In the Forum
Proteins Based Heart Tissue Repair System
Volume: 24 (10/07/2006)
Researchers at the University of Pennsylvania School of Medicine are studying the possibilities of using a protein to “switch on” the ability to repair damaged heart tissue. By triggering the cell-cycle signal, researchers found they can manipulate cells in animal models to regenerate damaged heart tissue. They are hoping to translate this research successfully to humans soon, as it could drastically change the approach to treating heart disease, the leading killer worldwide. “This is a different concept in terms of how to address heart disease. The classic thinking is to replace a valve, or place a bypass graft. Traditionally, when the heart gets injured, there’s dead tissue, and we work our way around it surgically, even
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replacing the heart with a transplant,” explained Principal Investigator Dr. Joseph Woo, MD, Director of the Minimally Invasive and Robotic Cardiac Surgery Program at Penn and Assistant Professor of Surgery. “So we asked, ‘What would be the most ideal, natural way of fixing any sort of problem like this?’ If you look at nature, the best way is to simply re-grow the tissue. We know if we take out a piece of the liver, our body has programming to grow it back to how it was.”
This rule however does not readily apply to the heart. Without the body receiving some kind of a shock or “jump start,” the body does not start healing or re-growing dead tissues in the heart. Such an inability of the body leads to devastating effects. When heart tissue dies either due to some disease or due to a heart attack, the heart is not able to contract fully or function normally. In such a situation, its ability to effectively pump oxygenated blood throughout the body is curtailed, in turn forcing the heart to exert extra pressure. This puts it under further duress, which could ultimately lead to heart failure and death.
As part of their efforts to better understand how this damage could be reversed in humans, Dr. Woo’s team first identified the signals in the rat heart that prevent the ability to re-grow damaged heart tissue. Thereafter the team worked to manipulate those signals so the heart could work on regenerating itself.
In particular, the research team attempted to initiate heart cell division and replication in order to understand its effects on myocardial regeneration. To achieve this, the researchers caused expression of the cell-cycle regulator protein – cyclin A2. This protein is unique in the body in the sense that it controls two major transactions of the cell cycle and is the only cyclin that becomes completely dormant after child birth in mice, rats as well as humans. Positive results were achieved from this approach as the expression of cyclin A2 via gene transfer gave improved myocardial function.
“Penn is the first to do this kind of research with damaged heart tissue, by ramping up the body's native reparative system,” stated Dr. Woo. “We are examining the potential role of this regenerative strategy as a future therapy for heart failure. Someday, this could lead to less surgery and perhaps even less medicine in treating heart disease.” At the same time Dr. Woo cautioned this research work was not yet tried on human and so they might be several years away from achieving actually applicable results. The findings of the study have been published in the online version of Circulation, the journal of the American Heart Association.
This rule however does not readily apply to the heart. Without the body receiving some kind of a shock or “jump start,” the body does not start healing or re-growing dead tissues in the heart. Such an inability of the body leads to devastating effects. When heart tissue dies either due to some disease or due to a heart attack, the heart is not able to contract fully or function normally. In such a situation, its ability to effectively pump oxygenated blood throughout the body is curtailed, in turn forcing the heart to exert extra pressure. This puts it under further duress, which could ultimately lead to heart failure and death.
As part of their efforts to better understand how this damage could be reversed in humans, Dr. Woo’s team first identified the signals in the rat heart that prevent the ability to re-grow damaged heart tissue. Thereafter the team worked to manipulate those signals so the heart could work on regenerating itself.
In particular, the research team attempted to initiate heart cell division and replication in order to understand its effects on myocardial regeneration. To achieve this, the researchers caused expression of the cell-cycle regulator protein – cyclin A2. This protein is unique in the body in the sense that it controls two major transactions of the cell cycle and is the only cyclin that becomes completely dormant after child birth in mice, rats as well as humans. Positive results were achieved from this approach as the expression of cyclin A2 via gene transfer gave improved myocardial function.
“Penn is the first to do this kind of research with damaged heart tissue, by ramping up the body's native reparative system,” stated Dr. Woo. “We are examining the potential role of this regenerative strategy as a future therapy for heart failure. Someday, this could lead to less surgery and perhaps even less medicine in treating heart disease.” At the same time Dr. Woo cautioned this research work was not yet tried on human and so they might be several years away from achieving actually applicable results. The findings of the study have been published in the online version of Circulation, the journal of the American Heart Association.
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