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BRCA-1 depletion impairs pro-inflammatory polarization and activation of RAW 264.7 macrophages in a NF-κB-dependent mechanism

da Silva Morrone, Maurilio; Somensi, Nauana; Franz, Lucas; de Miranda Ramos, Vitor; Gasparotto, Juciano; Taís da Rosa, Helen; Sartori, Marcelo; Figueiró, Fabrício; Gelain, Daniel; ZANOTTO-FILHO, ALFEU; Moreira, José Cláudio Fonseca (Universidad de la Costa, 2019-12)

BRCA-1 is a nuclear protein involved in DNA repair, transcriptional regulation, and cell cycle control. Its involvement in other cellular processes has been described. Here, we aimed to investigate the role of BRCA-1 in ...
Characterization and modulation of microglial phenotypes in an animal model of severe sepsis

Michels, Monique; Rocha Abatti, Mariane; Avila, Pricila; Vieira, Andriele; Borges, Heloisa; Carvalho Junior, Celso; Wendhausen, Diogo; Gasparotto, Juciano; Tiefensee Ribeiro, Camila; Moreira, José Cláudio Fonseca; Pens Gelain, Daniel; Dal‐Pizzol, Felipe (Journal of Cellular and Molecular Medicine, 2019-10-26)

We aim to characterize the kinetics of early and late microglial phenotypes after systemic inflammation in an animal model of severe sepsis and the effects of minocycline on these phenotypes. Rats were subjected to CLP, ...
Eugenol mitigated acute lung but not spermatic toxicity of C60 fullerene emulsion in mice

Gomes Pinheiro, Felipe; Moreira-Gomes, Maria Diana; Nascimento Machado, Mariana; dos Santos Almeida, Tailane; da Penha Apolinario Barboza, Priscila; Silva Oliveira, Luis Felipe; Sales Avila Cavalcante, Francisco; Henrique Leal-Cardoso, Jose; Soares Fortunato, Rodrigo; Araujo Zin, Walter (Corporación Universidad de la Costa, 2021)

C60 fullerene (C60) is a nano-pollutant that can damage the respiratory system. Eugenol exhibits significant anti-inflammatory and antioxidant properties. We aimed to investigate the time course of C60 emulsion-induced ...
High fat diet-induced obesity causes a reduction in brain tyrosine hydroxylase levels and non-motor features in rats through metabolic dysfunction, neuroinflammation and oxidative stress

Bittencourt, Aline; Ozorio Brum, Pedro; Tiefensee Ribeiro, Camila; Gasparotto, Juciano; Bortolin, Rafael Calixto; Rodrigues de Vargas, Amanda; Heimfarth, Luana; Farina de Almeida, Roberto; Moreira, José Cláudio Fonseca; de Oliveira, Jade; Pens Gelain, Daniel (Corporación Universidad de la Costa, 2020-10-20)

Obesity is a health problem that has been associated with neuroinflammation, decreased cognitive functions and development of neurodegenerative diseases. Parkinson’s disease (PD) is a chronic neurodegenerative condition ...
Obese rats are more vulnerable to inflammation, genotoxicity and oxidative stress induced by coal dust inhalation than non-obese rats

Gasparotto, Juciano; Chaves Rodrigues, Paloma; Da Boit Martinello, Katia; Da Rosa Siva, Helen Tais; Bortolin, Rafael Calixto; Silva Oliveira, Luis Felipe; Rabelo, Thallita Kelly; Da Silva, Jeferson D; Da Silva, Fernanda Rabaioli; Nordin, Adriane Perachi; Soares, Karina; Borges, Malu Siqueira; Gelain, D. P; Moreira Fonseca, José Cláudio (Ecotoxicology And Environmental Safety, 2018-08-26)

Obesity is an important nutritional disorder worldwide. Its association with environmental pollution may trigger an increase in oxidative stress and inflammatory parameters. Coal is a resource used throughout the world as ...
Obesity associated with coal ash inhalation triggers systemic inflammation and oxidative damage in the hippocampus of rats

Gasparotto, Juciano; Rodrigues Chaves, Paloma; Boit Martinello, Katiada; Silva Oliveira, Luis Felipe; Pens Gelain, Daniel; Fonseca Moreira, José Claudio (Universidad de la Costa, 2019)

People with large amounts of adipose tissue are more vulnerable and more likely to develop diseases where oxidative stress and inflammation play a pivotal role, than persons with a healthy weight. Atmospheric contamination ...

