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Characterizing the transcriptomic profile of the cortex within the long-term window of ischemic tolerance mediated by resveratrol preconditioning

ABSTRACT: To identify novel genes and adaptations induced by resveratrol preconditioning that could promote long-term cerebral ischemic tolerance. After analyzing the results, we identified only 155 differentially expressed genes among which the majority of genes consisting of 126 were downregulated and only 29 genes were upregulated. The downregulated genes clustered into biological processes involved in regulating the memebrane potential, gene expression regulation, and neurotrasmitter transport secrection. While the upregulated gene included immediate early genes and genes involved in antioxidant defense.

ORGANISM(S): Mus musculus

PROVIDER: GSE113298 | GEO | 2019/01/01

REPOSITORIES: GEO

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Project description:Background: Resveratrol has been demonstrated to exert pleiotropic health beneficial effects. Among the various mechanisms of action antioxidant, anti-inflammatory, cardio- and cancer-protective outcomes have been reported. Particularly, an important function of this natural compound against atherosclerosis has been postulated and the action of resveratrol on lipids and lipoprotein levels seems to be of relevance in this pathology, but also for other metabolic diseases. Accordingly, taking into consideration the straight contact of resveratrol with the intestine, this study aimed to gain insights into the protective effects of trans-resveratrol on enterocyte physiology and metabolism in proinflammatory conditions. For this purpose, a DNA microarray analysis was conducted in Caco-2 cells where global gene expression profile at intestinal level was screened. Cells were pretreated with 50 Î¼Î? of trans-resveratrol and, subsequently, lipopolysaccharide (LPS) was added for 48 h. Results: The microarray analysis revealed 121 genes differentially expressed between resveratrol-treated and non-treated cells (B> 0). Four genes, inhibitor of DNA binding 1(ID1), histidine-rich glycoprotein (HRG), NADPH oxidase (NOX1) and sprouty homolog 1 (SPRY), were upregulated by LPS treatment, but significantly downregulated with trans-resveratrol pretreatment (padj< 0.05). Moreover, genes implicated in pathways related to lipid metabolism, such as synthesis of lipids (z-score= -1.195) and concentration of cholesterol (z-score= -0.109), were markedly downregulated by trans-resveratrol. Other genes implicated in lipid metabolism, but also in cell death and survival function, such as transcription factors KrÃ¼ppel-like factor 5 (KLF5) and amphiregulin (AREG), were also significantly inhibited by trans-resveratrol pretreatment. RT-qPCR-data confirmed the microarray results. Special mention deserves acyl-CoA synthetase long-chain family member 3 (ACSL3) and endothelial lipase (LIPG), which were downregulated by the stilbene and have been previously associated with fatty acid synthesis and obesity in other tissues. Conclusions: This study envisages that trans-resveratrol might exert important anti-lipogenic effect at intestinal level under proinflammatory conditions, which have not been previously described. The experiment was conducte in Caco-2 cells. There were three experimental groups (n=5), Caco-2 cells stimulated with lipopolysaccharides (LPS), Caco-2 cells stimulated with LPS and pre-treated with trans-resveratrol (LPS+RSV) and non-treated Caco-2 cells.

Project description:Background: Resveratrol has been demonstrated to exert pleiotropic health beneficial effects. Among the various mechanisms of action antioxidant, anti-inflammatory, cardio- and cancer-protective outcomes have been reported. Particularly, an important function of this natural compound against atherosclerosis has been postulated and the action of resveratrol on lipids and lipoprotein levels seems to be of relevance in this pathology, but also for other metabolic diseases. Accordingly, taking into consideration the straight contact of resveratrol with the intestine, this study aimed to gain insights into the protective effects of trans-resveratrol on enterocyte physiology and metabolism in proinflammatory conditions. For this purpose, a DNA microarray analysis was conducted in Caco-2 cells where global gene expression profile at intestinal level was screened. Cells were pretreated with 50 μΜ of trans-resveratrol and, subsequently, lipopolysaccharide (LPS) was added for 48 h. Results: The microarray analysis revealed 121 genes differentially expressed between resveratrol-treated and non-treated cells (B> 0). Four genes, inhibitor of DNA binding 1(ID1), histidine-rich glycoprotein (HRG), NADPH oxidase (NOX1) and sprouty homolog 1 (SPRY), were upregulated by LPS treatment, but significantly downregulated with trans-resveratrol pretreatment (padj< 0.05). Moreover, genes implicated in pathways related to lipid metabolism, such as synthesis of lipids (z-score= -1.195) and concentration of cholesterol (z-score= -0.109), were markedly downregulated by trans-resveratrol. Other genes implicated in lipid metabolism, but also in cell death and survival function, such as transcription factors Krüppel-like factor 5 (KLF5) and amphiregulin (AREG), were also significantly inhibited by trans-resveratrol pretreatment. RT-qPCR-data confirmed the microarray results. Special mention deserves acyl-CoA synthetase long-chain family member 3 (ACSL3) and endothelial lipase (LIPG), which were downregulated by the stilbene and have been previously associated with fatty acid synthesis and obesity in other tissues. Conclusions: This study envisages that trans-resveratrol might exert important anti-lipogenic effect at intestinal level under proinflammatory conditions, which have not been previously described.

Project description:Ischemic preconditioning represents the most powerful mechanism of cardioprotection. The mechanisms mediating the second window of preconditioning (SWOP) differ from those mediating first window preconditioning. We hypothesized that chronic ischemia induced by repetitive ischemic stimuli would be mediated by yet different molecular mechanisms. Accordingly, conscious, chronically instrumented pigs (n=5/group) were submitted to a protocol of classical SWOP (two 10-min episodes of coronary artery occlusion followed by 24 hr reperfusion) and compared to pigs submitted to repetitive occlusion/reperfusion (RCO) by repeating 6 episodes of SWOP 12 hrs apart, and to a model of repetitive coronary stenosis (RCS), in which 6 episodes of 90 min coronary stenosis were performed 12 hrs apart. Microarray analysis was performed on the three models. There was an 85% homology in gene response between both models of RCO and RCS, whereas SWOP was qualitatively different. Both models of RCO and RCS but not SWOP showed a down-regulation of genes encoding proteins involved in oxidative metabolism, and an up-regulation of genes involved in protein synthesis and unfolded protein response, autophagy, heat shock response, protein secretion, and a strong activation of the NF-ÎºB signaling pathway. Two thirds of the genes regulated in the three models showed a gradual pattern of up- or down-regulation, in which RCO was quantitatively intermediary between RCS and SWOP. Therefore, the regulated genes in response to chronic, repetitive episodes of ischemia differ radically from classical first or second window preconditioning. Four groups of pigs were used for the study, i.e., control (n=5), SWOP (n=5), RCO (n=5), and RCS (n=5). SWOP was induced by two episodes of 10 min coronary artery occlusion (CAO), each followed by 10 min coronary artery reperfusion (CAR). RCO was induced by the same stimulus as SWOP (two cycles of 10 min CAO and 10 min CAR), but repeated six times every 12 hrs. RCS was induced by 90 min low-flow ischemia repeated six times every 12 hrs.

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Characterizing the transcriptomic profile of the cortex within the long-term window of ischemic tolerance mediated by resveratrol preconditioning

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