Japanese scientists have claimed that a number of toxins found in snake venom could help develop new therapies for chronic diseases like heart attack, stroke and cancer.
The scientists, who reported their findings in the Journal of Biological Chemistry, said that inhibiting a protein found on the surface of blood cells known as platelets may combat both irregular blood clotting and the spread of certain cancers throughout the body.
“The finding that platelets not only play a role in blood clotting but also in the development of vessels that allow tumours to flourish was quite unexpected and paves the way for new research on the role or roles of platelets,” said Ms Katsue Suzuki-Inoue, the associate professor at the University of Yamanashi.
She said: “When a blood clot, or thrombus, forms during the body’s normal repair process, it’s doing its job. But, thrombotic diseases, such as heart attack and stroke, are leading causes of death in developed countries.”
“Understanding and manipulating the underlying chemical reactions could help us save many lives.”
The researchers said that snake venom contains a vast number of toxins that target proteins in platelets.
“Some of those toxins prevent platelets from clotting, which can lead to profuse bleeding in snake bite victims. Others potently activate platelets, which results in blood clots,” said Yonchol Shin, an associate professor at Kogakuin University who specialises in snake toxins.
“Identification of the molecular targets of many of these toxins has made an enormous contribution to our understanding of platelet activation and related diseases.”
In 2000, researchers had come across a protein on the surface of platelets, called CLEC-2. At the time, it remained unclear how CLEC-2 was produced or what its job was, but the team suspected it was worth further study.
In 2006, the team discovered how rhodocytin — a molecule purified from the venom of the Southeast Asia pit viper Calloselasma rhodastoma — binds to the CLEC-2 receptor protein on the platelet surface, spurring the platelet to clot with others like it.
Then, in 2007, Suzuki-Inoue and her colleagues reported how a separate molecule, called podoplanin, binds to the CLEC-2 platelet receptor protein very much like the venom molecule does.