Want to protect yourself from the next polar vortex? Add some antifreeze protein to your genome and you may never have to worry about frostbite again. This is precisely what researchers from a Yale-led study have been able to demonstrate recently by transgenically adding an antifreeze protein into mice.
Several species of animals, such as ticks, frogs, and fish, have evolved the ability to survive and even thrive in harsh cold weather environments. They achieve this feat through the expression of various proteins in their genomes that aid in cold weather protection. However, by contrast, these proteins are relatively absent in the genetic make-up of mammals, a key reason for cold temperature injuries such as frostbite.
“We wanted to ask if you put antifreeze in mammals, can you protect them from a cold injury,” said Erol Fikrig, M.D., professor of medicine at Yale School of Medicine, investigator for the Howard Hughes Medical Institute, and senior author on the study. Dr. Fikrig and his team published their findings recently in PLoS ONE through an article entitled “Frostbite Protection in Mice Expressing an Antifreeze Glycoprotein”.
The investigators transfected an antifreeze glycoprotein, named IAFGP, from the black-legged tick, into mouse cells and whole live mice. Specifically, they tested the frostbite resistance of skin cells derived from IAFGP-transgenic mice and control mice. The team cultured the cells at 4°C for four days and found that the IAFGP-treated cells not only held up better, but had increased proliferation rates in comparison to controls.
Additionally, Dr. Fikrig and his team observed the effect of the antifreeze protein on whole mice tails. They found that after seven days of exposure to cold temperatures, 60% of the IAFGP-treated mice had no visible signs of frostbite, compared to 11% of the untreated control mice. Moreover, the IAFGP-treated tails were observed to have decreased indications of inflammation damage caused by frostbite when compared to controls.
“This study shows that if you put an antifreeze protein into warm-blooded animals, it does elicit antifreeze activity and it can protect the animal from frostbite,” Dr. Fikrig explained.
Research is still ongoing into the exact mechanism that allows IAFGP to protect mammalian cells from cold damage, but the team’s current hypothesis is that the protein prevents the growth of ice crystals within the cells. If crystals are allowed to form, they puncture through the cell and organellar membranes causing tissue necrosis and eliciting an inflammatory response — hallmarks of frostbite.
The benefits of this research could be far-reaching. For example, proteins such as IAFGP could potentially extend the length of time tissue is placed in cold storage, prior to it being used for transplantation. Furthermore, certain disorders such as scleroderma and Raynaud's disease, which are characterized by extreme cold sensitivity, may benefit immensely from this type of study.