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First published online December 1, 2003

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Stretch-activated channels lead the way

Cell migration requires cycles of cytoplasmic protrusion, adhesion, contraction and de-adhesion as the cell travels over the underlying substratum. Cells must be able to `sense' the substrate and possess mechanisms that allow them to respond to mechanical signals such as stretching. Release of calcium from stretch-activated channels could play an important role in this. Yu-Li Wang and co-workers have combined state-of-the-art traction force microscopy with conventional calcium biochemistry to examine the function of these channels and map their locations (see p. 53). They show that stretching forces trigger increases in intracellular calcium concentration and traction in fibroblasts, which can be blocked by the stretch-activated channel inhibitor gadolinium or removal of extracellular calcium. They then use focal delivery of gadolinium to show that – contrary to previous speculation – it is the channels at the leading edge rather than those at the tail that are important. Furthermore, they demonstrate that gadolinium significantly reduces the levels of phosphotyrosine and the structural protein vinculin at focal adhesions. The authors therefore conclude that calcium entry through stretch-activated channels regulates mechanical forces produced at the leading edge as well as the organization of cell-substratum attachments.

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