Anti-inflammatory activity of ghrelin in human carotid artery cells

Receptors for eicosanoids such as prostaglandin E(2), prostacyclin and thromboxane A(2), as well as the ghrelin receptor polypeptide (GHS-R1b), can all regulate ghrelin (GHS-R1a) receptor activity, by the process of hetero-oligomerization, when heterologously expressed in human embryonic kidney (HEK 293) cells. To determine if such regulation might occur in inflammatory diseases of the vasculature, we incubated human coronary artery endothelial cells and human coronary artery smooth muscle cells with lipopolysaccharide and determined mRNA expression levels of these proteins using real-time PCR. Acute inflammation increased GHS-R1a mRNA in smooth muscle cells and increased cyclo-oxygenase-2 mRNA in endothelial cells; both these changes were attenuated by pretreatment of cells with ghrelin. Lipopolysaccharide did not affect expression of GHS-R1b or prostanoid receptor mRNA. Therefore, hetero-oligomerization of GHS-R1a with GHS-R1b or prostanoid receptors is unlikely to influence GHS-R1a activity in the vasculature; at least under conditions of acute vascular inflammation.