A Queen's University study sheds new light on the way one of our cell enzymes, implicated in causing tissue damage after heart attacks and strokes, is normally kept under control.
Led by Biochemistry professor Peter Davies, the research team's discovery will be useful in developing new drug treatments that can aid recovery in stroke and heart disease, as well as lessen the effects of Alzheimer's and other neurologically degenerative diseases.
"This is particularly exciting because the enzyme structure we were seeking - and the way its inhibitor blocks activity without itself being damaged - have proved so elusive until now," says Dr. Davies, Canada Research Chair in Protein Engineering.
The team's findings will be published on-line in the international journal, Nature , on Thursday Nov. 20.
In remodeling proteins needed for cell growth and movement, our cells use the enzyme calpain to break off pieces from other proteins. Calpain is activated when the cell releases short bursts of calcium.
During heart attacks or strokes, however, blood supply to cells is interrupted. When the blockage is re-opened, the influx of blood causes calcium levels in the cell to become dangerously high, and the calpain activity to increase. The result is significant damage to tissues. "While you want the enzyme to switch on and off, you don't want it to go out of control," says Biochemistry research associate Rob Campbell, a member of the Queen's team.