A Novel Approach against Vascular Intimal Hyperplasia Through the Suppression of Girdin

Abstract

Intimal hyperplasia is an impediment to patency in both arteries after percutaneous angioplasty (PTA) and veingraft. It is well known that migration and proliferation of vascular smooth muscle cells (SMCs) influence the vascular remodeling process, there are no therapies to prevent intimal hyperplasia of post-PTA arteries and vein grafts. Girdin (girders of actin filaments), also known as Gα-interacting vesicle associated protein (GIV) is a novel actin-binding Akt substrate.Girdin is highly expressed in limited types of cells such as smooth muscle cells, neuroblasts, and cancer cells. Girdin is involved in the cell migration, proliferation and remodeling of actin filaments. This study revealed that Girdin is involved with intimal hyperplasia in carotid arteries after balloon injury and vein grafts and vascular SMCs migration and proliferation. There are suggestions that Girdin has pivotal roles in migration and proliferation of vascular SMCs and that gene therapy targeting Girdin could be a novel therapeutic strategy for restenosis after PTA and vein graft failure.