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BRCA-1 depletion impairs pro-inflammatory polarization and activation of RAW 264.7 macrophages in a NF-κB-dependent mechanism
...
da Silva Morrone, Maurilio | 2019-12

BRCA-1 is a nuclear protein involved in DNA repair, transcriptional regulation, and cell cycle control. Its involvement in other cellular processes has been described. Here, we aimed to investigate the role of BRCA-1 in macrophages M(LPS), M(IL-4), and tumor cell-induced differentiation. We used siRNAs to knockdown BRCA-1 in RAW 264.7 macrophages exposed to LPS, IL-4, and C6 glioma cells conditioned medium (CMC6), and evaluated macrophage differentiation markers and functional phagocytic activity as well as DNA damage and cell survival in the presence and absence of BRCA-1. LPS and CMC6, but not by IL-4, increased DNA damage in macrophages, and this effect was more pronounced in BRCA-1-depleted cells, including M(IL-4). BRCA-1 depletion impaired expression of pro-inflammatory cytokines, TNF-α and IL-6, and reduced the phagocytic activity of macrophages in response to LPS. In CMC6-induced differentiation, BRCA-1 knockdown inhibited TNF-α and IL-6 expression which was accompanied by upregulation of the anti-inflammatory markers IL-10 and TGF-β and reduced phagocytosis. In contrast, M(IL-4) phenotype was not affected by BRCA-1 status. Molecular docking predicted that the conserved BRCA-1 domain BRCT can interact with the p65 subunit of NF-κB. Immunofluorescence assays showed that BRCA-1 and p65 co-localize in the nucleus of LPS-treated macrophages and reporter gene assay showed that depletion of BRCA-1 decreased LPS and CMC6-induced NF-κB transactivation. IL-4 had no effect upon NF-κB. Taken together, our findings suggest a role of BRCA-1 in macrophage differentiation and phagocytosis induced by LPS and tumor cells secretoma, but not IL-4, in a mechanism associated with inhibition of NF-κB.

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Characterization and modulation of microglial phenotypes in an animal model of severe sepsis
...
Michels, Monique | 2019-10-26

We aim to characterize the kinetics of early and late microglial phenotypes after systemic inflammation in an animal model of severe sepsis and the effects of minocycline on these phenotypes. Rats were subjected to CLP, and some animals were treated with minocycline (10 ug/kg) by i.c.v. administration. Animals were killed 24 hours, 5, 10 and 30 days after sepsis induction, and serum and hippocampus were collected for subsequent analyses. Real‐time PCR was performed for M1 and M2 markers. TNF‐α, IL‐1β, IL‐6, IL‐10, CCL‐22 and nitrite/nitrate levels were measured. Immunofluorescence for IBA‐1, CD11b and arginase was also performed. We demonstrated that early after sepsis, there was a preponderant up‐regulation of M1 markers, and this was not switched to M2 phenotype markers later on. We found that up‐regulation of both M1 and M2 markers co‐existed up to 30 days after sepsis induction. In addition, minocycline induced a down‐regulation, predominantly, of M1 markers. Our results suggest early activation of M1 microglia that is followed by an overlap of both M1 and M2 phenotypes and that the beneficial effects of minocycline on sepsis‐associated brain dysfunction may be related to its effects predominantly on the M1 phenotype.

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Eugenol mitigated acute lung but not spermatic toxicity of C60 fullerene emulsion in mice
...
Gomes Pinheiro, Felipe | 2021

C60 fullerene (C60) is a nano-pollutant that can damage the respiratory system. Eugenol exhibits significant anti-inflammatory and antioxidant properties. We aimed to investigate the time course of C60 emulsion-induced pulmonary and spermatic harms, as well as the effect of eugenol on C60 emulsion toxicity. The first group of mice (protocol 1) received intratracheally C60 emulsion (1.0 mg/kg BW) or vehicle and were tested at 12, 24, 72 and 96 h (F groups) thereafter. The second group of mice (protocol 2) received intratracheally C60 emulsion or vehicle, 1 h later were gavaged with eugenol (150 mg/kg) or vehicle, and experiments were done 24 h after instillation. Lung mechanics, morphology, redox markers, cytokines and epididymal spermatozoa were analyzed. Protocol 1: Tissue damping (G) and elastance (H) were significantly higher in F24 than in others groups, except for H in F72. Morphological and inflammatory parameters were worst at 24 h and subsequently declined until 96 h, whereas redox and spermatic parameters worsened over the whole period. Eugenol eliminated the increase in G, H, cellularity, and cytokines, attenuated oxidative stress induced by C60 exposure, but had no effect on sperm. Hence, exposure to C60 emulsion deteriorated lung morphofunctional, redox and inflammatory characteristics and increased the risk of infertility. Furthermore, eugenol avoided those changes, but did not prevent sperm damage.

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High fat diet-induced obesity causes a reduction in brain tyrosine hydroxylase levels and non-motor features in rats through metabolic dysfunction, neuroinflammation and oxidative stress
...
Bittencourt, Aline | 2020-10-20

Obesity is a health problem that has been associated with neuroinflammation, decreased cognitive functions and development of neurodegenerative diseases. Parkinson’s disease (PD) is a chronic neurodegenerative condition characterized by motor and non-motor abnormalities, increased brain inflammation, α-synuclein protein aggregation and dopaminergic neuron loss that is associated with decreased levels of tyrosine hydroxylase (TH) in the brain. Diet-induced obesity is a global epidemic and its role as a risk factor for PD is not clear. Herein, we showed that 25 weeks on a high-fat diet (HFD) promotes significant alterations in the nigrostriatal axis of Wistar rats. Obesity induced by HFD exposure caused a reduction in TH levels and increased TH phosphorylation at serine 40 in the ventral tegmental area. These effects were associated with insulin resistance, increased tumor necrosis factor-α levels, oxidative stress, astrogliosis and microglia activation. No difference was detected in the levels of α-synuclein. Obesity also induced impairment of locomotor activity, total mobility and anxiety-related behaviors that were identified in the open-field and light/dark tasks. There were no changes in motor coordination or memory. Together, these data suggest that the reduction of TH levels in the nigrostriatal axis occurs through an α-synuclein-independent pathway and can be attributed to brain inflammation, oxidative/nitrosative stress and metabolic disorders induced by obesity

