Gene expression in human umbilical vein endothelial cells exposed to fine particulate matter: RNA sequencing analysis

Zhou, Zhixiang; Qin, Mengnan; Khodahemmati, Sara; Li, Wenke; Niu, Bingyu; Li, Jiangshuai; Liu, Yanghua; Gao, Jingfeng

doi:10.1080/09603123.2021.1935785

Cited by 5 publications

(3 citation statements)

References 31 publications

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“…The analysis revealed a robust regulation of the gene expression profile in PBMCs after their treatment with PM KRK, which was detected both in patients and HD. Similar changes were observed in the study on endothelial cells after their exposure to PM 2.5 [ 52 ]. In this context, Huang et al documented that bronchial epithelial cells undergo genome-wide alterations in gene expression and DNA methylation patterns after exposition to PM 2.5 [ 53 ].…”

Section: Discussionsupporting

confidence: 87%

Transcriptional Response of Blood Mononuclear Cells from Patients with Inflammatory and Autoimmune Disorders Exposed to “Krakow Smog”

Gałuszka-Bulaga

Hajto

Borczyk

et al. 2022

Cells

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Despite the general awareness of the need to reduce air pollution, the efforts were undertaken in Poland to eliminate the pollutants and their harmful effect on human health seem to be insufficient. Moreover, the latest data indicate that the city of Krakow is at the forefront of the most polluted cities worldwide. Hence, in this report, we investigated the impact of particulate matter isolated from the air of Krakow (PM KRK) on the gene expression profile of peripheral blood mononuclear cells (PBMCs) in healthy donors (HD) and patients with atherosclerosis (AS), rheumatoid arthritis (RA) and multiple sclerosis (MS), after in vitro exposure. Blood samples were collected in two seasons, differing in the concentration of PM in the air (below or above a daily limit of 50 µg/m3 for PM 10). Data show that PBMCs exposed in vitro to PM KRK upregulated the expression of genes involved, among others, in pro-inflammatory response, cell motility, and regulation of cell metabolism. The transcriptional effects were observed predominantly in the group of patients with AS and MS. The observed changes seem to be dependent on the seasonal concentration of PM in the air of Krakow and may suggest their important role in the progression of AS, MS, and RA in the residents of Krakow.

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Section: Discussionsupporting

confidence: 87%

Transcriptional Response of Blood Mononuclear Cells from Patients with Inflammatory and Autoimmune Disorders Exposed to “Krakow Smog”

Gałuszka-Bulaga

Hajto

Borczyk

et al. 2022

Cells

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“…Genetic predisposition appears to play a crucial role in response to air pollution ( 22 ). Previous studies have revealed that exposure to PM2.5 causes negative health consequences driven by alteration of gene expression ( 23 , 24 ). A study conducted by Yao et al showed that participants with 2 alleles of SIRT1_391 can counteract the adverse effect of PM2.5 and reduce the 26.1% risk of premature mortality ( 25 ).…”

Section: Introductionmentioning

confidence: 99%

Causality of particulate matter on cardiovascular diseases and cardiovascular biomarkers

Wang,

Chen

et al. 2023

Front. Public Health

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BackgroundPrevious observational studies have shown that the prevalence of cardiovascular diseases (CVDs) is related to particulate matter (PM). However, given the methodological limitations of conventional observational research, it is difficult to identify causality conclusively. To explore the causality of PM on CVDs and cardiovascular biomarkers, we conducted a Mendelian randomization (MR) analysis.MethodIn this study, we obtained summary-level data for CVDs and cardiovascular biomarkers including atrial fibrillation (AF), heart failure (HF), myocardial infarction (MI), ischemic stroke (IS), stroke subtypes, body mass index (BMI), lipid traits, fasting glucose, fasting insulin, and blood pressure from several large genome-wide association studies (GWASs). Then we used two-sample MR to assess the causality of PM on CVDs and cardiovascular biomarkers, 16 single nucleotide polymorphisms (SNPs) for PM2.5 and 6 SNPs for PM10 were obtained from UK Biobank participants. Inverse variance weighting (IVW) analyses under the fixed effects model were used as the main analytical method to calculate MR Estimates, followed by multiple sensitivity analyses to confirm the robustness of the results.ResultsOur study revealed increases in PM2.5 concentration were significantly related to a higher risk of MI (odds ratio (OR), 2.578; 95% confidence interval (CI), 1.611–4.127; p = 7.920 × 10−5). Suggestive evidence was found between PM10 concentration and HF (OR, 2.015; 95% CI, 1.082–3.753; p = 0.027) and IS (OR, 2.279; 95% CI,1.099–4.723; p = 0.027). There was no evidence for an effect of PM concentration on other CVDs. Furthermore, PM2.5 concentration increases were significantly associated with increases in triglyceride (TG) (OR, 1.426; 95% CI, 1.133–1.795; p = 2.469 × 10−3) and decreases in high-density lipoprotein cholesterol (HDL-C) (OR, 0.779; 95% CI, 0.615–0.986; p = 0.038). The PM10 concentration increases were also closely related to the decreases in HDL-C (OR, 0.563; 95% CI, 0.366–0.865; p = 8.756 × 10−3). We observed no causal effect of PM on other cardiovascular biomarkers.ConclusionAt the genetic level, our study suggested the causality of PM2.5 on MI, TG, as well HDL-C, and revealed the causality of PM10 on HF, IS, and HDL-C. Our findings indicated the need for continued improvements in air pollution abatement for CVDs prevention.

