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. [ABSTRACT FROM AUTHOR]