In the hopes of better understanding microRNA’s function, Craig Morrell, D.V.M., Ph.D., infected mice lacking microRNA 451 with malaria, thinking the missing microRNA would cause the mice to succumb more quickly.
Instead, they all got better.
“So like most things we do, it was an accidental discovery,” quipped Morrell, associate professor of medicine in the Aab Cardiovascular Research Institute.
The discovery led to an application for a CTSI Pilot Grant, which allowed Morrell and Lesley Chapman, a fifth year predoctoral student in the translational biomedical science program, to further their study of microRNA 451, which plays a role in T-cell proliferation.
Normally, when the body fights a disease, T-cells help to identify and respond to the invasive microbe.
“We thought that platelets stuck to the malaria-infected red blood cells would deliver the microRNA and slow down the parasite growth, so we expected the mice without that microRNA to have a higher number of parasites,” said Morrell. “But it turns out that the whole animal is much more complicated. Without that microRNA, they cleared the infection.”
Now, Morrell suspects that the microRNA blunts T-cell proliferation in some way. While this could potentially lead to an effective malaria treatment, Morrell thinks that developing such a treatment would mean encountering some tricky socioeconomic barriers along the way.
But the research could lead to breakthroughs in other areas. One potential example would be the use of microRNA 451 to reduce T-cell responses following organ transplant, where one of the primary complications is an immune response to the new organ.
“It was really your classic pilot project,” said Morrell. “The CTSI got us started with a nice sum of money to really support some preliminary data, and now we can get that publication we need to move things along.”