Affiliations: [a] Biomechanics and Medical Information Institute, Beijing Polytechnic University, Beijing, 100022, China | [b] Lab of Microcirculation, Chinese PLA General Hospital, Beijing, 100853, China | [c] Lab of Neuroscience, Chinese PLA General Hospital, Beijing, 100853, China
Abstract: Intercellular adhesion molecule-1 (ICAM-1) is an adherence molecule that is an important factor in many pathophysiological processes such as atherosclerosis, thrombosis and inflammation. It is secretion of endothelial cells by a variety of biochemical stimulations. But hemodynamic forces can also induce various functional changes in vascular endothelium. Some researches have proved that shear stress can modulate the expression of ICAM-1. But most of them examine the regulation of expression of ICAM-1 in human umbilical vein endothelial cells. There is no detail on the effect of shear stress (SS) on ICAM-1 expression of microvascular endothelial cells (RBMECs). In this experiment, we use cultured rat brain microvascular endothelial cells (RBMECs). By using the parallel plate flow chamber method, we give two magnitudes of lamminar shear stresses (0.2 dyn/cm2, 0.4 dyn/cm2) for different perieods of time on the slides of cells. Immunostaining method and image analysis shows a specific upregulation in ICAM-1 expression on RBMECs, which is different from endothelial cells of other species or vascular beds. Expression of ICAM-1 is increased 0.5h after the onset of SS, and reached its highest level 4h after onset of SS, then declines after that. The effect is time-dependent, not force magnitude-dependent. Endothelial cell surface expression of ICAM-1 in the supernatants of RBMECs exposed to SS was not modified excluding the possibility that RBMECs exposed to SS synthesize factors that upregulate ICAM-1. The experiment data are relevant to the current understanding of basic mechanisms that explain the signal transudation pathway occurring inside the endothelial cells under the effect of SS.
