Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1066500 | ENA |
REPOSITORIES: ENA
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Project description:MPs/NPs-associated anaerobic microbiome Transcriptome
| PRJNA1065101 | ENA
Project description:Exposure to titanium dioxide (TiO2) food additive by ingestion increased over the years. TiO2 is used in food to give a brighter, fresher colour to sweets, cookies, salad dressing under the name E171. New studies on E171 showed that after ingestion in a colorectal cancer mouse model, a significant increased number of colorectal tumours were found. In addition, short-term exposure to E171 induces gene expression changes in relation to oxidative stress responses, an impairment of the immune system, activation of signalling and cancer-related genes. Furthermore, dysregulation of the immune system was also observed after ingestion of E171 in rats. E171 comprises nanoparticles (NPs) and microparticles (MPs). Previous in vitro studies showed the capacity of E171, TiO2 NPs and MPs to induce oxidative stress, DNA damage, and induction of the micronuclei. The aim of our study was to investigate the relative contribution of the NPs and MPs fractions to the effects of E171 at the molecular level. This investigation was performed using in vitro exposure of Caco-2 cells to E171 as well as the NPs and MPs fractions of TiO2 and assessing effects with genome wide gene expression analysis. Results showed that the E171, TiO2 NPs and MPs induce gene expression changes in signalling, inflammation, immune system, transport, and cancer. Contribution of NPs was observed on genes involved in TLR cascade, MHC class I and II presentation, late cornified envelope, potassium channels, and cell cycle. MPs contribution was observed with changes in gene expression on a target to Hedgehog family, α-defensins, cadherin and cholinergic receptors. The gene expression changes associated with the immune system and inflammation induced by E171, MPs, and NPs suggest the creation of a favourable environment for cancer development.
2019-11-22 | GSE110410 | 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:Many observations suggest that mutations of mtDNA could be responsible of the neurodegenerative changes associated with AD. We examined the signal intensity of the four alleles for each mtDNA nucleotide position (np) in whole blood of AD patients and age-matched controls utilizing a resequencing array, the MitoChip v2.0, and identified 275 statistically different nps which all, with the exception of one, showed an increased contribution of non-reference alleles for AD patients. PCA and cluster analysis showed that 5 of these nps, characterized by low-level heteroplasmy, could discriminate AD from control subjects with 80% of cases correctly classified.
2014-03-11 | GSE49160 | GEO
Project description:Many observations suggest that mutations of mtDNA could be responsible of the neurodegenerative changes associated with AD. We examined the signal intensity of the four alleles for each mtDNA nucleotide position (np) in whole blood of AD patients and age-matched controls utilizing a resequencing array, the MitoChip v2.0, and identified 275 statistically different nps which all, with the exception of one, showed an increased contribution of non-reference alleles for AD patients. PCA and cluster analysis showed that 5 of these nps, characterized by low-level heteroplasmy, could discriminate AD from control subjects with 80% of cases correctly classified. This study included a total of 18 AD patients and 18 age-matched controls. Data acquisition was performed using the Affymetrix Genechip Command Console (AGCC) software and data analysis was carried out with GSEQ 4.1.
2014-03-11 | E-GEOD-49160 | biostudies-arrayexpress
Project description:The epidermis, the most superficial layer of human skin, serves a critical barrier function, protecting the body from external pathogens and allergens. Dysregulation in the epidermal differentiation process contributes to barrier dysfunction and is implicated in the pathology of various dermatological diseases, including atopic dermatitis (AD). Mucopolysaccharide polysulfate (MPS) is used as a moisturizing agent for xerosis in AD patients. However, its mechanism of action on keratinocytes, the main constituent of the epidermis, remains unclear. In this study, we investigated the impact of MPS on keratinocytes by subjecting adult human epidermal keratinocyte (HEKa) cells and three-dimensional cultured keratinocytes to MPS treatment, followed by transcriptome analysis. The analysis revealed that MPS treatment enhances keratinocyte differentiation and suppresses proliferation. We focused on amphiregulin (AREG), a membrane protein that belongs to the epidermal growth factor (EGF) family and possesses a heparin-binding domain, as a significant target of the MPS among the genes altered by MPS. It is revealed that MPS exerts an inhibitory effect directly on AREG, rather than on the EGF receptor or other members of the EGF family. Furthermore, it is suggested that AREG leads to a reduction in epidermal barrier function, whereas MPS contributes to barrier enhancement through AREG inhibition. Collectively, these findings suggest that MPS modulates barrier function through the inhibition of AREG, offering insights into potential therapeutic strategies for skin barrier restoration.
2024-07-03 | GSE268656 | GEO