Researchers identify protein to prevent damage to donated vital organs

By Hudson Institute communications

Melbourne researchers have identified a protein (follistatin) that could prevent damage to donated organs before and after transplantation, and potentially stop the body rejecting them.

Professor David de Kretser - Melbourne researchers have identified a protein, follistatin, that could prevent damage to donated organs before and after transplantation.
Professor David de Kretser

At any given time, 1500 Australians are on the waiting list for an organ transplant and many of these transplants fail after a short period of time. The discovery could prove crucial to the thousands of Australians who require an organ due to injury or disease.

The collaborative study, involving researchers from Hudson Institute of Medical Research, Monash University, St Vincent’s Hospital and the University of Melbourne has just been published in the journal, Transplantation Direct.

Donated organs are deprived of their blood supply and oxygen during transplantation, before they are reconnected to the blood supply of the recipient.  This results in inflammation, which can cause permanent damage to the organ. The scientists showed that follistatin markedly reduces this inflammation, providing better outcomes for the patient.

Co-investigator, Professor David de Kretser from the Hudson Institute of Medical Research and Monash University in Melbourne, is also a Director of Paranta Biosciences, a company that developed follistatin, a protein with anti-inflammatory and anti-fibrotic properties for clinical use.

“Follistatin is a naturally occurring protein found in almost every organ in the body. We have shown that follistatin works by blocking the actions of another protein called activin, a key initiator of the inflammatory response,” Professor de Kretser said.

“During an organ transplant, follistatin decreases the inflammation caused by the restoration of the blood supply to the transplanted organ, halting or preventing a process called ischemia-reperfusion injury (IRI),”

“IRI causes the release activin, which causes the inflammation and the fibrosis or scarring that follows. The scarring impairs the function of the transplanted organ to varying degrees.”

The team showed that the use of follistatin during kidney transplants in pre-clinical models reduced the damage that would have otherwise resulted in kidney failure.

Paranta Biosciences is discussing the use of follistatin as a valuable additive to solutions that preserve the function of organs during transplantation with companies who produce these products.

A pioneer of reproductive health research at Hudson Institute, Professor de Kretser says follistatin is well-known for its role in the body’s reproductive processes, but his current work with the protein surprises even him.

“Back in 1987 , we could never have predicted that we would be working to develop follistatin as an anti-inflammatory and anti-fibrotic drug which could be used to help any type of inflammation that progresses to fibrosis, including the kidneys, liver, lungs and skin,” he said.

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