Naoto Kawasaki

Effects of cold exposure and shear stress on endothelial nitric oxide synthase activation.

Endothelial nitric oxide synthase (eNOS) is the primary enzyme that produces nitric oxide (NO), which plays an important role in blood vessel relaxation. eNOS activation is stimulated by various mechanical forces, such as shear stress. Several studies have shown that local cooling of the human finger causes strong vasoconstriction, followed after several minutes by cold-induced vasodilation (CIVD). However, the role played by endothelial cells (ECs) in blood vessel regulation in respond to cold temperatures is not fully understood. In this study, we found that low temperature alone does not significantly increase or decrease eNOS activation in ECs. We further found that the combination of shear stress with temperature change leads to a significant increase in eNOS activation at 37°C and 28°C, and a decrease at 4°C. These results show that ECs play an important role in blood vessel regulation under shear stress and low temperature.

Growth of Endothelial Cells on Surfaces Modified by a Plasma-Polymerized Coating

Endothelial cell adhesion and growth were investigated on three types of surfaces with a plasma-polymerized coating (PPC): (1) the pristine surface of a hexamethyldisiloxane (HMDS) PPC (hydrophobic, electrically neutral surface); (2) an HMDS PPC surface with nitrogen-containing plasma treatment (hydrophilic, positively charged surface); and (3) an HMDS PPC surface treated with oxygen plasma (hydrophilic, negatively charged surface). Endothelial cells grew on surface (2) but not on surfaces (1) or (3). Next, endothelial cell adhesion and growth was investigated on a surface on which 80-μm squares were micro-patterned at 160-μm intervals in a mosaic composed of two different (cell-adhesive and non-cell-adhesive) regions. Cell growth on the patterned surfaces was different from that on non-patterned surfaces. PPC was shown to be a simple process for modulating cell adhesion to surfaces.