The presence of GSSG is linked to an excessive amount of glutamate that is released in the brain after a stroke. Glutamate is a neurotransmitter that, in tiny amounts, has important roles in learning and memory. Too much of it triggers a sequence of reactions that lead to the death of brain cells the most damaging effects of a stroke.
This experiment showed for the first time that the loss of MRP1 function impairs the clearance of GSSG, and that MRP1 cells were recruited to the site of the stroke in normal mice, indicating this protein has a protective role in the brain after a stroke.
The researchers searched databases containing genomic data for a microRNA that appeared to have potential to influence production of MRP1. MicroRNAs bind to messenger RNA, which contains the actual set of instructions for building proteins. When that connection is made, however, the microRNA inhibits the building of protein from messenger RNA. So an inverse relationship exists between a microRNA and a protein it controls.
The researchers saw this very relationship in the cell study in which they manipulated the candidate microRNA levels and observed the effects of changing those levels on the presence of the MRP1 protein.
Finally, the researchers compared mice that were treated with TCT supplements or corn oil as a control for 13 weeks before a stroke was induced. The amount of damaged brain tissue was smaller in the mice that received TCT supplementation than in the mice receiving corn oil. In addition, TCT supplementation was associated with a lower level of the candidate microRNA in the damaged brain tissue, as well as an increase in the abundance of MRP1 cells at the stroke site.
"Essentially what we are showing with mechanistic explanatio
|Contact: Chandan Sen|
Ohio State University