Endothelial cell dysfunction underlies the development of vascular inflammatory diseases. The cellular stiffness of endothelial cells has been shown to increase during chronic inflammation. Abnormalities of endothelial gap junctions facilitate endothelial dysfunction and participate in the progression of cardiovascular diseases; however, the impact of gap junction on endothelial cellular stiffness remains poorly understood. 
To evaluate the cellular stiffness, we have measured the force curve of live human umbilical vein endothelial cells (HUVECs) by using atomic force microscopy. We have shown that stimulation of HUVECs with tumor necrosis factor-α (TNF-α) increased the endothelial cellular stiffness. We have also shown that the blockade of gap junctions not only increases endothelial cellular stiffness, but also enhances focal adhesion formation and cytoskeletal rearrangement. Inhibition of gap junctions appeared to prolong the effects of TNF-α, increasing endothelial stiffness. 
Aberrant regulation of gap junctions may be involved in the vascular stiffening commonly observed in vascular inflammatory diseases. Our study provides a new insight into the potential pathogenic role of endothelial cellular stiffening driven by vascular inflammation.