We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
N6-methyladenosine methylation mediates non-coding RNAs modification in microplastic-induced cardiac injury
Summary
Researchers found that microplastic exposure in mice led to accumulation in organs and triggered cell death, particularly affecting heart tissue. Using advanced sequencing techniques, they discovered that microplastics altered chemical modifications (m6A methylation) on non-coding RNA molecules in heart cells, which may disrupt important gene regulatory networks. The study suggests a potential molecular mechanism through which microplastic exposure could contribute to heart damage, though more research is needed to understand the full implications.
Owing to their potential adverse health effects, global contamination by microplastics (MPs) has attracted increased scientific and societal concerns. However, in vivo studies on MP toxicity, along with its effects and underlying mechanisms, remain limited. We recently found that non-coding RNA (ncRNAs) contribute to MP-mediated vascular toxicity. Moreover, previous studies have identified N6-methyladenosine (m6A) modifications in ncRNAs as influencing factors in cardiovascular disease. However, whether and how m6A modifications in ncRNAs are affected by MP-induced cardiotoxicity remain unknown. Herein, we profiled differentially expressed ncRNAs and their related m6A modification profiles in MP-exposed myocardial tissue using RNA sequencing (RNA-seq) and methylated RNA immunoprecipitation sequencing (MeRIP-seq). First, we observed that MPs accumulated in different organs and upregulated apoptosis in the heart, liver, spleen, and kidney cells. Furthermore, total m6A and METTL3 levels increased in the myocardium after exposure to MPs. RNA-seq results revealed that 392 lncRNAs and 302 circRNAs were differentially expressed in MP-treated mouse myocardium compared to the control group. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that these altered lncRNAs and circRNAs were closely associated with endocytosis, cellular senescence, and cell cycle signaling pathways, which may cause cardiotoxicity. Furthermore, MeRIP-seq data showed different distributions and abundances of m6A modifications in lncRNAs and circRNAs. Additionally, we identified differentially m6A methylated lncRNAs and circRNAs through conjoint analysis of the two high-throughput sequencing datasets and found that both m6A modifications and the expression of circ-Arfgef2 and lncG3bp2 were upregulated after exposure to MPs. This suggests that MP-induced m6A modifications in ncRNAs are involved in cardiotoxicity. Our findings contribute to a better understanding of MP-induced cardiotoxicity and new molecular targets for treating cardiac injury.
Sign in to start a discussion.
More Papers Like This
Transcriptome-wide m6A modification mediates cardiotoxicity in mice after chronic exposure to microplastics
Researchers exposed mice to microplastics and examined the resulting heart tissue damage and changes in gene regulation through a chemical modification called m6A methylation. They found that microplastic exposure caused cardiac inflammation, fibrosis, and increased lipid accumulation, along with widespread changes in m6A methylation patterns across the transcriptome. The study suggests that microplastics may contribute to heart tissue damage through epigenetic modifications that alter gene expression.
Polystyrene nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis
Scientists found that tiny plastic particles called nanoplastics can damage heart cells by disrupting their powerhouses (mitochondria) and reducing their ability to produce energy. When researchers exposed human heart cells and mice to these nanoplastics, they observed weakened heart function and signs of early heart damage. This research suggests that the growing amount of microscopic plastic pollution in our environment could pose previously unknown risks to heart health.
Nanoplastics as Epigenetic Disruptors: A Biochemical Review of Environmental Pollutants and Gene Regulation
This biochemical review examined how nanoplastics disrupt epigenetic regulation, focusing on their ability to alter DNA methylation patterns, histone modifications, and non-coding RNA expression. The authors argued that nanoplastic-induced epigenetic changes could have lasting developmental and health consequences, especially during vulnerable life stages.
N6-methyladenosine RNA methylation regulates microplastics-induced cell senescence in the rainbow trout liver
Rainbow trout exposed to microplastics at 500 µg/L for two weeks accumulated plastic particles in their livers, which triggered oxidative stress, liver tissue damage, and — importantly — premature cell ageing (senescence) driven by changes in RNA regulation. Specifically, microplastics disrupted a molecular "reader" system (m6A RNA methylation) that normally controls cell proliferation and growth. This pathway-level finding is significant because cellular senescence is associated with tissue degeneration and disease, suggesting microplastic exposure may have long-term liver health consequences in fish — and potentially in other vertebrates.
A study on the roles of long non-coding RNA and circular RNA in the pulmonary injuries induced by polystyrene microplastics
Researchers exposed rats to polystyrene microplastics through the airways and found evidence of lung tissue damage, including destroyed air sacs and inflammation. The study identified changes in the activity of long non-coding RNAs and circular RNAs, types of genetic regulators that may help explain how microplastics cause lung injury at the molecular level. These findings provide new insight into the biological mechanisms behind potential respiratory harm from inhaling microplastic particles.