Earlier research showed that calcium ions are involved in wound response. In the current study published in the Biophysical Journal, led by Shane Hutson and Andrea Page-McCaw, cells on the back of fruit fly pupae were targeted which expressed a protein that fluoresces in the presence of calcium ions. The changes in calcium ion concentrations in the cells around wounds in living tissue were tracked with an unprecedented, millisecond precision.
In the current study, two prevailing hypotheses for the wound-response trigger were tested. Firstly, the proteins released by the damaged and dying cells are sensed by the surrounding cells and cause them to boost their internal calcium levels and in turn triggers the wound healing mechanism. Secondly, the trigger signal spreads from cell to cell through gap junctions. The ions, molecules and electrical impulses are exchanged through the microscopic gates.
Creating a wound generated complex series of calcium signals in the surrounding tissue:
- Firstly, a rapid influx of calcium into the cells around the wound matches the footprint of the cavitation bubble. The calcium levels in the extracellular fluid are higher than intracellular fluids. As the process occurs rapidly, the researchers disagreed that micro-tears created by the force of the micro-explosion caused influx.
- Then, a short-ranged wave spreads through healthy neighbouring cells: while the wave spreads rapidly if the wound is bigger. The speed of wave suggests that it travels through gap junctions and is made up of calcium ions or some other small signalling molecule.
- There is a second wave which appears about 45 seconds after wounding which move gradually than the first wave but spreads considerably farther. Researchers found that the special signalling proteins play the role here. They move more slowly than ions although the evidence is unclear. The second wave only occurs when cells are killed which signifies that it is dependent on the extent of the damage.
- The first two waves spread relatively symmetrically through the tissue. After the second wave, however, the area of high calcium concentration begins sending out "flares". Each flare lasts for ten seconds and new flares continue starting for more than 30 minutes after the injury.
Hutson concluded, “Outlining the trigger mechanisms would help in finding ways to stimulate the wound healing in diabetic patients as well as hastening normal wound healing.”