Dataset Information

Disease type and Pathogenic Mechanism induced by PM2.5 in five Human Systems using omics and Human Disease Database

ABSTRACT: Disease type and Pathogenic Mechanism induced by PM2.5 in five Human Systems using omics and Human Disease Database

PROVIDER: PRJNA1060619 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	SRR27407003_1.fastq.gz	Fastqsanger.gz
	SRR27407003_2.fastq.gz	Fastqsanger.gz
	SRR27407004_1.fastq.gz	Fastqsanger.gz
	SRR27407004_2.fastq.gz	Fastqsanger.gz
	SRR27407005_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Project description:PM2.5 can harm various systems in the human body. However, due to the limitations of epidemiology and toxicology, the disease types, shared and specific pathogenic mechanisms induced by PM2.5 in various human systems are not comprehensive and in-depth revealed. Thus, this study conducted an analysis on the aforementioned issues in respiratory, circulatory, endocrine, female, and male urogenital systems. According to this study, PM2.5 was more likely to induce pulmonary emphysema, reperfusion injury, malignant neoplasm of thyroid, endometriosis of ovary, nephritis in above each system respectively. FOS, extracellular matrix, urogenital system development, extracellular matrix structural constituent conferring tensile strength, and ferroptosis was the most important co-existing gene, cellular component, biological process, molecular function, and pathway in five systems targeted by PM2.5. Furthermore, BTG2, BIRC5, NFE2L2, TBK1, and STAT1 were significantly uniquely targeted by PM2.5 in each system respectively. Important disease related cellular component, biological process, and molecular function were highly specially induced by PM2.5, such as response to wounding, blood vessel morphogenesis, body morphogenesis, negative regulation of response to endoplasmic reticulum stress, and response to type I interferon were the top 1 uq-existing biological processes in each system respectively. PM2.5 highly specially acted on the key disease related pathway, such as PD-L1 expression and PD-1 checkpoint pathway in cancer (respiratory), cell cycle (circulatory), apoptosis (endocrine), antigen processing and presentation (female), and neuroactive ligand-receptor interaction (male). This study provides a new analysis method to clarify PM2.5-related disease types, which is an important supplement to epidemiological investigation. Furthermore, this study has clarified the risks of PM2.5 exposure, elucidated the pathogenic mechanisms, and provided scientific support for promoting precise prevention and treatment of PM2.5-related diseases.

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.

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.

Dataset Information

Disease type and Pathogenic Mechanism induced by PM2.5 in five Human Systems using omics and Human Disease Database

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets