Abstract
The mechanisms involved in vascular homeostasis and disease are mostly dependent on the interactions between blood, vascular smooth muscle, and endothelial cells. There is an accumulation of evidence for the involvement of prostanoids, the arachidonic acid metabolites derived from the cyclooxygenase enzymatic pathway, in physiological and/or pathophysiological conditions. In humans, the prostanoids activate different receptors. The classical prostanoid receptors (DP, EP1–4, FP, IP, and TP) are localized at the cell plasma or nuclear membrane. In addition, CRTH2 and the nuclear PPAR receptors are two other targets for prostanoids, namely, prostacyclin (PGI2) or the natural derivatives of prostaglandin D2. While there is little information on the role of CRTH2, there are many reports on PPAR activation and the consecutive expression of genes involved in the human vascular system. The role of the classical prostanoid receptors stimulated by PGI2 and thromboxane in the control of the vascular tone has been largely documented, whereas the other receptor subtypes have been overlooked. There is now increasing evidence that suggests a role of PGE2 and the EP receptor subtypes in the control of the human vascular tone and remodeling of the vascular wall. These receptors are also present on leukocytes and platelets, and they are implicated in most of the inflammatory processes within the vascular wall. Consequently, the EP receptor subtypes or isoforms would provide a novel and specific cardiovascular therapeutic approach in the near future.
Highlights
Prostanoids are derived from membrane phospholipids and the metabolism of arachidonic acid via the rate-limiting enzyme prostaglandin H synthase more commonly known as cyclooxygenase (COX)
The different effects of prostanoids are dependent on the activation of specific receptors, namely, the eight classical prostanoid receptors (DP, EP1–4, FP, IP, and TP; Table 1), as well as the recently described chemoattractant receptor CRTH2 and nuclear receptors (PPARα,δ,γ)
They are responsible for many physiological events, for example, the activation of PPARα receptors expressed in human aortic smooth muscle cells promotes their proliferation[59]
Summary
INSERM U698: Haemostasis, Bioengineering and Cardiovascular Remodeling CHU X. There is increasing evidence that suggests a role of PGE2 and the EP receptor subtypes in the control of the human vascular tone and remodeling of the vascular wall. Some isoforms derived from splice variants have been described in human tissues for the EP3 receptor (EP3-I, EP3-II, EP3-III, EP3-IV, EP3-V, EP3-VI, EP3-e, EP3-f)[1], the FP receptor (FP-A, FPB), and the TP receptor (TP-α, TP-β)[2] These receptors, as well as the CRTH2, are found on the cytoplasmic membranes and they are seven transmembrane domain G-protein coupled receptors (Table 1). Their activation leads to increased or decreased production of different intracellular second messengers (Table 1) This situation has been further complicated by the increasing evidence for the presence of the classical prostanoid receptors at the nuclear and/or perinuclear region[3].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
