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Jefferson scientists use gene therapy to restore function of damaged heart cells in lab

eptors are more or less turned off.

"We have thought that inhibiting ARK activity could increase signaling and increase function," he explains. In the laboratory dish, the researchers infected heart cells from patients who underwent cardiac transplantation due to end-stage heart failure with an adenovirus that encoded both ARKct a peptide that can block ARK and a so-called "reporter gene" protein, which glows green. The latter provided a signal to the scientists that the inhibitor was indeed present in the heart cells. They then were able to use a video camera to actually measure how strong the individual heart cells were beating. The virus used in this study is a version of the common cold virus that has been rendered non-infectious and serves to carry the therapeutic gene to the failing heart cells.

"We put the ARKct into the cells, and failing human hearts become more like normal hearts, based on their ability to contract and other functional properties of these cells was also improved," Dr. Koch says. "This is the first work in actual human hearts to show efficacy of ARKct as a potential therapy and more importantly, proves that the enzyme ARK1 is a target for heart failure treatment."

"This study is the last proof of concept," he adds, noting that years of previous work in various animal models enabled the research team to reach this point. "Now we are dealing with human cells from failing human hearts," he says, noting that essentially these studies in human heart cells "confirm all we have done."

Congestive heart failure affects nearly 5 million Americans, many of whom have poor long-term prognoses, despite recent therapeutic advances. Dr. Koch hopes that such studies will move gene therapy forward as a viable option for heart failure patients. He notes that pre-clinical studies in "clinically relevant" large animal models are progressing, and should eventually lead to human trials using the ARKct gene.


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5-Apr-2004


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