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Protein May Hold Key to Decreasing Organ Dysfunction Rates in Heart Transplants

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02.05.2007

Genetically Disabling a Protein Decreases Inflammation in Transplanted Hearts

A new study, led by Felix Aigner, M.D., has identified a protein known as Lipocalin-2 (Lcn-2) as potentially responsible for regulating the body’s inflammatory response during heart transplants. One of the major complications involved with many transplantations is the damage done to the transplanted heart during and immediately following surgery, known as ischemia and reperfusion (IR). In particular, inflammatory cells infiltrate the donated heart, which then releases enzymes and other proteins that attack the transplanted tissue, and can seriously impair the viability of replacement organs and jeopardize the health of the patient. The identification of Lcn-2 could be a first step towards reducing this inflammatory response and increasing the success rate of heart transplants worldwide. The study appears in American Journal of Transplantation.

Building on earlier work, the study finds that Lcn-2 is released by inflammatory cells attacking transplanted hearts in mice, and suggests that the protein is responsible for attracting further inflammatory response. Inflammation was found to decrease dramatically in mice in which the production of Lcn-2 was genetically disabled.

The study also found elevated levels of Lcn-2 in the kidneys of mice that had undergone heart transplants, suggesting the protein’s possible involvement in the systemic response to IR. “The major goal of our research activities is therefore to understand the exact mechanisms of this injury concomitant to organ transplantation,” notes Aigner, stressing the value of this research to the development of new treatment options in organ transplantation.

Sean Wagner | Source: alphagalileo
Further information:
www.blackwellpublishing.com/press/pressitem.asp?ref=1208

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