MicroRNA microarray of mouse in response to atmospheric PM2.5 inhalation
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE93967 | GEO | 2017/01/24
SECONDARY ACCESSION(S): PRJNA362955
REPOSITORIES: GEO
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Project description:Outdoor atmospheric PM2.5 Raw sequence reads
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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:PM2.5 exposure is closely linked to the exacerbation of asthma. Estrogen related receptor gamma (Esrrg), an orphan nuclear receptor, exerts a crucial role as a transcription factor in various metabolic diseases. Nevertheless, the impacts of Esrrg on PM2.5-triggered asthma aggravation have not been investigated. Herein, ovalbumin (OVA)-induced asthmatic mice were exposed to PM2.5 to establish a mouse model of asthma aggravation by PM2.5. In view of mRNA sequencing, Esrrg was the only member of nuclear receptor superfamily in the up-regulated differentially expressed genes in OVA compared with Naive groups as well as OVA+PM2.5 compared with OVA groups (|log2 (fold change)|>1 and p<0.05). In vivo, adeno-associated virus carrying Esrrg shRNA (AAV-shEsrrg) was applied to silencing Esrrg. In addition, Esrrg activity was suppressed pharmacologically with an inverse agonist GSK5182. Either AAV-shEsrrg or GSK5182 ameliorated airway inflammation in the PM2.5-aggravated asthmatic mice. In vitro, isolated mouse primary tracheobronchial epithelial cells (MTEC) from mice were identified by detecting cytokeratin 7-positive cells. The treatment of adenovirus vector with shEsrrg or GSK5182 mitigated the cell damage induced by PM2.5. Notably, phosphodiesterase 3B (Pde3b) expression was declined by Esrrg inhibition in vivo and in vitro. Dual luciferase reporter and ChIP-PCR assays showed the binding of Esrrg to the Pde3b promoter. Taken together, these results revealed that Esrrg inhibition alleviated airway inflammation in the PM2.5-deteriorated asthmatic mouse model and prevented PM2.5-driven MTEC injury through binding to the Pde3b promoter, which might contribute to further study the therapy of PM2.5-aggravated asthma.
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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. 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: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:Yangyinqingfei Decoction (YYQFD), a traditional Chinese prescription, is well known in the treatment of diphtheria and lung-related diseases in clinic. However, the underlying mechanism how to treat lung-related diseases remains unclear. In the present study, the intervention effect of YYQFD on PM2.5-induced lung injury mice and its potential mechanism were investigated by metabolomics and proteomic techniques. The results showed that YYQFD could significantly improve pulmonary functions, relieve lung injury, as well as reduce IL-6, TNF-α and MDA, and increase SOD levels in serum and BALF of PM2.5-induced lung injury mice. Furthermore, the protein-metabolite joint analysis presented that YYQFD regulated the pathways of arachidonic acid metabolism, linoleic acid metabolism, and biosynthesis of unsaturated fatty acids with significantly down-regulating arachidonic acid, 20-HETE, prostaglandin E2, lecithin, linoleic acid, α-linolenic acid, eicosatetraenoic acid, and γ-linolenic acid, and up-regulating PTGES2, GPX2 and CBR3 protein expressions in lung tissue. A regulatory metabolic network map was further constructed, which provide us a better understanding about the role of YYQFD on PM2.5-induced lung injury mice and new insight into YYQFD application for the treatment of lung-related diseases.
2022-12-22 | PXD037163 | Pride
Project description:To elucidate the molecular mechanism underlying lifespan reduction induced by PM2.5 exposure in Caenorhabditis elegans, we performed global gene expression profiling by RNA-sequencing technology, and compared the gene expression pattern change induced by PM2.5 exposure.
2023-02-22 | GSE214215 | GEO
Project description:MicroRNAs (miRNA) are small, non-coding RNAs mediating post-transcriptional regulation of gene expression. miRNAs have recently been implicated in hippocampus-dependent functions such as learning and memory, although the roles of individual miRNAs in these processes remain largely unknown. Here, we achieved stable inhibition using AAV-delivered miRNA sponges of individual, highly expressed and brain-enriched miRNAs; miR-124, miR-9 and miR-34, in hippocampal neurons. Molecular and cognitive studies revealed a role for miR-124 in learning and memory. Inhibition of miR-124 resulted in an enhanced spatial learning and working memory capacity, potentially through altered levels of genes linked to synaptic plasticity and neuronal transmission. In contrast, inhibition of miR-9 or miR-34 led to a decreased capacity of spatial learning and of reference memory, respectively. On a molecular level, miR-9 inhibition resulted in altered expression of genes related to cell adhesion, endocytosis and cell death, while miR-34 inhibition caused transcriptome changes linked to neuroactive ligand-receptor transduction and cell communication. In summary, this study establishes distinct roles for individual miRNAs in hippocampal function. Three RNA samples containing bilateral entire hippocampi from three different mice, per group. Group 1 were injected with vector containing GFP and a miR34sp/miR9sp and the other group were subjected to a vector expressing GFP only.
2016-03-01 | E-GEOD-68884 | biostudies-arrayexpress
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.
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