We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Transcriptome-wide m6A modification mediates cardiotoxicity in mice after chronic exposure to microplastics
Summary
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.
The widespread presence of microplastics (MPs) has garnered attention owing to their possible adverse effects. However, the cardiotoxicity of MPs and their underlying mechanism remains unclear. N6-methyladenosine (m6A) modification contributes to post-transcriptional modulation of gene expression, but whether this modification is relevant to MP-induced cardiotoxicity is unknown. First, we detected damage to the myocardial tissue among MP-exposed and -unexposed (control) mice by staining them with hematoxylin and eosin, Masson trichrome, and Oil Red O. Then, we comprehensively measured the transcriptome-wide m6A methylome and m6A-altered genes using high-throughput sequencing assays, such as methylated RNA immunoprecipitation sequencing and RNA sequencing. Our data indicated MP-induced myocardial inflammatory injury and histological alterations in vivo, evidenced by the severity of cardiac fibrosis and increased lipid accumulation. We found 878 increased and 316 decreased methylation peaks mostly distributed in the 3' UTR among the MP-exposed group compared with the control group. We found 779 upregulated and 340 downregulated genes in the MP-exposed group. In addition, conjoint analysis of results from the two high-throughput sequencings showed that 109 and 11 hypermethylated genes were upregulated and downregulated, respectively; 12 and 21 hypomethylated genes were upregulated and downregulated, respectively. Results of the cross-link analysis showed that several potential signals, such as ECM-receptor interactions, cell adhesion molecules, cytokine-cytokine receptor interactions, and NF-κB signaling, contributed to MP-induced cardiotoxicity. Our findings indicated that m6A modifications of genes were involved in MP-induced cardiotoxicity and reported new information regarding the chronic cardiotoxicity caused by MP exposure in mice.
Sign in to start a discussion.
More Papers Like This
N6-methyladenosine methylation mediates non-coding RNAs modification in microplastic-induced cardiac injury
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.
Microplastic exposure is associated with epigenomic effects in the model organism Pimephales promelas (fathead minnow)
Researchers exposed fathead minnows to microplastics and found changes in DNA methylation -- a chemical modification that controls which genes are turned on or off -- across multiple organs including the brain, liver, and gonads. These epigenetic changes are heritable, meaning microplastic exposure could affect not just the exposed fish but also future generations, raising concerns about long-term ecological and evolutionary impacts.
Beyond genetics: can micro and nanoplastics induce epigenetic and gene-expression modifications?
This review gathers existing research on whether micro and nanoplastics can cause epigenetic changes, which are modifications that alter how genes work without changing the DNA itself. Although studies are still limited, the evidence so far shows that both short-term and long-term plastic particle exposure can trigger these gene-level changes in various organisms. This is concerning because epigenetic changes can potentially be passed to future generations and may contribute to disease.
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.
Changes in global methylation patterns of Mytilus galloprovincialis exposed to microplastics
Researchers found that exposing mussels to polystyrene microplastics caused changes in their DNA methylation patterns, an epigenetic modification that controls how genes are turned on and off. Higher microplastic concentrations led to greater loss of methylation, and similar patterns were seen in wild mussels from polluted areas. This suggests microplastics could affect organisms at the genetic regulation level, potentially influencing metabolism and cell division.