Airborne fine particulate matter alters the expression of endothelin receptors in rat coronary arteries.

Exposure to airborne fine particulate matter (PM _2.5 ) is associated with cardiovascular diseases. However, a comprehensive understanding of the underlying mechanisms by which PM _2.5 induces or aggravates these diseases is still insufficiently clear. The present study investigated whether PM _2.5 alters the expression of the endothelin subtype B (ET _B ) and endothelin subtype A (ET _A ) receptors in the coronary artery and examined the underlying mechanisms. Rat coronary artery segments were cultured with PM _2.5 in the presence or absence of MEK/ERK1/2, JNK, and p38 pathway inhibitors. Contractile reactivity was measured by myography. ET _B and ET _A receptor expression was evaluated using RT-PCR, western blot and immunohistochemistry. Compared with fresh arteries, the cultured coronary arteries showed a significantly enhanced contraction mediated by the ET _B receptor and an unaltered contraction mediated by the ET _A receptor. Culture with PM _2.5 significantly enhanced the contraction and the mRNA and protein expression levels of the ET _B and ET _A receptors in the coronary arteries, suggesting that PM _2.5 induces an upregulation of ET _A and ET _B receptors. In addition, the PM _2.5 -induced increases in ET _B - and ET _A -mediated vasoconstriction and receptor expressions could be notably decreased by MEK1/2 inhibitor, U0126 and Raf inhibitor, SB386023, suggesting that the upregulation of ET _B and ET _A receptors is related with MEK/ERK1/2 pathway. In conclusion, PM _2.5 induces the ET _B and ET _A receptor upregulation in rat coronary arteries, and the MEK/ERK1/2 pathway may be involved in this process.
(Copyright © 2016 Elsevier Ltd. All rights reserved.)