Engineered protein restores heart function

NIH | APRIL 10, 2016

When someone has had a heart attack or has heart failure, the heart isn’t able to contract with enough force to meet an increased energy demand. A team from Ohio State University set out to improve the ability of the heart to contract by using protein engineering.

Heart attack. Photo: Jonn Leffmann/Wikimedia Commons (CC BY 3.0)

Heart cell contraction is regulated by calcium binding to a protein called troponin C. The researchers designed troponin C types with varying sensitivity to calcium. They then used a harmless virus commonly used for gene therapy to deliver the engineered form into heart cells.

They found that TnC L48Q, a troponin C form that was more sensitive to calcium, improved several characteristics of function and performance in rabbit myofibrils (contractile machinery) and mouse heart cells as well as in normal mice.

The scientists injected mice with TnC L48Q and then induced a heart attack. The altered troponin C was protective; it improved heart function and performance without adversely affecting electrical activity and other characteristics.

Mice given TnC L48Q after an induced heart attack also showed improved heart performance, illustrating that the engineered protein could also serve as a treatment.

The researchers found that TnC L48Q improved function even when it only partially replaced the animal’s normal existing troponin C. The engineered form didn’t adversely influence cell death or inflammation, or alter the heart’s electrical activity.

The team is working to customize several forms of troponin C to increase or decrease contraction force to respond to a range of disorders.

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