Adhesion and Function of Human Endothelial Cells Co-cultured on Smooth Muscle Cells

Abstract

To evaluate interactions between human endothelial cells (ECs) and smooth muscle cells (SMCs) for the development of tissue-engineered vessels, we examined the adhesion and key cell properties of human ECs grown on quiescent human aortic SMCs. ECs attached to SMCs spread more slowly than ECs attached to fibronectin surfaces, and ECs aligned along the direction of the SMCs. ECs attached firmly and less than 5% of the cells were removed by shear stresses as high as 300 dyn cm(-2). Unlike porcine SMCs and co-cultures, human SMCs or co-cultures do not contract under flow, and the human ECs and SMCs in co-culture align toward the direction of flow. A confluent endothelium could be maintained in co-culture for over 30 days, and some of the ECs reoriented perpendicular to the SMCs after 9 days in static culture. Surface tissue factor levels in ECs and SMCs were less in co-culture than in monoculture. Co-culture induced an increase in calponin expression in SMCs. These findings show that human co-cultures can be maintained for long culture periods, where the endothelium remains confluent and responds to long-term exposure to flow, and EC-SMC interactions lead to an increase in SMC differentiation and an EC surface that is less thrombotic.

Effect of cellular senescence on the albumin permeability of blood-derived endothelial cells

“…We (48) have found that when ECs are cultured on quiescent vascular smooth muscle cells that EC proliferation is greatly reduced. This coculture system could then be used to mimic vessel wall structure and reduce hCB-EC proliferation toward in vivo values.…”

Characterization of Umbilical Cord Blood–Derived Late Outgrowth Endothelial Progenitor Cells Exposed to Laminar Shear Stress

“…This high strength of adhesion has only been observed a few times for such short attachment times. 32,37 Expression and blocking of a 5 b 1 and a V b 3 integrins Both a 5 b 1 and a V b 3 integrins affect EC adhesion to FN, 32,34 and expression of these integrins may affect the adhesion (Fig. 4A, p < 0.05, n ¼ 4).…”

Biomechanical regulation of vascular smooth muscle cell functions: from in vitro to in vivo understanding

“…EC-VSMC interactions lead to an increase in VSMC differentiation [114]. Atheroprone flow decreases VSMC gene expression (a-SMA and myocardin) and induces a proinflammatory phenotype in ECs and VSMCs by upregulating expression of VCAM-1, IL-8 and monocyte chemoattractant protein-1 (MCP-1) [111].…”