Juliana Fiúza-Fernandes’s research while affiliated with University of Minho and other places

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Publications (1)

RSP extract (0.01–5.0 mg/mL) shows no toxic effect in C. elegans. Toxicity was assessed using the food clearance assay. The optical density of the OP50 suspension with RSP extract-treated animals (N2) at the concentrations depicted, was measured daily. The mean optical density (OD) was calculated for each day from triplicate samples and plotted over time. Control DMSO (1%) corresponds to drug vehicle and DMSO at 5% was used as positive (toxic compound) control, n = 5 (independent experiments).
Improvement of motor impairments of the MJD C. elegans model with RSP extract treatment is independent of ATXN3 aggregation load. (A) Locomotion defective behavior of MJD (AT3q130) animals, comparison between treated (RSP extract 0.1–5.0 mg/mL), untreated animals (1% DMSO solvent control), wild type (N2) and AT3q14 controls (1% DMSO). Statistical significant difference was determined using One-way ANOVA and Dunnett’s multiple comparison analysis compared to AT3q130 control: ∗∗∗p ≤ 0.001, ∗∗p ≤ 0.01, ∗p ≤ 0.05; n = 5. (B) Comparison of locomotion defective behavior of N2, AT3q14, and AT3q130 untreated (1% DMSO vehicle control) and RSP extract treated (4 mg/mL) animals. Statistical significant difference determined using Two-way ANOVA and Tukey’s multiple comparisons test compared to untreated (1%DMSO) control: ∗∗∗p ≤ 0.001, ns-not significant, n = 6. (C) Confocal imaging of head region of AT3q130 strain treated with RSP (4 mg/mL, right) in comparison to vehicle control (1% DMSO, left). Confocal microscopy pictures are representative for the three independent experiments. (D) Aggregation load (number and area of aggregations) of AT3q130 animals upon treatment with RSP extract (4 mg/mL) compared to solvent control (1% DMSO). Values shown are the mean (normalized to vehicle treated control) of 10 or more animals per group; number of experiments n = 3, no significant difference, p > 0.05 (unpaired t-test). Data normalized to the 1% DMSO control. Scale bar 50 μm in all represented pictures.
Protective effects of RSP extract supplementation (4 mg/mL) on DAergic neurodegeneration in C. elegans. C. elegans strain with GFP expression in all DAergic neurons (Pdat-1:GFP) grown in media supplemented with 1% DMSO (solvent control) and treated with (A): 0 mM 6-OHDA and 0 mM AA, (B): 10 mM 6-OHDA and 2 mM AA, (C): 25 mM 6-OHDA and 5 mM AA. C. elegans strain expressing GFP proteins in all DAergic neurons (Pdat-1:GFP) grown in media supplemented with (D,E) 4 mg/mL RSP extract pre- and post- treated with (D): 10 mM 6-OHDA and 2 mM AA, (E) 25 mM 6-OHDA and 5 mM AA. The fluorescence signals of DAergic neurons in the animals’ head (CEPs and ADEs) were photographed at 60× magnification using confocal fluorescence microscopy. Scale bar 50 μm in all represented pictures. (F) Total number of DAergic neurons were scored for each condition. Data are expressed as the median ± 10–90 percentile, with results obtained from three independent experiments (n = 3 with ≥ 10 animals per treatment). Significant differences between conditions were determined by non-parametric Kruskal–Wallis test and outlier analysis. #p < 0.05, ###p < 0.001 compared with vehicle alone (no 6-OHDA), ns, ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 compared with respective 6-OHDA concentration control. 6-OHDA: 6-hydroxydopamine; AA: ascorbic acid; DAergic-dopaminergic neurons.
Supplementation with RSP extract suppressed loss of DAergic neurons mediated by alpha-synuclein and tyrosine hydroxylase overexpression in C. elegans. Confocal imaging and quantification of total number of DAergic neurons in Pdat-1:GFP animals (A, day 7 and G, day 10), in Pdat-1:GFP; Pdat-1:α-syn (B, day7 and H, day 10) and in Pdat-1:GFP; Pdat-1:cat-2 (C, day7 and I, day 10) vehicle treated (1% DMSO) animals, as well as in Pdat-1:GFP; Pdat-1:α-syn (D, day7 and J, day 10) and in Pdat-1:GFP; Pdat-1:cat-2 (E, day 7 and K, day 10) RSP extract (4 mg/mL) treated animals. Quantification of total number of DAergic neurons is shown in F (day 7) and L (day 10). Confocal microscopy pictures represent the head region of C. elegans and the pictures are representative of three independent experiments. Data is shown as the median ± 10–90 percentile with results obtained from three independent experiments (n = 3 with ≥ 10 animals per treatment). Significant differences between strains and treatment were determined by Kruskal–Wallis analysis, after outlier analysis: ns no significant difference. ###p < 0.001 compared with Pdat-1:GFP; ns ∗∗∗p < 0.001 compared with respective vehicle treated strain control. Scale bar 50 μm in all represented pictures.
RSP extract supplementation activated transcriptional activity of gst-4 and sod-3, but not of gcs-1 gene promoters in C. elegans reporter strains. Brightfield and widefield fluorescence images of vehicle-(1% DMSO) and RSP-(4 mg/mL) treated Psod-3:GFP (A), Pgst-4:GFP (B) and Pgcs-1:GFP (C) animals. Graphical results shown in (D) represents the GFP fluorescence intensity divided by the total area of each worm (n ≥ 9) normalized to the respective 1% DMSO control. Statistical comparison was done via two-way ANOVA and Bonferroni’s multiple comparisons test after Shapiro–Wilk normality test and outlier analysis, graph shows a representative example of three experimental replicates (n = 3). ns, no significant difference and ∗∗∗p < 0.001 compared with respective control. The pictures presented are from the same experimental day. Time of exposure is maintained constant in vehicle- and RSP-treated animals. Fluorescence intensity of each worm was measured using Fiji (ImageJ, 1.51n) and divided by the total area of the respective animal and normalized to the mean of the vehicle treated worms. Scale bar 100 μm in all represented pictures.

