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Transcriptomics changes and the candidate pathway in human macrophages induced by different PM2.5 extracts.

Jing An1, Waner Tang1, Lu Wang1

  • 1School of Environmental and Chemical Engineering, Shanghai University, Shanghai, 200444, China.

Environmental Pollution (Barking, Essex : 1987)
|August 6, 2021
PubMed
Summary
This summary is machine-generated.

Fine particulate matter (PM2.5) triggers oxidative stress and inflammation via water-soluble components. Organic PM2.5 components disrupt cell cycle regulation, impacting human health.

Keywords:
BioinformaticsCell cycleInflammationParticulate matterTranscriptomics

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Area of Science:

  • Environmental Health
  • Molecular Toxicology
  • Transcriptomics

Background:

  • Ambient fine particulate matter (PM2.5) is a global environmental hazard with significant health implications.
  • The precise molecular mechanisms and toxic components of PM2.5 remain incompletely understood.
  • Investigating PM2.5's impact on cellular pathways is crucial for understanding its toxicity.

Purpose of the Study:

  • To elucidate the transcriptomic alterations in macrophages exposed to different PM2.5 extracts.
  • To identify key molecular pathways and genes involved in PM2.5 toxicity.
  • To explore the differential effects of seasonal PM2.5 components on cellular responses.

Main Methods:

  • Utilized RNA sequencing to analyze whole transcriptomic changes in THP-1 derived macrophages.
  • Applied bioinformatics analyses including Gene Ontology (GO), KEGG pathway, and protein-protein interaction (PPI) networks.
  • Compared the effects of water extracts (WEs) and dichloromethane extracts (DEs) from PM2.5 collected in different seasons.

Main Results:

  • PM2.5 water extracts significantly modulated genes and pathways associated with oxidative stress and inflammation.
  • PM2.5 dichloromethane extracts specifically impacted cell cycle-related genes and signaling.
  • Non-heating season WEs induced higher expression of calcium-associated genes, suggesting enhanced inflammation.
  • Heating season DEs exhibited extensive cell cycle pathway dysregulation, potentially due to higher polycyclic aromatic hydrocarbons (PAHs).

Conclusions:

  • Water-soluble PM2.5 components induce oxidative stress and inflammation in macrophages.
  • Organic PM2.5 components contribute to cell cycle dysregulation, a key factor in PM2.5's biological effects.
  • Seasonal variations in PM2.5 composition, including PAHs and metal ions, influence transcriptomic responses.