α-smooth muscle actin (blue) joins stress fibers that are under a lot (top) but not less (bottom) tension.
In vivo, the extracellular matrix rearranges and increases in rigidity in response to wounding. This change, along with the release of growth factors, induces fibroblasts to take on a contractile phenotype, including expression of α-SMA. The question remains, however, as to what triggers incorporation of α-SMA into stress fibers in these cells.
When differentiated myofibroblasts were cultured on flexible substrates, FAs remained relatively small. However when the cells were grown on rigid substrates, supermature FAs formed. Once formed, supermature FAs were able to withstand substantially larger physical forces and generated higher intracellular tension than did FAs of a more typical size. This higher tension in turn triggered α-SMA recruitment to stress fibers, which did not occur in cells with smaller FAs.
The team is working to identify the cellular component that senses the increased tension in stress fibers and recruits α-SMA. In the meantime, they are convinced that tension and size are intimately linked in the formation of supermature FAs and α-SMA stress fibers.
