The research team led by Drs Benjamin Kile and David Huang has discovered that platelet life span is controlled by two key molecules. The discovery raises the prospect of developing a new drug to prolong the life span of platelets stored in blood banks, effectively increasing the availability of this life-saving blood product.
An undesirable side effect of cancer chemotherapy is extensive bruising and potentially life-threatening bleeding. This is caused by the unintended depletion of platelets, tiny circulating blood cells that are essential for blood clotting and wound healing. Consequently, the well being of some patients depends upon platelet transfusions, particularly during the vulnerable periods that follow anti-cancer treatment. The significant demand for high quality platelets, coupled with their short shelf life of only five days, presents major logistical challenges in clinical practice.
The scientific team has found that two specialised molecules act in opposition to each other to control platelet life span by regulating the process known as "apoptosis." This term refers to the normal and healthy self destruction of old, damaged and surplus cells. One protein (known as Bcl-xL) acts to preserve the life of the platelet, while the other protein (Bak) prepares the cell to self-destruct after its usual life span within the body - about a week.
WEHI's Dr David Huang said, "Apoptosis is an essential process, common in other cells, but the central role it plays in controlling the life span of the highly specialised platelet has not been previously appreciated. With this new knowledge, we are in a much stronger position to devise better therapies for the management of platelet-related diseases."
Dr Kile added, "For fifty years doctors have speculated about what controls platelet life span. We now know the identity of the precise molecular switch responsible. The team is now actively pursuing a drug development program
Contact: Brad Allan