Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1123503 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29413485.fastq.gz | Fastqsanger.gz | |||
| SRR29413486.fastq.gz | Fastqsanger.gz | |||
| SRR29413487.fastq.gz | Fastqsanger.gz | |||
| SRR29413488.fastq.gz | Fastqsanger.gz | |||
| SRR29413489.fastq.gz | Fastqsanger.gz |
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Project description:Proteomics analysis of the underlying mechanisms of PS-NPs-induced reproductive toxicity in females
| PXD080517 |
Project description:The emerging environmental health issue posed by micro (nano) plastics (MNPs) has raised significant concerns. Accumulating evidence suggested that MNPs can bioaccumulate in gonads and impair fertility in animals, yet the underlying cellular mechanisms and tissue-specific responses remain poorly understood. In this study, we employed in vivo and in vitro models to systematically investigate the impact of polystyrene microplastics (PS-MPs; 100 nm and 5 µm) on ovarian development and function in pubertal female mice. Following 35 days of exposure, we observed size-dependent reproductive toxicity, with 100 nm PS-MPs causing reduced body weight gain and ovarian size, and compromised ovarian structures and functions, including altered follicle and corpora lutea counts, alongside disrupted hormone levels. Leveraging single-cell RNA-sequencing (scRNA-seq), we uncovered profound alterations in intracellular communication networks and signaling flow patterns across seven identified ovarian cell types. Granulosa cells (GCs) were identified as the primary target PS-MPs, exhibiting marked transcriptional changes, including dysregulation of FSCN1, a critical actin cytoskeleton regulator. In vitro experiments confirmed that only 100 nm PS-MPs were internalized by GCs, leading to cell cycle arrest, necroptosis and hormonal dysfunction. Mechanistically, PS-MPs triggered F-actin cytoskeleton remodeling, increasing cell stiffness and reducing histone marks (H3K4me3, H3K27ac) associated with chromatin accessibility. Integrated ATAC-seq and RNA-seq analyses implicated STAT1 as a key transcriptional regulator driving PS-MP-induced epigenetic and transcriptional changes. Overall, this study first revealed PS-MP-mediated reproductive toxicity from a single-cell perspective, identifying granulosa cells as particularly vulnerable targets. It uncovered novel mechanisms involving cytoskeletal disruption and epigenetic reprogramming, while demonstrating size-dependent internalization patterns that directly correlate with reproductive impairment. These findings provide unprecedented insights into the molecular and epigenetic consequences of MNPs in mammalian reproduction, emphasizing the potential health risks of environmental MNPs exposure.
2026-08-02 | GSE306390 | GEO
Project description:The emerging environmental health issue posed by micro (nano) plastics (MNPs) has raised significant concerns. Accumulating evidence suggested that MNPs can bioaccumulate in gonads and impair fertility in animals, yet the underlying cellular mechanisms and tissue-specific responses remain poorly understood. In this study, we employed in vivo and in vitro models to systematically investigate the impact of polystyrene microplastics (PS-MPs; 100 nm and 5 µm) on ovarian development and function in pubertal female mice. Following 35 days of exposure, we observed size-dependent reproductive toxicity, with 100 nm PS-MPs causing reduced body weight gain and ovarian size, and compromised ovarian structures and functions, including altered follicle and corpora lutea counts, alongside disrupted hormone levels. Leveraging single-cell RNA-sequencing (scRNA-seq), we uncovered profound alterations in intracellular communication networks and signaling flow patterns across seven identified ovarian cell types. Granulosa cells (GCs) were identified as the primary target PS-MPs, exhibiting marked transcriptional changes, including dysregulation of FSCN1, a critical actin cytoskeleton regulator. In vitro experiments confirmed that only 100 nm PS-MPs were internalized by GCs, leading to cell cycle arrest, necroptosis and hormonal dysfunction. Mechanistically, PS-MPs triggered F-actin cytoskeleton remodeling, increasing cell stiffness and reducing histone marks (H3K4me3, H3K27ac) associated with chromatin accessibility. Integrated ATAC-seq and RNA-seq analyses implicated STAT1 as a key transcriptional regulator driving PS-MP-induced epigenetic and transcriptional changes. Overall, this study first revealed PS-MP-mediated reproductive toxicity from a single-cell perspective, identifying granulosa cells as particularly vulnerable targets. It uncovered novel mechanisms involving cytoskeletal disruption and epigenetic reprogramming, while demonstrating size-dependent internalization patterns that directly correlate with reproductive impairment. These findings provide unprecedented insights into the molecular and epigenetic consequences of MNPs in mammalian reproduction, emphasizing the potential health risks of environmental MNPs exposure.
