expression of chondroitin sulphate, vimentin, α‐actin and MMP‐9. In spite of the high cell density in prostate, the proliferative activity was lower in the prostates of obese rats, indicating that hyperplasia was established during the early phases in this obesity model. AR levels increased significantly, whereas the ERα decreased in this group. Moreover, the levels of catalase and GST were changed considerably. These findings indicate that long‐term obesity, besides disturbing the antioxidant control, causes intense stromal remodelling and release of factors that create an environment that can promote proliferative disorders in the gland, culminating with diffuse hyperplasia.

10.1111/iep.12107

Cite

Citations (37)

Pathological lesions and global DNA methylation in rat prostate under streptozotocin‐induced diabetes and melatonin supplementation

Cell Biology International (2017)

Marina Guimarães Gobbo Guilherme Henrique Tamarindo Daniele Lisboa Ribeiro Silvana G. P. Campos Sebastião Roberto Taboga

Chronic hyperglycemia increases production of reactive oxygen species, which favors carcinogenesis. The association between diabetes and prostate cancer is controversial. Melatonin has antioxidant, anti-inflammatory, and antiproliferative properties. We investigated whether low doses of melatonin prevent the tissue alterations caused by diabetes and alter prostate histology of healthy rats. We also investigated whether experimental diabetes promoted the development of pathological lesions in the ventral prostate of rats. Melatonin was provided in drinking water (10 μg/kg/day) from age 5 weeks until the end of experiment. Diabetes was induced at 13 weeks by administration of streptozotocin (40 mg/kg, ip). Rats were euthanized at 14 or 21 weeks. Histological and stereological analyses were carried out and the incidence and density of malignant and pre-malignant lesions were assessed. Immunohistochemical assays of α-actin, cell proliferation (PCNA), Bcl-2, glutathione S-transferase (GSTPI), and DNA methylation (5-methylcytidine) were performed. Melatonin did not elicit conspicuous changes in the prostate of healthy animals; in diabetic animals there was a higher incidence of atrophy (93%), microinvasive carcinoma (10%), proliferative inflammatory atrophy, PIA (13%), prostatitis (26%), and prostate intraepithelial neoplasia, PIN (20%) associated with an increase of 40% in global DNA methylation. Melatonin attenuated epithelial and smooth muscle cell (smc) atrophy, especially at short-term diabetes-and normalized incidence of PIN (11%), inflammatory cells infiltrates, prostatitis (0%) and PIA (0%) at long-term diabetes. MLT was effective in preventing inflammatory disorders and PIN under diabetic condition. Although MLT has antioxidant action, it did not influence DNA methylation and not avoid carcinogenesis at low doses.

10.1002/cbin.10920

Cite

Citations (7)

Differential ontogenetic exposure to obesogenic environment induces hyperproliferative status and nuclear receptors imbalance in the rat prostate at adulthood

The Prostate (2016)

Eloísa Zanin Pytlowanciv Maria Etelvina Pinto‐Fochi Vanessa Reame Marina Guimarães Gobbo Daniele Lisboa Ribeiro

BACKGROUND Experimental data indicate that high-fat diet (HFD) may alter proliferative activity and prostate health. However, the consequences of HFD exposure during different periods of ontogenetic development on prostate histophysiology remain to be elucidated. Herein, we compare the influence of obesogenic environment (OE) due to maternal obesity and HFD at different periods of life on proliferative activity and nuclear receptors frequency in the rat ventral prostate and a possible relationship with metabolic and hormonal alterations. METHODS Male Wistar rats (19 weeks old), treated with balanced chow (Control group—C; 3% high-fat, 3.5 Kcal/g), were compared with those exposed to HFD (20% high-fat, 4.9 kcal/g) during gestation (G—maternal obesity), gestation and lactation (GL), from post-weaning to adulthood (WA), from lactation to adulthood (LA) and from gestation to adulthood (GA). After the experimental period, the ventral prostate lobes were removed and analyzed with different methods. RESULTS Metabolic data indicated that G and GL rats became insulin resistant and WA, LA, and GA became insulin resistant and obese. There was a strong inverse correlation between serum testosterone (∼133% lower) and leptin levels (∼467% higher) in WA, LA, and GA groups. Estrogen serum levels increased in GA, and insulin levels increased in all groups, especially in WA (64.8×). OE-groups exhibited prostatic hypertrophy, since prostate weight increased ∼40% in G, GL, LA, and GA and 31% in WA. As indicated by immunohistochemistry, all HFD-groups except G exhibited an increase in epithelial cell proliferation (PCNA-positive) and a decrease in frequency of AR- and ERβ-positive epithelial cells; there was also an increment of ERα-positive stromal cells in comparison with control. Cells containing PPARγ increased in both epithelium and stroma of all OE groups and those expressing LXRα decreased, particularly in groups OE-exposed during gestation (G, GL and GA). CONCLUSIONS OE leads to prostate hypertrophy regardless of the period of development and, except when restricted to gestation, leads to a hyperproliferative status which was correlated to downregulation of AR and LXRα and upregulation of ERα and PPARγ signaling. Prostate 76:662–678, 2016. © 2016 Wiley Periodicals, Inc.

