Ontology highlight
ABSTRACT:
PROVIDER: PRJNA611046 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11263247.fastq.gz | Fastqsanger.gz |
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Project description:Forty-six percent of the world's population resides in rural areas, the majority of whom belong to vulnerable and low-income groups. They mainly use cheap solid fuels for cooking and heating, which release a large amount of PM2.5 and cause adverse effects to human health. PM2.5 exhibits urban-rural differences in its health risk to the respiratory system. However, the majority of research on this issue has focused on respiratory diseases induced by atmospheric PM2.5 in urban areas, while rural areas have been ignored for a long time, especially the pathogenesis of respiratory diseases. This is not helpful for promoting environmental equity to aid low-income and vulnerable groups under PM2.5 pollution. Thus, this study focuses on rural atmospheric PM2.5 in terms of its chemical components, toxicological effects, respiratory disease types, and pathogenesis, represented by PM2.5 from rural areas in the Sichuan Basin, China (Rural SC-PM2.5). In this study, organic carbon is the most significant component of Rural SC-PM2.5. Rural SC-PM2.5 significantly induces cytotoxicity, oxidative stress, and inflammatory response. Based on multiomics, bioinformatics, and molecular biology, Rural SC-PM2.5 inhibits ribonucleotide reductase regulatory subunit M2 (RRM2) to disrupt the cell cycle, impede DNA replication, and ultimately inhibit lung cell proliferation. Furthermore, this study supplements and supports the epidemic investigation. Through an analysis of the transcriptome and human disease database, it is found that Rural SC-PM2.5 may mainly involve pulmonary hypertension, sarcoidosis, and interstitial lung diseases; in particular, congenital diseases may be ignored by epidemiological surveys in rural areas, including tracheoesophageal fistula, submucous cleft of the hard palate, and congenital hypoplasia of the lung. This study contributes to a greater scientific understanding of the health risks posed by rural PM2.5, elucidates the pathogenesis of respiratory diseases, clarifies the types of respiratory diseases, and promotes environmental equity.
2024-12-08 | GSE246730 | GEO
Project description:Outdoor atmospheric PM2.5 Raw sequence reads
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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:MicroRNA microarray of mouse in response to atmospheric PM2.5 inhalation
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Project description:Characterization of Risks and Pathogenesis of Respiratory Diseases Caused by Rural Atmospheric PM2.5
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Project description:Examine the toxic effect and molecular mechanisms of PM2.5 in primary human umbilical vein endothelial cells (HUVECs) . We used microarrays to detail the global programme of gene expression in HUVECs exposed to PM2.5 and identified distinct classes of up-regulated genes. Cultured HUVECs which were treated with PM2.5 at the concentrations of 50 μg/mL or DMEM for 24 h were collected for RNA extraction and hybridization on Affymetrix microarrays.
2016-08-11 | E-GEOD-85468 | 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:Objectives: To explore the molecular mechanisms of PM2.5-induced dysfunction in human corneal epithelial cells (HCECs). Methods: RNA-Seq was performed to identify the differentially expressed genes (DEGs) in PM2.5-exposed HCECs compared to unexposed condition, which was followed by validation via real-time PCR (qRT-PCR). Results: A total of 434 DEGs—240 up-regulated and 194 down-regulated—were identified in PM2.5-exposed HCECs rather than unexposed HCECs. The expression of a few genes related to proliferation, inflammation, and aryl hydrocarbon stimulation were significantly altered by PM2.5 exposure, which may contribute to PM2.5-related corneal diseases. Conclusion: The present study identified the altered expression of hundreds of genes in HCECs exposed to PM2.5, which suggests the importance of PM2.5 for cornea health.
2022-08-01 | GSE135262 | 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: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