Glycation of matrix proteins in the artery inhibits migration of smooth muscle cells from the media to the intima

Abstract

Formation and growth of atherosclerotic plaques have serious clinical consequences. One mechanism that occurs during atherogenesis is migration of smooth muscle cells from the middle layer of the artery to the intima, where they proliferate and are transformed into foam cells. This degenerative process is accompanied by glycation, by which proteins are modified and change the biomechanical and biochemical properties. The aim of the study was to determine whether glycation of collagen and elastin building the walls of blood vessels alters the adhesion and rate of myocyte migration. In vitro experiments included migration assays and immunocytochemical staining with anti α-actin, β-catenin anti-collagen type IV antibodies. It turns out that there is a tendency to decrease the number of cells that had migrated through the barrier consisting of glycated proteins as compared to the control. Adversely, the morphology of the cells cultured in the presence of glycated substrates is changed. The lower intensity of β-catenin staining indicates lower adhesiveness of such cells. It is proposed that glycation inhibits migration of smooth muscle cells from the media to the intima, which represents part of the anti-atherogenic mechanism.