Inhibitory effects of RAGE-aptamer on development of monocrotaline-induced pulmonary arterial hypertension in rats

AbstractBackground The receptor for advanced glycation end products (RAGE), a transmembrane belonging to the immunoglobulin superfamily, is overexpressed in pulmonary artery smooth muscle cells (PASMCs) patients with arterial hypertension (PAH) and implicated etiology of PAH. Recently, we reported that RAGE-aptamer, short single-stranded DNA directed against RAGE, inhibited an inappropriate increase cultured PASMCs aim this study was determine efficacy RAGE-aptamer monocrotaline-induced PAH rats. Methods Results Rats were assigned either untreated control group, group received continuous subcutaneous administration immediately after monocrotaline injection, or control-aptamer injection. All rats survived 21 days injection RAGE-aptamer. Injection delivery resulted higher right ventricular systolic pressure compared controls. This attenuated by proportion small arteries full muscularization greater than group. Continuous significantly reduced percentage muscularization. Conclusions suppresses development Inhibition RAGE ameliorates arteries. Treatment might be new therapeutic option