Endothelial cell responses to mechanical forces such as shear stress and tensile stress have been a subject of intense investigations. However, there is a substantial lack of studies addressing the effects/mechanism of hydrostatic pressure on endothelial cell function. It is known that pathologies such as venous congestion, compartment syndrome etc., are closely associated to the increased intravascular and/or interstitial hydrostatic pressure.
In this study we examined vascular endothelial cell (HUVEC) responses to increased hydrostatic pressure (IHP). To this end, HUVEC were seeded into μ-Slide IV (ibidi) channels and grown to confluence. Subsequently, one end of the channel was connected to the pressure monitor and the other end was connected to the cell culture medium reservoir, which was elevated to the height to induce 30mmHg hydrostatic pressure within the channel under conditions of “no flow”. HUVEC were exposed to the IHP (30mmHg) for 4 hrs in 5%CO2 cell culture incubator at 37°C. Control HUVEC were cultured at ambient pressure (0mmHg) under the same conditions.
The obtained results indicate that exposure of HUVEC to 30mmHg IHP results in: 1) prominent formation of F-actin stress fibers (Phalloidin staining), 2) changes in VE-cadherin junctional staining pattern, 3) induction of oxidative stress (DHR123 oxidation), 4) induction of apoptosis (caspase-3 activity assay), and 5) increased neutrophil adhesion to HUVEC.
These results indicate that increased hydrostatic pressure per se is a critical factor contributing to endothelial cell activation and dysfunction.
Available at: http://works.bepress.com/douglas-fraser/30/