Archived News


March 19, 2002

Platelets, the clot-forming cells that stop you bleeding to death from a shaving cut, are always in high demand from blood banks but have a short shelf life. Using a new process discovered at the University of California, Davis, platelets can be freeze-dried and stored for at least a year at room temperature before being reconstituted with water.

Blood banks store whole platelets at room temperature because they are damaged by cold. Under federal regulations, platelets have to be discarded after five days. Freeze-drying could extend their shelf life and allow them to be transported easily.

Usually, dehydration kills human cells. Wim Wolkers, Naomi Walker, John Crowe and Fern Tablin at the UC Davis Biostabilization Laboratory used trehalose, a sugar, to protect the cells during the freeze-drying process. Animals and plants that are naturally able to withstand extreme drying often use trehalose as a protectant, Crowe said.

Trehalose replaces water in the “shell” around proteins and other large molecules in the cell. This seems to protect the structure of these proteins as water is removed.

Wolkers found a simple method to make platelets take up trehalose, and showed that they could then be freeze-dried.  The dried platelets can be resurrected after at least a year.  The method is currently in clinical trials for use with human and animal blood, Crowe said.

Dried platelets might also be used for novel devices, such as “smart” bandages that promote clotting and wound healing, Crowe said.

The UC Davis group is also investigating freeze-drying of more complex cells. The technology could, for example, be used to store human stem cells or for bioelectronic devices with living cells fused to a microchip.


Platelets, the cells that make blood clot, are in high demand from blood banks. Blood banks store them at room temperature and throw them out after five days. They would last longer refrigerated, but if you chill platelets, they activate and form a useless clot in the bag. Researchers have now shown that a key step for that activation is the formation of “lipid raft” structures in the membranes enclosing the cells.

Discovering how and why platelets get activated is also important for understanding how blood clots can cause heart attacks and strokes.

Karine Gousset and colleagues from the University of California, Davis, Biostabilization Laboratory, led by John Crowe and Fern Tablin, have shown that chilling causes changes in the platelets’ outer membrane. At body temperature, cell membranes are fairly fluid, like a soap bubble. The fatty molecules that make up the membrane can jostle and move around next to each other.

When the temperature drops, some of the molecules in the membrane, such as cholesterol and another molecule called sphingomyelin, clump into distinct islands in the membrane called “lipid rafts.” Some proteins attached to the surface, including some that carry signals from the cell surface to the inside, are also collected into these rafts.

After rafts form, the cells show other signs of activation, such as increased calcium levels, Crowe said. Platelets respond to other signals in the same way, showing that lipid raft formation is a general first step in platelet activation, Crowe said.

The news tips above were originally distributed March 15, 2002 by the Campus News Service, University of California, Davis.

Dr. Fern TablinIn 2001, School of Veterinary Medicine professor Fern Tablin, Department of Anatomy, Physiology and Cell Biology, was one of two veterinary faculty elected to the American Association for the Advancement of Science, the world’s largest scientific organization. Two of Tablin’s recent publications include “Animal models for studies on cold-induced platelet activation in human beings” in the Journal of Laboratory and Clinical Medicine, 2000, and “Membrane reorganization during chilling: Implications for long-term storage” in Cryobiology, now in press.