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Obese rats are more vulnerable to inflammation, genotoxicity and oxidative stress induced by coal dust inhalation than non-obese rats
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Gasparotto, Juciano | 2018-08-26

Obesity is an important nutritional disorder worldwide. Its association with environmental pollution may trigger an increase in oxidative stress and inflammatory parameters. Coal is a resource used throughout the world as an important fuel source for generating electricity. The ashes released by the coal combustion cause serious problems for human health due to their high toxicity and their capacity to bioaccumulate. The aim of this work was to investigate the effects of coal dust inhalation in the organs of obese and non-obese Wistar rats. Pro-inflammatory cytokines, oxidative stress, oxidative damage, histological analysis, comet assay, and micronuclei were investigated. Both obesity and coal dust inhalation increased the pro-inflammatory cytokines IL-1β and TNF-α and decreased HSP70 levels in serum, however, in obese animals that inhaled coal dust these changes were more pronounced. Liver histological analysis showed severe microvesicular steatosis in obese animals that inhaled coal dust. Lung histologic investigation showed abnormalities in lung structure of animals exposed to coal dust and showed severe lung distensibility in obese animals exposed to coal dust.

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Obesity associated with coal ash inhalation triggers systemic inflammation and oxidative damage in the hippocampus of rats
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Gasparotto, Juciano | 2019

People with large amounts of adipose tissue are more vulnerable and more likely to develop diseases where oxidative stress and inflammation play a pivotal role, than persons with a healthy weight. Atmospheric contamination is a reality to which a large part of the worldwide population is exposed. Half of today's global electrical energy is derived from coal. Each organism, in its complexity, responds in different ways to dietary compounds and air pollution. The objective of this study was to investigate the effects of obesity and coal ash inhalation within the parameters of oxidative damage and inflammation in different regions of the brain of rats. A diet containing high-fat concentration was administered chronically to rats, along with exposure to coal ash, simulating the contamination that occurs daily throughout human life. High-resolution transmission electron microscopy was performed to identify the particles present in coal ash samples. Our results demonstrated that obese rats exposed to coal ash inhalation were more affected by oxidative damage with subsequent systemic inflammation in the hippocampus. Since there is an inflammatory predisposition caused by obesity, the inhalation of nanoparticles increases the levels of free radicals, resulting in systemic inflammation and oxidative damage, which can lead to chronic neurodegeneration.

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Browsing by Subject "Inflammation"

BRCA-1 depletion impairs pro-inflammatory polarization and activation of RAW 264.7 macrophages in a NF-κB-dependent mechanism ﻿

Characterization and modulation of microglial phenotypes in an animal model of severe sepsis ﻿

Eugenol mitigated acute lung but not spermatic toxicity of C60 fullerene emulsion in mice ﻿

High fat diet-induced obesity causes a reduction in brain tyrosine hydroxylase levels and non-motor features in rats through metabolic dysfunction, neuroinflammation and oxidative stress ﻿

Obese rats are more vulnerable to inflammation, genotoxicity and oxidative stress induced by coal dust inhalation than non-obese rats ﻿

Obesity associated with coal ash inhalation triggers systemic inflammation and oxidative damage in the hippocampus of rats ﻿

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BRCA-1 depletion impairs pro-inflammatory polarization and activation of RAW 264.7 macrophages in a NF-κB-dependent mechanism

Characterization and modulation of microglial phenotypes in an animal model of severe sepsis

Eugenol mitigated acute lung but not spermatic toxicity of C60 fullerene emulsion in mice

High fat diet-induced obesity causes a reduction in brain tyrosine hydroxylase levels and non-motor features in rats through metabolic dysfunction, neuroinflammation and oxidative stress

Obese rats are more vulnerable to inflammation, genotoxicity and oxidative stress induced by coal dust inhalation than non-obese rats

Obesity associated with coal ash inhalation triggers systemic inflammation and oxidative damage in the hippocampus of rats

BRCA-1 depletion impairs pro-inflammatory polarization and activation of RAW 264.7 macrophages in a NF-κB-dependent mechanism

Characterization and modulation of microglial phenotypes in an animal model of severe sepsis

Eugenol mitigated acute lung but not spermatic toxicity of C60 fullerene emulsion in mice

High fat diet-induced obesity causes a reduction in brain tyrosine hydroxylase levels and non-motor features in rats through metabolic dysfunction, neuroinflammation and oxidative stress

Obese rats are more vulnerable to inflammation, genotoxicity and oxidative stress induced by coal dust inhalation than non-obese rats

Obesity associated with coal ash inhalation triggers systemic inflammation and oxidative damage in the hippocampus of rats