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Protein Responsible for Heart Transplant Failure Identified

      Volume: 36 (29/04/2007)
Researchers at the Innsbruck Medical University in Austria have identified a protein known as Lipocalin-2 (Lcn-2) which they believe is responsible for controlling the inflammatory response of the body during heart transplants. The study was led by Dr. Felix Aigner, a researcher in the Department of General and Transplant Surgery.

The damage suffered by the transplanted heart during and immediately following surgery often leads to complications in many heart transplants. This damage is known as ischemia and reperfusion (IR). The main response of the body to the transplanted heart is to release inflammatory cells which infiltrate the donated organ.

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This infiltration causes the release of enzymes and other proteins which then attack the transplanted tissue. Such an attack can seriously undermine the viability of replacement organs and also adversely affect the health of the patient.

The researchers based their study on earlier work and used laboratory mice to study the effect of Lcn-2 on the heart. They found that in mice, inflammatory cells attacking the heart released Lcn-2. This led them to hypothesize that the protein is potentially responsible for inducing further inflammatory response in the donated organ. When the researchers genetically disabled the production of Lcn-2 in the mice, they found a dramatic reduction in inflammation.

Elevated levels of Lcn-2 were also observed in the kidneys of those mice that had had heart transplants. According to the researchers, this suggests that the protein might be involved in the systemic response to IR.

Stressing the value their research can provide to the development of new treatment options in organ transplantation, Dr. Aigner said, “The major goal of our research activities is therefore to understand the exact mechanisms of this injury concomitant to organ transplantation.”

In the researchers’ opinion, the identification of Lcn-2 could provide a major boost to the efforts for reducing the body’s inflammatory response to heart transplantation. If successful, such reduction could increase the success rate of transplants worldwide. The study has been published in the American Journal of Transplantation.

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