Effects of PM2.5 exposure in utero on heart injury, histone acetylation and GATA4 expression in offspring mice

Li, Ruijin; Zhao, Yufei; Shi, Jing; Zhao, Chao; Xie, Peisi; Wei, Huang; Yong, Ting Ting; Cai, Zongwei

doi:10.1016/j.chemosphere.2020.127133

Cited by 16 publications

(13 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results further indicate that acetyltransferase p300 plays a pivotal role in pathological cardiac hypertrophy and remodeling in adult mice those exposed to PM 2.5 in utero [ 69 ]. Similarly, a recent study also showed that PM 2.5 exposure in utero is associated with cardiac injury related phenotypes including cardiac inflammation, interstitial edema and hypertrophy in adult offspring [ 70 ]. However, unlike previous reports [ 69 ], this study showed that PM 2.5 exposure in utero causes downregulation of acetyltransferase p300 activity especially in male offspring, and that is associated with decreased recruitment of acetylated H3K9 to GATA4 promoter and its transcriptional repression.…”

Section: Acetyltransferase P300 Boosts Cardiac Hypertrophy Myocardial Fibrosis and Heart Failurementioning

confidence: 99%

“…However, unlike previous reports [ 69 ], this study showed that PM 2.5 exposure in utero causes downregulation of acetyltransferase p300 activity especially in male offspring, and that is associated with decreased recruitment of acetylated H3K9 to GATA4 promoter and its transcriptional repression. As GATA4 is a key transcription factor for embryonic heart development, authors suggested that downregulation as well as decreased acetylation of GATA4 may contribute to PM 2.5 -induced in utero heart injury and cardiac dysfunction in adult offspring [ 70 ]. However, the reason for the discrepancy between the results of these two studies is unclear.…”

Section: Acetyltransferase P300 Boosts Cardiac Hypertrophy Myocardial Fibrosis and Heart Failurementioning

confidence: 99%

See 1 more Smart Citation

Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease

Ghosh

2021

Cells

View full text Add to dashboard Cite

Cardiovascular disease is the leading cause of accelerated as well as chronological aging-related human morbidity and mortality worldwide. Genetic, immunologic, unhealthy lifestyles including daily consumption of high-carb/high-fat fast food, lack of exercise, drug addiction, cigarette smoke, alcoholism, and exposure to environmental pollutants like particulate matter (PM)-induced stresses contribute profoundly to accelerated and chronological cardiovascular aging and associated life threatening diseases. All these stressors alter gene expression epigenetically either through activation or repression of gene transcription via alteration of chromatin remodeling enzymes and chromatin landscape by DNA methylation or histone methylation or histone acetylation. Acetyltransferase p300, a major epigenetic writer of acetylation on histones and transcription factors, contributes significantly to modifications of chromatin landscape of genes involved in cellular aging and cardiovascular diseases. In this review, the key findings those implicate acetyltransferase p300 as a major contributor to cellular senescence or aging related cardiovascular pathologies including vascular dysfunction, cardiac hypertrophy, myocardial infarction, cardiac fibrosis, systolic/diastolic dysfunction, and aortic valve calcification are discussed. The efficacy of natural or synthetic small molecule inhibitor targeting acetyltransferase p300 in amelioration of stress-induced dysregulated gene expression, cellular aging, and cardiovascular disease in preclinical study is also discussed.

show abstract

Section: Acetyltransferase P300 Boosts Cardiac Hypertrophy Myocardial Fibrosis and Heart Failurementioning

confidence: 99%

Section: Acetyltransferase P300 Boosts Cardiac Hypertrophy Myocardial Fibrosis and Heart Failurementioning

confidence: 99%

Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease

Ghosh

2021

Cells

View full text Add to dashboard Cite

show abstract

“…Cardiac damage and myocardial hypertrophy with an overexpression of mir-208b/β-MHC has been observed in rats [ 29 ]. Additionally, at the epigenomic level, the increased acetylation of histone GATA4 has occurred [ 30 ].…”

Section: Introductionmentioning

confidence: 99%

Particle Debris Generated from Passenger Tires Induces Morphological and Gene Expression Alterations in the Macrophages Cell Line RAW 264.7

et al. 2023

View full text Add to dashboard Cite

Air pollution in the urban environment is a topical subject. Aero-suspended particles can cause respiratory diseases in humans, ranging from inflammation to asthma and cancer. One of the components that is most prevalent in particulate matter (PM) in urban areas is the set of tire microparticles (1–20 μm) and nanoparticles (<1 μm) that are formed due to the friction of wheels with asphalt and are increased in slow-moving areas that involve a lot of braking actions. In this work, we studied the effect that microparticles generated from passenger tires (PTWP, passenger tire wear particles) have in vitro on murine macrophages cells RAW 264.7 at two concentrations of 25 and 100 μg/mL, for 24 and 48 h. In addition to the chemical characterization of the material and morphological characterization of the treated cells by transmission electron microscopy, gene expression analysis with RT-PCR and active protein analysis with Western blotting were performed. Growth curves were obtained, and the genotoxic effect was evaluated with a comet assay. The results indicate that initially, an induction of the apoptotic process is observable, but this is subsequently reversed by Bcl2. No genotoxic damage is present, but mild cellular abnormalities were observed in the treated cells.

show abstract

“…Additionally, PM 2.5 could lead to down-regulation of lncRNA (PEAMIR) expression in heart tissue, of which the effect as competing endogenous RNAs (ceRNAs) was reduced, and thus weakened the inhibition of miR-29b-3p, leading to elevation of cardiac inflammation and apoptosis [ 104 ]. An increased level of acetylated histone 3 lysine 9 (H3K9ac) was also found to be involved in the cardiovascular toxicity of PM 2.5 , resulting in myocardial injury and upregulation of inflammatory factors [ 105 ].…”

Section: Introductionmentioning

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

View full text Add to dashboard Cite

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

show abstract

Effects of PM2.5 exposure in utero on heart injury, histone acetylation and GATA4 expression in offspring mice

Cited by 16 publications

References 29 publications

Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease

Acetyltransferase p300 Is a Putative Epidrug Target for Amelioration of Cellular Aging-Related Cardiovascular Disease

Particle Debris Generated from Passenger Tires Induces Morphological and Gene Expression Alterations in the Macrophages Cell Line RAW 264.7

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

Contact Info

Product

Resources

About