Background: Prostaglandin E2 (PGE2) induces vasodilatation and vasoconstriction via EP receptors. Among PGE2 receptors, the EP3 receptor was the first to be cloned, although this receptor is known to express various isoforms. In humans, five receptor isoforms exist, which were named EP3-I, EP3-II, EP3-III, EP3-IV, and EP3-e. EP3-I isoform has three splice variants. These variants are designated EP3-Ia, EP3-Ib, and EP3-Ic. Each isoform can initiate distinct signaling pathways. In our recent works, we demonstrated PGE2 induced contraction via EP3 receptor in human coronary artery, the contraction was less pronounced when atherosclerotic coronary artery was used. On the other hand, in non-atherosclerotic preparations, perivascular adipose tissue induced relaxion via EP3 receptor. Material-method: Based on these our previous results, we investigated the EP3-1b, EP3-II, EP3-III and EP3-IV isoforms expression in both atherosclerotic and non-atherosclerotic coronary artery and perivascular adipose tissue by RT-PCR. Results: Our results demonstrated that atherosclerotic coronary artery expressed lower level of EP3-II and EP3-III isoforms versus non-atherosclerotic coronary artery. In atherosclerotic preparations, perivascular adipose tissue expressed greater levels of EP3-Ib and EP3-III isoforms versus coronary artery. In conclusion, there was a difference in EP3 isoforms expression between coronary artery and perivascular adipose tissue. Therefore, the activation of these receptors by PGE2 could result in different effect on vascular tone regulation.
Anahtar Kelimeler: EP3 receptor, coronary artery, perivascular adipose tissue, prostaglandin E2
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