The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that is involved in proliferation, migration and cell growth. It can be activated by binding of ligands, e.g. epidermal growth factor or heparin-bound growth factor or by vasoactive substances like vasopressin (ADH), endothelin (ET-1), phenylephrine (PE) after binding to their specific receptor by a process is called transactivation.

Vascular smooth muscle cells (VSMC) are involved in atheroscelrotic plaque formation, restenosis and vascular remodelling. To elucidate the role of EGFR in VSMC in cell migration, we generated a mouse model with a specific deletion of EGFR in VSMC (EGFR^VSMC-/-), thereby enabling the investigation of the contribution of EGFR to VSMC cell migration and proliferation. The effect of serum on proliferation of VSMC as well as migration in a reconstitution assay and in a boyden chamber model was more pronounced in wild type cells as compared to EGFR^VSMC-/- cells. Similarly cell migration was significantly reduced in EGFR^VSMC-/- cells compared to wildtype cells during vasopressin (ADH) incubation in a reconstitution assay.

Taken together our results show that EGFR is needed for proliferation and migration of VSMC under baseline condition and that increased migration of VSMC upon increased ADH concentration depends on the presence of EGFR.