Zeitschrift für klinische Toxikologie
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Claudin 5 Transcripts Following Acrolein Exposure Affected by Epigenetic Enzyme

Kuk-Young Moon, Pureun-Haneul Lee, Byeong-Gon Kim, Moo-Kyun Park and An-Soo Jang

Background and objective: Acrolein is a highly reactive α, β-unsaturated aldehyde and a respiratory irritant that is ubiquitously present in the environment but that can also be generated endogenously at sites of inflammation. Apical junctional protein claudin 5 can be affected by acrolein. This study aimed to determine the impact of aberrant expression of DNMT1, DNMT3b, MBD3, and MeCP2 on acrolein induced claudin 5.
Methods: EA.hy926 cell lines were exposed to acrolein 30 nm for 1 h, 2 h, and 4 h. Epigenetic enzyme such as DNMT1, DNMT3b, MBD3 and MeCP2 were quantified in the cell line using real time PCR. Claudin 5 methylation was checked by methtyl specific PCR.
Results: After acrolein 30 nm exposure, MBD3 and MeCP2 transcript were decreased at 1 h and increased at 2 h and 4 h compared to control. DNMT3b transcript was decreased at 1 h, 2 h, and 4 h following acrolein 30 nm exposure. DNMT1 transcript was not different between control and acrolein 30 nm exposure. Claudin 5 methylation transcript /total Claudin 5 transcript was decreased at 1 h, 2 h and 4 h following acrolein 30 nm exposure.
Conclusion: These findings demonstrate that acrolein exposure modify epigenetic enzyme leading to Claudin 5 methylation change, suggesting that acrolein contribute to enzyme pathway involved in epigenetic regulation.