A new study conducted by researchers at UC has identified a potential genetic target for heart disease.
The study, led by WenFeng Cai, shows that a micro-RNA, known as miR765, which regulates gene expressions, can down-regulate the expression of protein phosphatase 1 inhibitor-1 (I-1) and reduce the contractility of cells that make up cardiac muscle.
Using a gene transfer agent-or virus-researchers moved either miR-765 or a control agent into ventricular cells of animal models.
Data showed that the expression of I-1 messenger RNA was decreased by 20 percent in the miR765 cells of these models when compared with the control models.
"Under resting conditions, the contractile parameters were decreased in miR765-treated animal models," Cai said.
"Although beta adrenergic agonist, used to speed up the pumping action of the heart, had a positive effect, the contractile function remained suppressed in the miR765 group."
Cai adds that analysis showed both phosphorylations of phospholamban and ryanodine receptor, the proteins that regulate calcium uptake and calcium release, were significantly reduced in the miR765 group both in the presence and in the absence of beta adrenergic agonist.
"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," Cai said.
"This leads us to believe that miR765 may play a role in the development of heart failure," Cai added.
The finding has at the American Heart Association's (AHA) Scientific Sessions in Chicago.