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“…Studies have shown that PM 2.5 can cause the destruction of the balance of oxidants and antioxidants by up-regulating the production of intracellular ROS (KE 1115) and the expression of oxidative stress-related genes, leading to oxidative stress (KE 1392), including the reduction of superoxide dismutase activity, the release of lactate dehydrogenase and the increase of cell membrane permeability. Subsequently, activation of related pathways can cause cardiac fibrosis (KE 1924), significantly enhance vascular endothelial permeability and other cardiovascular damage, leading to CVD [90][91][92][93]. Inflammatory pathways activation (KE 151) and systemic inflammation (KE 149) were observed after exposure to PM 2.5 , which in turn led to increased secretion of a range of pro-inflammatory factors (KE 1496) and vascular endothelial dysfunction (KE 1928) [94,95].…”

Section: The Effects and Mechanisms Of Pm On Cardiovascular Systemmentioning

confidence: 99%

A comprehensive understanding of ambient particulate matter and its components on the adverse health effects based from epidemiological and laboratory evidence

Sun

et al. 2022

Part Fibre Toxicol

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The impacts of air pollution on public health have become a great concern worldwide. Ambient particulate matter (PM) is a major air pollution that comprises a heterogeneous mixture of different particle sizes and chemical components. The chemical composition and physicochemical properties of PM change with space and time, which may cause different impairments. However, the mechanisms of the adverse effects of PM on various systems have not been fully elucidated and systematically integrated. The Adverse Outcome Pathway (AOP) framework was used to comprehensively illustrate the molecular mechanism of adverse effects of PM and its components, so as to clarify the causal mechanistic relationships of PM-triggered toxicity on various systems. The main conclusions and new insights of the correlation between public health and PM were discussed, especially at low concentrations, which points out the direction for further research in the future. With the deepening of the study on its toxicity mechanism, it was found that PM can still induce adverse health effects with low-dose exposure. And the recommended Air Quality Guideline level of PM2.5 was adjusted to 5 μg/m3 by World Health Organization, which meant that deeper and more complex mechanisms needed to be explored. Traditionally, oxidative stress, inflammation, autophagy and apoptosis were considered the main mechanisms of harmful effects of PM. However, recent studies have identified several emerging mechanisms involved in the toxicity of PM, including pyroptosis, ferroptosis and epigenetic modifications. This review summarized the comprehensive evidence on the health effects of PM and the chemical components of it, as well as the combined toxicity of PM with other air pollutants. Based on the AOP Wiki and the mechanisms of PM-induced toxicity at different levels, we first constructed the PM-related AOP frameworks on various systems. Graphical Abstract

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Gene expression in human umbilical vein endothelial cells exposed to fine particulate matter: RNA sequencing analysis

Cited by 5 publications

References 31 publications

Transcriptional Response of Blood Mononuclear Cells from Patients with Inflammatory and Autoimmune Disorders Exposed to “Krakow Smog”

Transcriptional Response of Blood Mononuclear Cells from Patients with Inflammatory and Autoimmune Disorders Exposed to “Krakow Smog”

Causality of particulate matter on cardiovascular diseases and cardiovascular biomarkers

A comprehensive understanding of ambient particulate matter and its components on the adverse health effects based from epidemiological and laboratory evidence

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