10.1002/pros.23158

Cite

Citations (14)

Melatonin and Docosahexaenoic Acid Decrease Proliferation of PNT1A Prostate Benign Cells via Modulation of Mitochondrial Bioenergetics and ROS Production

Oxidative Medicine and Cellular Longevity (2019)

Guilherme Henrique Tamarindo Daniele Lisboa Ribeiro Marina Guimarães Gobbo Luiz Henrique Alves Guerra Paula Rahal

Prostate cancer development has been associated with changes in mitochondrial activity and reactive oxygen species (ROS) production. Melatonin (MLT) and docosahexaenoic acid (DHA) have properties to modulate both, but their protective role, mainly at early stages of prostate cancer, remains unclear. In this study, the effects of MLT and DHA, combined or not, on PNT1A cells with regard to mitochondria bioenergetics, ROS production, and proliferation-related pathways were examined. Based on dose response and lipid accumulation assays, DHA at 100 μ M and MLT at 1 μ M for 48 h were chosen. DHA doubled and MLT reduced (40%) superoxide anion production, but coincubation (DM) did not normalize to control. Hydrogen peroxide production decreased after MLT incubation only (p<0.01). These alterations affected the area and perimeter of mitochondria, since DHA increased whereas MLT decreased, but such hormone has no effect on coincubation. DHA isolated did not change the oxidative phosphorylation rate (OXPHOS), but decreased (p<0.001) the mitochondrial bioenergetic reserve capacity (MBRC) which is closely related to cell responsiveness to stress conditions. MLT, regardless of DHA, ameliorated OXPHOS and recovered MBRC after coincubation. All incubations decreased AKT phosphorylation; however, only MLT alone inhibited p-mTOR. MLT increased p-ERK1/2 and, when combined to DHA, increased GSTP1 expression (p<0.01). DHA did not change the testosterone levels in the medium, whereas MLT alone or coincubated decreased by about 20%; however, any incubation affected AR expression. Moreover, incubation with luzindole revealed that MLT effects were MTR1/2-independent. In conclusion, DHA increased ROS production and impaired mitochondrial function which was probably related to AKT inactivation; MLT improved OXPHOS and decreased ROS which was related to AKT/mTOR dephosphorylation, and when coincubated, the antiproliferative action was related to mitochondrial bioenergetic modulation associated to AKT and ERK1/2 regulation. Together, these findings point to the potential application of DHA and MLT towards the prevention of proliferative prostate diseases.

Bioenergetics

Mitochondrial ROS

10.1155/2019/5080798

Cite

Citations (22)

Evaluation of doxorubicin in three-dimensional culture of breast cancer cells and the response in PI3K/AKT/PTEN signaling pathways: a pilot study

Women & Health (2022)

Marina Guimarães Gobbo G Fernandes Rafael Fernandes-Ferreira Lennon Pereira Caires Heloisa Cristina Caldas

Breast cancer (BC) has a high mortality rate, which is attributed to the absence of effective treatment markers. Doxorubicin (DOX) was evaluated by molecular docking in vitro in cultured BC spheroids and its association with genes involved in the PI3K/AKT/PTEN signaling pathway. Spheroids were obtained from a primary BC. The selected compound was used for molecular docking experiments. Spheroids were treated with DOX for 1 (D1) and 9 (D9) days. qPCR was used to evaluate PIK3CA, HIF-1α, VEGF-A, PTEN expression. Treatment with DOX (1 µM) significantly increased the number of spheroids (D1), whereas exposure to chemotherapy at 2 µM on D9 was more effective. DOX treatment resulted in significantly higher expression of VEGF-A, HIF-1α and PIK3CA by D1 and HIF-1α and PTEN were upregulated by D9. Compared to treatment on D1 with D9 (1 μM) had significantly higher PTEN and lower PIK3CA gene expression. The genes HIF-1α and PTEN were more expressed with 2 μM of DOX while VEGF-A was downregulated. D1 vs. D9 exhibited reduced VEGF-A, HIF-1α, and PIK3CA expression and upregulation of PTEN expression. DOX effects at the molecular mechanisms can be involved the modulation of genes related to angiogenesis cell proliferation and tumor growth in BC tissue spheroids.

10.1080/03630242.2022.2085842

Cite

Citations (0)

[Effects of ketanserin on glucose metabolism in hypertensive diabetic subjects].

PubMed (1990)

R Carleo Marina Guimarães Gobbo M. S. Bonavita De Matteo A Marco Gallo

In this report the Authors have verified the effects of Ketanserin on glycaemic metabolism of type II diabetic subjects with a moderately high blood pressure. They think that a therapeutic dose of drug is not able to considerably inhibit insulin production. The Authors can assert that the Ketanserin does not influence the glycaemic regulation by therapeutic dose, neither does it increase the diabetic disease, nor disturb the oral hypoglycaemic therapy though it normalizes high blood pressure.

Ketanserin

Carbohydrate Metabolism

Source

Cite

Citations (0)

The protective role of exogen melatonin on the prostate gland under experimental models of metabolic diseases

Marina Guimarães Gobbo Guilherme Henrique Tamarindo Sebastião Roberto Taboga Rejane M. Góes

Department of Biology Institute of Biosciences Humanities and Exact Sciences Universidade Estadual Paulista UNESP

Source

Cite

Citations (0)