RNAseq analysis of PM2.5 treated mouse cardiomyocyte cell line
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ABSTRACT:
PROVIDER: PRJNA873040 | ENA |
REPOSITORIES: ENA
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Project description:We report the gene expression profile in mouse cardiomyocyte cell line after treatment of PM2.5.
2022-09-27 | GSE211949 | 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.
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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.
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Project description:RNAseq analysis of U251 cell line treated with 100nM of LLY-283 compared to Vehicle treated cells to analyse the effect of LLY-283 on gene expression and mRNA splicing.
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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.
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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).
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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.
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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:Mitochondria are essential cellular organelles that participate in important cellular processes, including bioenergetics, metabolism, and signaling. Recent functional and proteomic studies have revealed the remarkable complexity of mitochondrial protein organization. Protein machineries with diverse functions such as protein translocation, respiration, metabolite transport, protein quality control and the control of membrane architecture interact with each other in dynamic networks. The goal of this study was to identify protein expression changes in a human cardiomyocyte cell line treated with several mitochondrial toxicants which inhibit mitochondrial membrane potential (MMP) and mitochondrial respiration. AC16 human cardiomyocyte cells were treated with carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP), dinoterb, picoxystrobin, pinacyanol and triclocarban for 18 h around the IC50 values generated from MMP assay. The samples were harvested and labeled with tandem mass tags with different mass isotopes. Peptide assignment was performed in Proteome Discoverer. Each dataset was analyzed in Ingenuity Pathway Analysis (IPA). In the proteomic profile, these compounds showed dysregulation of a group of mitochondrial proteins (e.g. NDUA, NDUB, BCS1, CYB5B and SDHF2), as well as proteins involved in lipid metabolism (e.g. CPT, MECR, and LPGAT1), cytoskeleton protein changes (e.g. CROCC, LAMC3, FBLN1 and FMN2) and stress response (e.g. IKBKG, IKBB, SYVN1, SOD2 and CPIN1). Proteomic data from the current study provides key insights into chemical induced cellular pathway dysregulation, supporting the use of proteomic profiling as a sensitive method to further explore molecular functions and disease pathogenesis upon exposure to environmental chemicals.
2021-09-09 | PXD019076 | Pride
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