A monoclonal antibody derived by inoculation of human umbilical vein endothelial cells is a potential inhibitor of acetylcholine receptor-linked vasorelaxation.

Abstract

In a previous study, we produced antibodies from rats immunized with human umbilical vein endothelial cells (HUVECs) and determined the vascular function of the monoclonal antibodies. However, unanswered question remains still about their role in vascular function. The current study explored vasoreactivity, in particular, focusing on the vascular contractility of a functional antibody against proteins expressed on the plasma membrane of HUVECs developed in a previous study. Among the antibodies developed, A-7 significantly attenuated endothelium-dependent vasorelaxation in response to acetylcholine (ACh) but not to sodium nitroprusside or histamine. In addition, the A-7 antibody did not affect norepinephrine-stimulated contraction in both endothelium-intact and -denuded aorta. Immunocytochemical and immunoblotting analyses showed that A-7 attenuated ACh-increased expression of ACh receptor on the plasma membrane of HUVECs. These findings suggest that the monoclonal A-7 antibody may act as an inhibitor of endothelium-dependent vasorelaxation, probably in part via downregulation of ACh receptor expression.