%0 journal article %@ 2352-3697 %A Franke, R.P.,Fuhrmann, R.,Krueger, A.,Jung, F. %D 2015 %J Journal of Cellular Biotechnology %N 1 %P 119-130 %R doi:10.3233/JCB-15012 %T Reaction of arterial endothelial cells to stent impression: In vitro study using a model of the human artery wall %U https://doi.org/10.3233/JCB-15012 1 %X Stenoses in arterial blood vessels by artherosclerotic processes can decrease the supply of downstream tissue dramatically. The implantation of stents by percutaneous coronary intervention is one method of choice to restore the physiological blood flow. In some cases in-stent re-stenoses by thrombotic events, vascular wall hyperplasia or endothelial dysfunction occur. Causes and nature underlying this processes are not fully understood.,Aim of the present study was to study the re-stenotic processes after stent impress on a cellular and molecular level in vitro. Therefore, human arterial endothelial cells (HUAEC) were seeded on a model vascular wall intima consisting of extracellular matrix secreted by bovine corneal endothelial cells. Subsequently, a pre-mounted balloon-expendable tubular stent made of 316 L was impressed through the HUAEC layer leading to an impairment of the vessel wall intima. After stent removal the wound healing process, HUAEC membrane integrity, vitality, proliferation and function were assessed.,Immediately after stent impress an increased level of lactate dehydrogenase (LDH) was observed indicating an impairment of the cell membrane integrity. After 24 h baseline LDH values presented again. HUAEC vitality adjacent to the stent impress induced wound was normal (investigated by inverted microscopy). The proliferation of HUAEC was the highest in the direct vicinity of the stent impress induced wound. Prostacyclin and nitric oxide decreased significantly indicating a temporary loss of cell function.,These results could imply that the healing process of the endothelial cell lesion is superior to the maintenance of vascular tonicity and downregulation of platelet aggregation.