It’s been pretty well established that miRNAs really get their hands dirty with various affairs of the heart like development and function (not romance and relationships). So it stands to reason that when things start to go haywire with the heart, like a myocardial infarction (MI), that miRNA expression gets out of whack, too.
Scientists from Harbin Medical University in China, armed with miRNA expression arrays and protein-protein interaction (PPI) software, conducted a study to see if they could ID some key miRNAs related to MI. The team used a rat MI model, and profiled miRNA expression in animals with and without treatment of propranolol, a ß-adrenoreceptor blocker used in MI patients. Here’s what their data revealed:
- Microarray results showed 31 miRNAs were dysregulated by MI, 18 of those were rescued by propranolol.
- PPI analysis found that three important miRNAs had a specific regulatory emphasis: miR-1 (myocyte growth), miR-29b (fibrosis) and miR-98 (inflammation).
Now that the role of miRNA regulation has been confirmed in ischemic heart, and some of the critical miRNAs in MI have been tagged, the dedicated group from China hopes that their process and techniques can be applied to other diseases in addition to aiding in the development of other propranolol-like therapeutics for heart disease.
Find all of the heart pumping details at PLoS One, March, 2011.