Fine particulate matter 2.5 exerted its toxicological effect by regulating a new layer, long non-coding RNA

Area of Science:

• Environmental Health
• Molecular Biology
• Toxicology

Background:

• Fine particulate matter (PM2.5) exposure, particularly its organic components, causes respiratory issues, but molecular mechanisms remain unclear.
• Long non-coding RNAs (lncRNAs) are implicated in various physiological and pathological processes.
• Understanding lncRNA roles in PM2.5 toxicology is crucial for respiratory health research.

Purpose of the Study:

• To investigate the role of lncRNAs in the toxicological effects of PM2.5 on human bronchial epithelial cells.
• To elucidate the molecular mechanisms underlying PM2.5-induced respiratory damage.
• To compare the toxicity of PM2.5 from different urban environments.

Main Methods:

• Human bronchial epithelial cell lines (BEAS-2B and A549) were exposed to organic extracts of PM2.5 from Nanjing and Shanghai.
• RNA sequencing was performed to analyze lncRNA and mRNA expression profiles.
• The expression of specific lncRNAs (n405968, MALAT1) and inflammatory factors (IL-6, IL-8) was quantified.
• The epithelial-mesenchymal transition (EMT) process was assessed.
• The involvement of the aryl hydrocarbon receptor (AHR) and CYP1A1 was investigated.

Main Results:

• PM2.5 exposure altered lncRNA and mRNA profiles, with Nanjing PM2.5 showing greater impact.
• Increased expression of lncRNA n405968 correlated with elevated inflammatory factors (IL-6, IL-8).
• Increased MALAT1 expression was associated with induced EMT.
• Higher polycyclic aromatic hydrocarbon (PAH) content in Nanjing PM2.5 likely contributed to its increased toxicity.
• Antagonism of AHR or inhibition of CYP1A1 reduced PM2.5-induced effects.

Conclusions:

• lncRNAs are involved in PM2.5 toxicology by regulating inflammation and EMT in bronchial epithelial cells.
• PM2.5 composition, such as PAH content, influences its toxicity.
• AHR and CYP1A1 pathways are implicated in mediating PM2.5 toxicity.