2026-08-02 | GSE306389 | GEO
Project description:The emerging environmental health issue posed by micro (nano) plastics (MNPs) has raised significant concerns. Accumulating evidence suggested that MNPs can bioaccumulate in gonads and impair fertility in animals, yet the underlying cellular mechanisms and tissue-specific responses remain poorly understood. In this study, we employed in vivo and in vitro models to systematically investigate the impact of polystyrene microplastics (PS-MPs; 100 nm and 5 µm) on ovarian development and function in pubertal female mice. Following 35 days of exposure, we observed size-dependent reproductive toxicity, with 100 nm PS-MPs causing reduced body weight gain and ovarian size, and compromised ovarian structures and functions, including altered follicle and corpora lutea counts, alongside disrupted hormone levels. Leveraging single-cell RNA-sequencing (scRNA-seq), we uncovered profound alterations in intracellular communication networks and signaling flow patterns across seven identified ovarian cell types. Granulosa cells (GCs) were identified as the primary target PS-MPs, exhibiting marked transcriptional changes, including dysregulation of FSCN1, a critical actin cytoskeleton regulator. In vitro experiments confirmed that only 100 nm PS-MPs were internalized by GCs, leading to cell cycle arrest, necroptosis and hormonal dysfunction. Mechanistically, PS-MPs triggered F-actin cytoskeleton remodeling, increasing cell stiffness and reducing histone marks (H3K4me3, H3K27ac) associated with chromatin accessibility. Integrated ATAC-seq and RNA-seq analyses implicated STAT1 as a key transcriptional regulator driving PS-MP-induced epigenetic and transcriptional changes. Overall, this study first revealed PS-MP-mediated reproductive toxicity from a single-cell perspective, identifying granulosa cells as particularly vulnerable targets. It uncovered novel mechanisms involving cytoskeletal disruption and epigenetic reprogramming, while demonstrating size-dependent internalization patterns that directly correlate with reproductive impairment. These findings provide unprecedented insights into the molecular and epigenetic consequences of MNPs in mammalian reproduction, emphasizing the potential health risks of environmental MNPs exposure.
2026-08-02 | GSE305839 | GEO
Project description:Aims: Polystyrene microplastics (PS-MPs) are emerging environmental pollutants, but their impact on lung cancer treatment remains unclear. This study investigates how PS-MPs affect radiotherapy efficacy in lung cancer, focusing on their role in ferroptosis regulation and NF-κB pathway activation. Results: PS-MPs were rapidly internalized by lung cancer cells and remained detectable across multiple passages. Exposure to PS-MPs promoted lung cancer cell proliferation, increased mitochondrial length, and elevated Ki67 and c-Myc expression. Following ionizing radiation, PS-MPs significantly attenuated radiation-induced ferroptosis, as evidenced by reduced mitochondrial damage, lipid peroxidation, and GSH depletion. Transcriptomic analysis revealed that PS-MPs activated the NF-κB pathway, leading to increased phosphorylation of IKKβ, IκBα degradation, and enhanced nuclear translocation of NF-κB. In vivo, PS-MPs accumulated in lung tumor-bearing mice, reducing radiotherapy efficacy by increasing tumor volume and weight while decreasing survival rates. Knockdown of NF-κB restored ferroptosis sensitivity and mitigated PS-MPs-induced radioresistance, confirming the NF-κB-dependent inhibition of ferroptosis. Innovation and Conclusion: This study provides the first evidence that PS-MPs impair radiotherapy efficacy in lung cancer by suppressing ferroptosis via NF-κB activation. Unlike previous research focusing on microplastic toxicity in normal tissues, our findings highlight their oncological impact and potential role as an environmental factor influencing cancer therapy resistance. These results emphasize the need for further investigation into microplastics as emerging disruptors of redox homeostasis in oncology and their broader implications for environmental and cancer research.
2025-09-08 | GSE307179 | GEO
Project description:The in vitro and in vivo toxicity of copper oxide nanoparticles (CuO NPs) is attributed to both particle and dissolved copper ion species. However, a clear understanding of 1) the specific cellular responses that are modulated by the two species and 2) the temporal dynamics in toxicity, as the proportional amount of particulate and ionic forms change over time, is lacking. In the current study, in vitro responses to microparticulate CuO (CuO MPs), CuO NPs, and dissolved Cu2+ were characterized in order to elucidate particle and ion induced kinetic effects. Particle dissolution experiments were carried out in relevant cell culture medium, using CuO NPs and MPs. Mouse lung epithelial cells were exposed for 2 - 48 h with 1 - 25 µg/mL CuO MPs, CuO NPs, or 7 & 54 µg/mL CuCl2. Cellular viability and genome-wide transcriptional responses were assessed. Dose and time dependent cytotoxicity was observed in CuO NP exposed cells, which was delayed and subtle in CuCl2 and not observed in CuO MPs treated cells. Analyses of differentially expressed genes and associated pathway perturbations showed that dissolved ions released by CuO NPs in extracellular medium are insufficient to account for the observed potency and cytotoxicity. Further organization of gene expression results in an Adverse Outcome Pathway (AOP) framework revealed a series of key events potentially involved in CuO NPs toxicity. The AOP is applicable to soluble metal oxide nanoparticle induced toxicity in general, and thus, can facilitate the development of in vitro alternative strategies to screen their toxicity.
