Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1265643 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To further explore the potential mechanism underlying PM2.5-induced lung tumorigenesis, we performed circRNA sequencing (circRNA-seq) using RNA isolated from control or chronic PM2.5 exposed HBE cells (control n=3 vs. PM2.5 n=3)
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Project description:Genome-wide analysis of lncRNA expression profiles in COPD rat model exposed by cigarette smoking (CS) and fine particulate matter (PM2.5). Goal was to explore the differences and similarities lncRNAs expression in rats model of COPD exposed by CS and PM2.5.
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Project description:Intra-tracheal instillation of saline or PM2.5 was performed in BALB/c Mice once a week for consecutive eight weeks. Genomewide transcriptome profiling of coding genes, long non-coding RNAs (lncRNA), and circular RNAs (circRNA) in mice lung were done by ribosomal RNA-depleted RNA sequencing.
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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: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:Fine particulate matter (PM2.5) is toxic to reproduction and can cause a range of reproductive disorders. However, the underlying mechanisms of female reproductive impairment due to cowshed PM2.5 exposure are unclear. The aim of this study was the investigation of the effects of PM2.5 on rat ovaries and its molecular mechanisms. Therefore, this study established a whole-body exposure model of PM2.5 in female rats to investigate the effects of PM2.5 on the ovaries. Exposure of rats to PM2.5 using a small animal whole-body PM2.5 exposure system. The device effectively simulates the exposure of animals or humans to PM2.5 within the barn environment, thereby offering enhanced scientific reference data. To put it briefly, for 30 days, the rats were exposed to six hours a day at four times the actual ambient PM2.5 concentration. Adult rats' respiratory coefficient, single-breath volume, and respiratory frequency were used to quantify their daily exposure to PM2.5. To study the effects of PM2.5 exposure on the ovaries of rats, the rats were divided into 2 groups: rats living in clean air were the Control group (Control), which received no additional treatments, and rats exposed to PM2.5 were the PM2.5-exposed group (PM2.5).
2025-10-10 | GSE294063 | GEO
Project description:Chronic exposure to ambient particulate matter <2.5µ (PM2.5) has been linked to cardiopulmonary disease. Tissue-resident (TR) alveolar macrophages (AΦ) are long lived, self-renew and critical to the health impact of inhalational insults. There is inadequate understanding of the impact of PM2.5 exposure on nature/time course of transcriptional responses and the proliferation/maintenance of AΦ including the contribution from bone marrow (BM) over chronic time periods. We investigated the effects of exposure to real-world concentrated PM2.5 or filtered air (FA) in chimeric (CD45.2/CD45.1) mice. Here, we show that PM2.5 exposure induces an influx of BM-derived monocytes to lungs at 4-weeks, with no contribution to TR-AΦ population. Chronic (32-weeks) PM2.5 exposure resulted in enhanced apoptosis (Annexin V+) and decreased proliferation (BrdU+) of TR-AΦ and presence of BM-AΦ in inflamed lungs. RNA-seq analysis of flow sorted TR-AΦ and BM-AΦ from 4 and 32-weeks exposed mice, revealed a unique time dependent pattern of differentially expressed genes, with PM2.5 exposure with a pro-inflammatory bias. PM2.5 exposure resulted in pulmonary fibrosis and reduced alveolar fraction which corresponded to protracted lung inflammation. Our findings suggest a time dependent PM2.5 entrainment of a BM-derived monocytes infiltration into PM2.5 exposed lungs with an inflammatory phenotype, that together with enhanced apoptosis of TR-AΦ and pro-inflammatory polarization may contribute to perpetuation of chronic inflammation and lung fibrosis.
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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