Mineralization rate and biochemical fate of natural polymers and microplastics in freshwaters
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PROVIDER: PRJEB51211 | ENA |
REPOSITORIES: ENA
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Project description:Microplastics represent a growing environmental concern for the oceans due to their potential capability to adsorb different classes of pollutants, thus representing a still unexplored source of exposure for aquatic organisms. In this study polystyrene (PS) microplastics were characterized for their capability to adsorb pyrene (PYR) as model compound for polycyclic aromatic hydrocarbons, and transfer this chemical to filter feeding mussels Mytilus galloprovincialis. Gene expression analyses of Mytilus galloprovincialis exposed to polystyrene (PS) microplastics and to polystyrene contaminated with pyrene (PS-PYR) have been performed trough a DNA microarray platform.
2014-12-27 | GSE57460 | GEO
Project description:The contamination of marine ecosystems with microplastics, such as the polymer polyethylene, a commonly used component of single-use packaging, is of global concern. Although it has been suggested that biodegradable polymers, such as polylactic acid, may be used to replace some polyethylene packaging, little is known about their effects on marine organisms. Blue mussels, Mytilus edulis, have become a “model organism” for investigating the effects of microplastics in marine ecosystems. We show here that repeated exposure, over a period of 52 days in an outdoor mesocosm setting, of M. edulis to polyethylene microplastics reduced the number of byssal threads produced and the attachment strength (tenacity) by ~50%. Exposure to either type of microplastic altered the haemolymph proteome and, although a conserved response to microplastic exposure was observed, overall polyethylene resulted in more changes to protein abundances than polylactic acid. Many of the proteins affected are involved in vital biological processes, such as immune- and stress- regulation, metabolism and cellular and structural development. Our study highlights the utility of mass spectrometry-based proteomics to assess the health of key marine organisms and identifies the potential mechanisms by which microplastics, both conventional and biodegradable, could affect their ability to form and maintain reefs.
2019-01-02 | PXD011567 | Pride
Project description:Polyethylene terephthalate microplastics generated from disposable water bottles induce interferon signalling pathway in mouse lung epithelial cells
2024-08-16 | GSE269348 | GEO
Project description:Microplastics (MPs) are considered as one of the main reasons for male and female infertility. However, the reproductive toxicity and its related mechanisms are understood by animal models with acute exposure to MPs at present. In the study, we show the low-dose polystyrene microplastics (PSMPs) exposure results in severely abnormal reproduction in female, but not male in mouse model, exhibiting failed oocyte meiotic maturation. Mechanistically, the PSMPs exposure induces the over-activation of cell metabolism pathways, insufficient HDACs and H4K16 hyperacetylation in oocytes in vivo and in vitro. By addition of HDAC3 inhibitor, the failed oocyte maturation, over-activation of cell metabolism pathways and H4K16 hyperacetylation are recapitulated, and the overexpression of HDAC3 can rescue the defects of meiotic maturation induced by PSMPs. Our observations suggest a direct link of the maturation defects induced by PSMPs to HDAC3 insufficiency. Thus, we propose the potential treatments for therapy of the failed meiotic maturation of oocyte from women highly exposed to MPs by activating or supplying HDAC3.
2024-03-06 | GSE259264 | GEO
Project description:Cartilage mineralization is a tightly controlled process, imperative for skeletal growth and fracture repair. However, in osteoarthritis (OA), cartilage mineralization may impact the joint range of motion, inflict pain and may increase chances for joint effusion. Here we attempt to understand the link between inflammation and cartilage mineralization by targeting SIRT1 and LEF1, both reported to have contrasting effects on cartilage.
2022-05-16 | GSE200522 | GEO
Project description:Candida albicans exposure to antifungal polymers
| PRJEB65085 | ENA
Project description:Riverine microplastics and associated microbial assemblages
| PRJEB41771 | ENA
Project description:Background: Circulating polymers of alpha1-antitrypsin (α1AT) are chemo-attractant for neutrophils and contribute to inflammation in pulmonary, vascular and adipose tissues. Cellular factors affecting the intracellular itinerary of mutant polymerogenic α1AT remain obscure. Methods: Here, we report on an unbiased genome-wide CRISPR/Cas9 screen for regulators of trafficking of the polymerogenic α1AT-H334D variant. Single guide RNAs targeting genes whose inactivation enhanced accumulation of polymeric α1AT were enriched by iterative construction of CRISPR libraries based on genomic DNA from fixed cells selected for high polymer content by fluorescence-activated cell sorting. This approach bypassed the limitation to conventional enrichment schemes imposed by cell fixation. Results: Our screen identified 121 genes involved in polymer retention at false discovery rate < 0.1. From that set of genes, the pathway ‘cargo loading into COPII-coated vesicles’ was overrepresented with 16 significant genes, including two transmembrane cargo receptors, LMAN1 (ERGIG-53) and SURF4. LMAN1 and SURF4-disrupted cells displayed a secretion defect extended beyond α1AT monomers to polymers, whose low-level secretion was especially dependent on SURF4 and correlated with SURF4-α1AT-H334D physical interaction and with enhanced co-localisation of polymeric α1AT-H334D with the endoplasmic reticulum (ER). Conclusions: These findings suggest that ER cargo receptors co-ordinate intracellular progression of α1AT out of the ER and modulate the accumulation of polymeric α1AT not only by controlling the concentration of precursor monomers but also through a previously-unrecognised role in secretion of the polymers themselves.
2021-06-02 | GSE158574 | GEO
Project description:The serpinopathies are human pathologies caused by mutations that promote polymerisation and intracellular deposition of proteins of the serpin superfamily, leading to a poorly understood cell toxicity. The dementia familial encephalopathy with neuroserpin inclusion bodies (FENIB) is caused by polymerisation of the neuronal serpin neuroserpin (NS) within the endoplasmic reticulum (ER) of neurons. We have generated transgenic neural progenitor cell (NPC) cultures from mouse embryonic cerebral cortex, stably expressing the control protein GFP (green fluorescent protein), or human wild type, G392E or deltaNS. We have characterised these cells in the proliferative state and after differentiation to neurons. Our results show that G392E NS formed polymers that were mostly retained within the ER, while wild type NS was correctly secreted as a monomeric protein into the culture medium. DeltaNS was absent at steady state due to its rapid degradation, but it was easily detected upon proteasomal block. Looking at their intracellular distribution, wild type NS was found in partial co-localisation with ER and Golgi markers, while G392E NS was localised within the ER only. Furthermore, polymers of NS were detected by ELISA and immunofluorescence in neurons expressing the mutant but not the wild type protein. We used our model system to investigate which cellular pathways were activated by intracellular polymers of G392E NS by performing RNA sequencing of differentiated cells expressing G392E NS or the negative control protein GFP, and identified 747 genes with a significant upregulation (623) or downregulation (124) in G392E NS-expressing cells. We focused our attention on genes involved in the defence against oxidative stress that were up-regulated in cells expressing G392E NS. Inhibition of these defences by specific pharmacological reagents uncovered the damaging effects of NS polymers. Our results support a role for oxidative stress in the cellular toxicity underlying the neurodegenerative dementia FENIB.
2017-03-11 | GSE96096 | GEO