2022-11-03 | GSE161017 | GEO
Project description:Nanoplastics (NPs), plastic particles smaller than 1 μm, have gained increasing attention due to their potential health effects. Experimental studies in animals have shown that NPs can pass biological barriers, reach the female reproductive tract, and enter the ovary. Their presence in the ovary might have profound consequences for reproductive endpoints, such as oocyte development. This study aimed to investigate the uptake and associated effects of polystyrene (PS) NPs on oocyte and embryo development using a bovine in vitro fertilization (IVF) model. Bovine cumulus-oocyte complexes (COCs) were exposed to pristine PS-NPs (50 nm or 200 nm) at different doses during in vitro maturation (23 hours), followed by IVF and embryo culture. RNA sequencing was performed to investigate mechanisms involved in possible effects on oocyte maturation. Confocal microscopy confirmed the internalization of 50 nm and 200 nm PS-NPs into cumulus cells, however, only 50 nm particles were able to transfer into oocytes. Additionally, exposure to 50 nm PS-NPs at 3 μg/mL significantly delayed oocyte nuclear maturation and early embryo development. At this dose, RNA sequencing did not identify differentially expressed genes in the COCs, however, gene set enrichment analyses did indicate effects on mitochondrial processes. Nevertheless, subsequent analysis on mitochondrial activity remained unaffected.
2026-02-06 | GSE299785 | GEO
Project description:Plastic pollution, especially from mismanaged waste degrading into nanoplastics (NPs), poses a growing threat to environmental and human health. Polystyrene NPs (PS-NPs) are particularly prevalent, infiltrating ecosystems and accumulating in organs, including the brain. While NPs are linked to behavioral, metabolic, and developmental effects, their impact on reproduction and fertility remains poorly understood. Declining fertility rates suggest environmental toxicants like NPs may contribute to adverse reproductive outcomes. Reproductive function relies on the hypothalamus-pituitary-gonad (HPG) axis, centrally regulated by gonadotropin-releasing hormone (GnRH) neurons. These neurons originate in the nasal placode and migrate to the hypothalamus during embryogenesis. Altered GnRH neuron development or release can lead to absent puberty and infertility, whose genetic causes explain only 50% of known cases. In this context, environmental factors including NPs might contribute to the etiology of these disorders. In this work, we take advantage of an established model of migrating GnRH neurons (GN11) to assess PS-NPs effects and to provide the first evidence that these environmental factors interfere with cellular and molecular processes of GnRH neurons, thus suggesting a novel mechanism contributing to idiopathic infertility.
2026-03-10 | GSE295898 | GEO
Project description:Plastic particles in water environment can adsorb heavy metals, leading to combined toxicity to aquatic organisms. However, current conclusions are mostly obtained based on cell population-average responses. Heterogeneity effects among cell populations in aquatic organisms remain unclear. This study analyzed the heterogeneity effects of 200 μg/L 100 nm polystyrene nanoplastics (PS-NPs), 50 μg/L lead (Pb), and their combined exposures on zebrafish intestine cells by single-cell RNA sequencing.A total of 38640 cells in the zebrafish intestine was obtained and identified as seven cell populations, including enterocytes, macrophages, neutrophils, B cells, T cells, enteroendocrine cells, and goblet cells.Co-exposure of PS-NPs and Pb caused similar transcriptome profiles with PS-NPs exposure in macrophages, which changed immunological recognition processes. The Pb exposure influenced the macrophages by direct cytotoxicity. However, the Pb alone and combined exposures induced similar modes of action in the enterocytes, including the generation of oxidative stress and abnormal lipid metabolism.
2022-02-25 | GSE165888 | GEO
Project description:Microplastics are emerging environmental pollutants with potential biological effects on human health. However, the molecular responses of colorectal cancer tissues following microplastic exposure remain poorly characterized. In this study, we performed bulk RNA sequencing to investigate transcriptomic alterations associated with polystyrene microplastics (PS-MPs) exposure in a murine colorectal cancer model. CT26 colorectal cancer cells were subcutaneously implanted into BALB/c mice to establish xenograft tumors. After tumor formation, mice received daily intratumoral injections of 1 μm PS-MPs suspension (10 μg/mL, 50 μL/day), while control mice received no PS-MPs treatment. Tumor tissues were collected for RNA extraction and high-throughput sequencing. Differential gene expression analysis and downstream bioinformatic analyses were performed to characterize molecular changes associated with PS-MPs exposure. This dataset provides transcriptomic profiles of CT26 colorectal cancer xenograft tumors following PS-MPs exposure and may facilitate further investigation of the biological responses associated with environmental microplastic exposure.
2026-08-23 | GSE343346 | GEO