Similar Datasets
Project description:This project unraveled the molecular mechanism of adaptive changes of strain PAH02 in the process of absorbing Cd and degrading Phe by Tandem Mass Tags proteomic technologies.The results show that strain PAH02 significantly upregulated the levles of proteins such as MerR and aerC to ensure energy utilization and cellular integrity under the stress of Cd-Phe co-contaminant.
2022-11-30 | PXD038463 |
Project description:Cadmium (Cd) is a prevalent environmental and industrial contaminant that causes significant damage to liver function. However, the role of m6A methylation─a critical epigenetic modification─in Cd-induced liver injury remains poorly understood. This study aimed to investigate the effects of m6A methylation in Cd-induced liver damage. A mouse model of Cd-induced liver injury was established, and exposure to CdCl2 (20 mg/kg) for 90 days resulted in reduced m6A methylation levels. Using methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-Seq), we characterized the m6A methylation profiles in both control and Cd-exposed groups. A total of 8355 unique m6A peaks and 1,101 unique m6A-modified genes were identified. Among these, 673 genes exhibited differential m6A methylated modifications, including 463 hyper-methylated and 210 hypo-methylated genes. Conjoint analysis of MeRIP-seq and RNA-Seq data unveiled genes that showed both differential methylation and expression. These genes were significantly enriched in the AGE-RAGE and PI3K-Akt signaling pathway. Through bioinformatics screening, five key genes (Il-1β, Ccl2, Tlr2, Itgax, and Ccr2) were identified, and expression validation indicated that Itgax and Ccr2 may play pivotal roles in Cd-induced liver injury. Notably, elevated expression of methyltransferase-like 14 (METTL14) was observed in both in vivo and in vitro models. Inhibition of Mettl14 can regulate Cd-induced liver inflammation through m6A-dependent regulation of Ccr2 expression. Collectively, our findings highlight the crucial role of Mettl14 and Ccr2 in Cd-induced liver injury, providing novel insights into the epigenetic mechanisms underlying liver diseases and potential biomarkers for diagnosis and therapy.
2025-04-07 | GSE286882 | GEO
Project description:Cadmium (Cd) is a prevalent environmental and industrial contaminant that causes significant damage to liver function. However, the role of m6A methylation─a critical epigenetic modification─in Cd-induced liver injury remains poorly understood. This study aimed to investigate the effects of m6A methylation in Cd-induced liver damage. A mouse model of Cd-induced liver injury was established, and exposure to CdCl2 (20 mg/kg) for 90 days resulted in reduced m6A methylation levels. Using methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-Seq), we characterized the m6A methylation profiles in both control and Cd-exposed groups. A total of 8355 unique m6A peaks and 1,101 unique m6A-modified genes were identified. Among these, 673 genes exhibited differential m6A methylated modifications, including 463 hyper-methylated and 210 hypo-methylated genes. Conjoint analysis of MeRIP-seq and RNA-Seq data unveiled genes that showed both differential methylation and expression. These genes were significantly enriched in the AGE-RAGE and PI3K-Akt signaling pathway. Through bioinformatics screening, five key genes (Il-1β, Ccl2, Tlr2, Itgax, and Ccr2) were identified, and expression validation indicated that Itgax and Ccr2 may play pivotal roles in Cd-induced liver injury. Notably, elevated expression of methyltransferase-like 14 (METTL14) was observed in both in vivo and in vitro models. Inhibition of Mettl14 can regulate Cd-induced liver inflammation through m6A-dependent regulation of Ccr2 expression. Collectively, our findings highlight the crucial role of Mettl14 and Ccr2 in Cd-induced liver injury, providing novel insights into the epigenetic mechanisms underlying liver diseases and potential biomarkers for diagnosis and therapy.
2025-04-07 | GSE286881 | GEO
Project description:The heavy metal Cadmium (Cd), a widespread environmental contaminant, poses serious hazards to human health, and is considered a metallohormone and carcinogen. In women with uterine fibroids, there is a significant association between blood Cd levels and fibroid tumor size. The aim of this study was to determine if benign uterine fibroid cells could be malignantly transformed in vitro by continuous Cd exposure, and if so, explore a molecular mechanism by which this could occur. We found when fibroid cells were exposed to 10 µM CdCl2 for 8 weeks, a robust and fast-growing Cd- Resistant Leiomyoma (CR-LM) culture was established. The CR-LM cells showed the ability to form viable colonies in soft agar, increased glycogen aggregates, enhanced cell motility, a higher percentage of cells in G2/M phase, and increased expression of the proliferation marker Ki-67. NanoString analysis showed downregulation of genes encoding for ECM components, such as collagens, fibronectins, laminins, and SLRP family proteins; whereas, genes involved in ECM degradation (MMP1, MMP3 and MMP10) were significantly upregulated. A volcano plot showed that the direction of expression changes of the top differentially genes favored cancer progression. Functional analysis by IPA predicted a significant inhibition of TGFβ signaling, leading to enhanced proliferation and attenuated fibrosis. Prolonged Cd exposure altered phenotypic characteristics and dysregulated genes in fibroid cells predicative of progression towards a cancer phenotype. Therefore, continuous Cd exposures changes the phenotype of benign fibroid cells in vitro and could possibly pose a health risk for women with uterine fibroids.
2023-11-13 | GSE161455 | GEO
Project description:The heavy metal Cadmium (Cd), a widespread environmental contaminant, poses serious hazards to human health, and is considered a metallohormone and carcinogen. In women with uterine fibroids, there is a significant association between blood Cd levels and fibroid tumor size. The aim of this study was to determine if benign uterine fibroid cells could be malignantly transformed in vitro by continuous Cd exposure, and if so, explore a molecular mechanism by which this could occur. We found when fibroid cells were exposed to 10 µM CdCl2 for 8 weeks, a robust and fast-growing Cd- Resistant Leiomyoma (CR-LM) culture was established. The CR-LM cells showed the ability to form viable colonies in soft agar, increased glycogen aggregates, enhanced cell motility, a higher percentage of cells in G2/M phase, and increased expression of the proliferation marker Ki-67. NanoString analysis showed downregulation of genes encoding for ECM components, such as collagens, fibronectins, laminins, and SLRP family proteins; whereas, genes involved in ECM degradation (MMP1, MMP3 and MMP10) were significantly upregulated. A volcano plot showed that the direction of expression changes of the top differentially genes favored cancer progression. Functional analysis by IPA predicted a significant inhibition of TGFβ signaling, leading to enhanced proliferation and attenuated fibrosis. Prolonged Cd exposure altered phenotypic characteristics and dysregulated genes in fibroid cells predicative of progression towards a cancer phenotype. Therefore, continuous Cd exposures changes the phenotype of benign fibroid cells in vitro and could possibly pose a health risk for women with uterine fibroids.
2023-11-13 | GSE161454 | GEO
Project description:Initial work for profiling contaminant response in Phaeodactylum cells exposed to contaminants and non contaminant stressors
2012-01-11 | GSE34988 | GEO
Project description:In this study, we investigated miRNA expression profiles in ileal mucosa from CD patients in different settings (post-operative recurrent (POR) CD, newly diagnosed CD and late stage CD)) and controls.
2019-03-01 | GSE102127 | GEO
Project description:To study the soil mcirobial functional communities and the nutrient cycles couplings changes after exposure to different contaminant
2020-12-31 | GSE135153 | GEO