Physicians treating patients with heart disease can probably benefit from the following tidbit. Researchers from the University of Cincinnati claim to have discovered a potential genetic target for heart disease. The findings can probably help in introducing novel for avoiding disease development.
Scientists assert that the micro-RNA called miR765, managing gene expressions can down-regulate the expression of protein phosphatase 1 inhibitor-1 (I-1). This micro-RNA may also decrease the contractility of cells that make up cardiac muscle. Prior investigations have suggested that the reduction in I-1 expression is a hallmark in pathogenesis of heart disease. Yet the underlying molecular mechanism leading to this down-regulation is apparently unknown. In the present investigation, researchers focused on affirming whether miR765 regulates this protein expression and creates an impact on the contractility of cardiac muscle cells.
“These findings show that miR765 can down-regulate the expression and reduce contractility of heart cells by decreasing or deactivating a number of proteins that help the heart function at full capacity. This leads us to believe that miR765 may play a role in the development of heart failure. Hopefully, these findings will lead to future studies, helping researchers and clinicians develop a therapeutic target to stop heart disease where it first starts: in the genes,” mentioned WenFeng Cai, PhD, a postdoctoral fellow and lead researcher.
With the help of a gene transfer agent or virus, experts were probably capable of moving miR-765 or a control agent into ventricular cells of animal models. It was pointed out that the expression of I-1 messenger RNA reduced by 20 percent in the miR765 cells of these models than the control models. The contractile parameters seemingly declined in miR765-treated animal models. Beta adrenergic agonist may be employed to speed up the pumping action of the heart, develops a positive effect and the contractile function remains suppressed in the miR765 group. The research findings affirm that both phosphorylations of phospholamban and ryanodine receptor are dramatically decreased in the miR765 group. This reduction was observed in the presence and in the absence of beta adrenergic agonist by the scientists.
The study was presented at the American Heart Association’s (AHA) Scientific Sessions in Chicago Nov. 17.