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AHR-mediated m

Cheng Ji1, Yizhou Tao1, Xiaoxiao Li2

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Summary
This summary is machine-generated.

Fine particle matter (PM2.5) exposure harms heart development by altering m6A RNA methylation via the aryl hydrocarbon receptor (AHR). This leads to apoptosis and cardiac defects in zebrafish larvae.

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Area of Science:

  • Environmental Toxicology
  • Molecular Biology
  • Developmental Biology

Background:

  • Ambient fine particle matter (PM2.5) is linked to inhibited heart development.
  • The precise molecular mechanisms underlying PM2.5 cardiac toxicity are not fully understood.
  • N6-methyladenosine (m6A) RNA methylation is crucial for cellular processes and development.

Purpose of the Study:

  • To investigate the role of m6A RNA methylation in PM2.5-induced cardiac developmental toxicity.
  • To elucidate the molecular pathways connecting PM2.5 exposure to heart defects.

Main Methods:

  • Zebrafish larvae were exposed to extractable organic matter (EOM) from PM2.5.
  • Measurements included global m6A RNA methylation levels, reactive oxygen species (ROS) generation, mitochondrial damage, and apoptosis.
  • Gene expression analysis focused on methyltransferases (METTL14, METTL3), aryl hydrocarbon receptor (AHR), and apoptosis-related genes (traf4a, bbc3).
  • Pharmacological interventions included betaine (methyl donor) and CH223191 (AHR inhibitor).
  • Gene knockdown and forced expression were used to assess gene function.

Main Results:

  • PM2.5 EOM significantly decreased cardiac m6A RNA methylation in zebrafish.
  • Betaine treatment restored m6A levels and attenuated EOM-induced ROS, mitochondrial damage, apoptosis, and heart defects.
  • EOM activated AHR, which repressed METTL14 and METTL3 transcription, leading to genome-wide m6A changes.
  • AHR inhibition alleviated aberrant m6A methylation.
  • EOM upregulated apoptosis-related genes traf4a and bbc3; forced METTL14 expression restored their levels.
  • Knockdown of traf4a or bbc3 reduced EOM-induced ROS and apoptosis.

Conclusions:

  • PM2.5 exposure induces cardiac malformations through m6A RNA methylation alterations.
  • The mechanism involves AHR-mediated downregulation of METTL14, leading to increased traf4a and bbc3 expression.
  • This results in apoptosis and subsequent cardiac defects, highlighting m6A RNA methylation as a key mediator of PM2.5 cardiotoxicity.