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GST-4-Dependent Suppression of Neurodegeneration in C. elegans Models of Parkinson’s and Machado-Joseph Disease by Rapeseed Pomace Extract Supplementation
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October 2019

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48 Citations

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Genetic mutations and aging-associated oxidative damage underlie the onset and progression of neurodegenerative diseases, like Parkinson’s disease (PD) and Machado-Joseph disease (MJD). Natural products derived from plants have been regarded as important sources of novel bioactive compounds to counteract neurodegeneration. Here, we tested the neuroprotective effect of an ethanolic extract of rapeseed pomace (RSP), a rapeseed (canola) oil production by-product, in C. elegans models of MJD and PD. The extract, containing sinapine and other phenolics, restored motor function of mutant ataxin-3 (ATXN3) animals (MJD) and prevented degeneration of dopaminergic neurons in one toxin-induced and two genetic models of PD. Whole-organism sensors of antioxidant and xenobiotic response activation revealed the induction of phase II detoxification enzymes, including glutathione S- transferase (GST-4) upon RSP extract supplementation. Furthermore in vivo pharmacogenetic studies confirmed gst-4 is required for the therapeutic effect of RSP extract in the two disease models. The results suggest that GST-4-mediated antioxidant pathways may constitute promising therapeutic co-targets for neurodegenerative diseases and confirm the utility of searching for bioactive compounds in novel sources, including food and agricultural waste/by-products, such as RSP.

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Citations (1)

... Additionally, SKN-1, a homolog of mammalian Nrf2, plays a crucial role in longevity and oxidative stress resistance and has been shown to extend the lifespan and mitigate Aβ toxicity in C. elegans [52,53]. The SKN-1-regulated gene gst-4 encodes glutathione S-transferase, which is implicated in many neurodegenerative diseases, with reduced activity observed in AD patients [54]. Moreover, hsp-70, which encodes heat shock proteins, plays a vital role in preventing protein misfolding, which is a common feature of neurodegenerative diseases [35]. ...

Reference:

Cremastra appendiculata Polysaccharides Alleviate Neurodegenerative Diseases in Caenorhabditis elegans: Targeting Amyloid-β Toxicity, Tau Toxicity and Oxidative Stress
GST-4-Dependent Suppression of Neurodegeneration in C. elegans Models of Parkinson’s and Machado-Joseph Disease by Rapeseed Pomace Extract Supplementation

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