Similar Datasets
Project description:Purpose: PM2.5 can impact mouse TH17 cell differentitation. To Investigator the genes altered by PM2.5 during TH17 differentiation, mRNA-seq was performed. Methods: Naïve T cells were isolated from mouse spleen by magnetic beads. These naïve T cells were stimulated by CD3/CD28 antibodies and cultured under TH17 polarization conditions for 4 days before harvested. For PM2.5 group, 100ug/ml of PM2.5 suspensions were added to culture medium 6 hours after stimulation. The total RNA was extracted using the TRIzol reagent (Invitrogen). The library construction and sequencing was performed by Illumina Xten at Shanghai Biotechnology Corporation.
2019-07-01 | GSE124660 | GEO
Project description:There is a lot of epidemiological evidence that PM2.5 causes liver disease, and metformin can alleviate these diseases.However, the precise mechanism remains unclear.Our study defined the dynamic changes of the differentially expressed genes related PM2.5 induced diseases, and provide basis for comprehensive understanding of the mechanism at the transcriptome level. We investigated PM2.5 induced gene expression alteration associated with the development of liver injury by microarray in a ob/ob mouse model.
2021-11-03 | GSE186900 | GEO
Project description:In order to assess the alteration of lncRNA expression in 16HBE cell treated with PM2.5 samples, we determined the lncRNA expression profiles in 16HBE cell treated with PBS (control group) and PM2.5 samples (low dose 125 μg/mL and high dose 500 μg/mL) using lncRNA Microarray. 16HBE Cells were treated with PM2.5 suspension at concentration of 125 μg/mL and 500 μg/mL, and PBS was used in the control group for 48 h. Then, total RNAs were extracted for lncRNA chip preparation and analysis.
2016-03-25 | E-GEOD-79570 | biostudies-arrayexpress
Project description:To determine the epigenetic mechanism by which PM2.5 deteriorated synaptic transmission and spatial learning and memory, we determined miRNA expression in hippocampi of mice in absent or present of PM2.5 exposure using GenoExplorer microRNA microarray analysis.
2017-01-24 | GSE93967 | GEO
Project description:Lung cancer cells exposed to PM2.5 for 90 days or overexpressed TMPRSS2 were employed as a cellular model to evaluate the effects of long-term exposure to PM2.5 on lung cancer progression.
2023-05-23 | GSE220252 | GEO
Project description:Several epidemiological pieces of evidence on air pollution health effects have notably accelerated in recent years. They have described the relationship between PM2.5 (ambient fine particulate matter of <2.5 μm in diameter) and kidney diseases. Previous research has shown that lactoferrin showed renoprotective effects against some kidney diseases. In the current study, we analyzed the transcriptional profiles of PM2.5 and lactoferrin using RNA sequencing (RNA-seq) and identified the key signaling pathway in the human kidney proximal tubular epithelial cell line (HK-2 cells).
2023-01-30 | GSE208331 | GEO
Project description:In order to assess the alteration of lncRNA expression in 16HBE cell treated with PM2.5 samples, we determined the lncRNA expression profiles in 16HBE cell treated with PBS (control group) and PM2.5 samples (low dose 125 μg/mL and high dose 500 μg/mL) using lncRNA Microarray.
2016-03-25 | GSE79570 | GEO
Project description:We have found that PM2.5 exposure can induce spermatocyte damage and inhibit GC-2spd cell proliferation in vivo and vitro studies. Transcriptomics was performed to explore the potential mechanism of PM2.5-induced reproductive toxicity. With RNA-sequencing technique, the differentially expressed genes induced by PM2.5 exposure were mainly enriched in the metabolism of xenobiotics by cytochrome P450 pathway, and Cyp1a1 was the most significantly changed gene.
2021-12-16 | GSE189187 | GEO
Project description:Atmospheric fine particulate matter (PM2.5) causes severe haze in China and is regarded as a threat to human health. The health effects of PM2.5 vary location by location due to the variation in size distribution, chemical com position, and sources. In this study, the cytotoxicity effect, oxidative stress, and gene expression regulation of PM2.5 in Chengdu and Chongqing, two typical urban areas in southern China, were evaluated. Urban PM2.5 in summer and winter significantly inhibited cell viability and increased reactive oxygen species (ROS) levels in A549 cells. Notably, PM2.5 in winter exhibited higher cytotoxicity and ROS level than summer. Moreover, in this study, PM2.5 commonly induced cancer-related gene expression such as cell adhesion molecule 1(PECAM1), interleukin 24 (IL24), and cytochrome P450 (CYP1A1); meanwhile, PM2.5 commonly acted on cancer-related biological functions such as cell-substrate junction, cell-cell junction, and focal adhesion. In partic ular, PM2.5 in Chengdu in summer had the highest carcinogenic potential among PM2.5 at the two sites in summer and winter. Importantly, cancer-related genes were uniquely targeted by PM2.5, such as epithelial splicing regu latory protein 1 (ESRP1) and membrane-associated ring-CH-type finger 1 (1-Mar) by Chengdu summer PM2.5; collagen type IX alpha 3 chain (COL9A3) by Chengdu winter PM2.5; SH2 domain-containing 1B (SH2D1B) by Chongqing summer PM2.5; and interleukin 1 receptor-like 1 (IL1RL1) and zinc finger protein 42 (ZNF423) by Chongqing winter PM2.5. Meanwhile, important cancer-related biological functions were specially induced by PM2.5, such as cell cycle checkpoint by Chengdu summer PM2.5; macromolecule methylation by Chengdu win ter PM2.5; endoplasmic reticulum-Golgi intermediate compartment membrane by Chongqing summer PM2.5;and cellular lipid catabolic process by Chongqing winter PM2.5. Conclusively, in the typical urban areas of southern China, both summer and winter PM2.5 illustrated significant gene regulation effects. This study contrib utes to evaluating the adverse health effects of PM2.5 in southern China and providing public health suggestions for policymakers.
2022-10-30 | GSE216512 | GEO
Project description:Epidemiological studies have demonstrated that fine particulate matter (PM2.5) is associated with adverse obstetric and postnatal metabolic health outcomes, but the mechanism remains unclear. This study aimed to investigate the toxicological pathways by which PM2.5 damaged placental trophoblasts in vivo and in vitro. We confirmed that PM2.5 induced adverse gestational outcomes such as increased fetal mortality rates, decreased fetal number and weight, damaged placental structure, and increased apoptosis of trophoblasts. Additionally, PM2.5 induced dysfunction of the trophoblast cell line HTR8/SVneo, including in its proliferation, apoptosis, invasion, migration and angiogenesis. Moreover, we comprehensively analyzed the transcriptional landscape of HTR8/SVneo cells exposed to PM2.5 through RNA-Seq and observed that PM2.5 triggered overexpression of pathways involved in oxidative stress and mitochondrial apoptosis to damage HTR8/SVneo cell biological functions through CYP1A1. Mechanistically, PM2.5 stimulated KLF9, a transcription factor identified as binding to CYP1A1 promoter region, which further modulated the CYP1A1-driven downstream phenotypes. Together, this study demonstrated that the KLF9/CYP1A1 axis played a crucial role in the toxic progression of PM2.5 induced adverse pregnancy outcomes, suggesting adverse effects of environmental pollution on pregnant females and putative targeted therapeutic strategies.
2023-08-01 | GSE237795 | GEO