Forced to bond
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《细胞学杂志》
The bonds between leukocytes and endothelial cells last longer when under some strain, as shown by Yago et al. (page 913). The results explain why these white blood cells attach to and roll along the vasculature only when blood flow is strong enough.
Most explanations of this flow-enhanced adhesion suggest that flow increases the number of bonds that form between L-selectin on leukocytes and PSGL-1 or other ligands on vascular cells, possibly by rotating or deforming the blood cell. But some scientists believe that force generated from flow might also increase the lifetime of existing bonds.
The new results show that catch bonds—those whose lifetimes are lengthened by force—between L-selectin and PSGL-1 control leukocyte rolling. The authors correlated the lasting power of individual bonds with the rolling stability of the cells. As the force imposed on bonds increased, their lifetimes increased. The blood cells thus rolled more slowly on PSGL-1 substrates. Slow rolling allows leukocytes to respond to chemokines and traverse the endothelium. The force requirement probably prevents inflammation and leukocyte clumping at vascular blockages.
Above optimum shear, when blood cells roll most slowly, catch bonds became slip bonds, whose lifetimes are shortened by force. Rolling velocities thus increased, and the cells detached from the substrate. The transition to slip bonds may explain why leukocytes usually do not adhere in arteries, where blood flow is very strong.(L-selectin bonds hold longer as force in)
Most explanations of this flow-enhanced adhesion suggest that flow increases the number of bonds that form between L-selectin on leukocytes and PSGL-1 or other ligands on vascular cells, possibly by rotating or deforming the blood cell. But some scientists believe that force generated from flow might also increase the lifetime of existing bonds.
The new results show that catch bonds—those whose lifetimes are lengthened by force—between L-selectin and PSGL-1 control leukocyte rolling. The authors correlated the lasting power of individual bonds with the rolling stability of the cells. As the force imposed on bonds increased, their lifetimes increased. The blood cells thus rolled more slowly on PSGL-1 substrates. Slow rolling allows leukocytes to respond to chemokines and traverse the endothelium. The force requirement probably prevents inflammation and leukocyte clumping at vascular blockages.
Above optimum shear, when blood cells roll most slowly, catch bonds became slip bonds, whose lifetimes are shortened by force. Rolling velocities thus increased, and the cells detached from the substrate. The transition to slip bonds may explain why leukocytes usually do not adhere in arteries, where blood flow is very strong.(L-selectin bonds hold longer as force in)