Molecule that hastens tissue regeneration following bone marrow transplants discovered

A new discovery of a molecule that could serve as a key factor in accelerating cell recovery after bone marrow transplants, in addition to liver disease, and colon disease has recently been discovered. Such a discovery came at the hands of a joint investigation comprised of UT Southwestern, Case Western Reserve, and the University of Kentucky. The study was published in the journal Science.

The partnership discovered an enzyme known as the 15-PGDH. This particular enzyme helps regulate the tissue that is responsible for regeneration in several of the body’s organs. Thus, by obstructing the 15-PGDH in test subjects such as mice using the newly acquired molecule, SWO33291, the team discovered that they can indeed salvage damaged bone marrow, liver tissue, and colon tissue; as tissue regeneration is crucial to total recovery from injury, disease, and certain medical procedures.

“Patients undergoing bone marrow transplants and patients with colitis may benefit from this approach. We propose that SW033291 will be useful in accelerating recovery of bone marrow cells following a bone marrow transplant and may also be a treatment for colitis,” noted Associate Dean of Oncology Programs, Director of the Harold C. Simmons Comprehensive Center, Professor of Internal Medicine, holder of the Lisa K. Simmons Distinguished Chair in Comprehensive Oncology, and co-author Dr. James K. Wilson.

Bone marrow transplants are a prevalent form of treatment for patients diagnosed with leukemia. The National Cancer Institute approximates that within the year of 2015 there will be 54,270 new cases of leukemia and an around 24,450 people will die from the disease. Prostaglandin, which is a hormone-like thick acid, is a prime element in chronic infections and cancer.

“These inhibitors increase prostaglandin levels in a variety of tissues. For this reason, they appear to help the healing process in at least the intestines, liver, and bone marrow. We are hopeful that inhibiting 15-PGDH represents a general strategy to promote tissue repair,” said Professor of Biochemistry, member of the Simmons Cancer Center, and co-author of the study, Joseph Ready.

The newly discovered SWO33291 molecule operates by singling out a 15-PGDH regulated pathway of bone marrow regeneration in which increased bone marrow prostaglandin steers the generation of hematopoietic cytokines by CD45 positive marrow cells.

As previously mentioned the UT Southwestern team discovered the molecule in a joint effort with the University of Kentucky and researchers at Case Western Reserve. Professor of Hematology and Oncology, and Head of the Cancer Genetics Program, Dr. Sanford Markowitz, along with Professor of Hematology and Oncology, and Director of the Case Comprehensive Cancer Center, Dr. Stanton Greson, and a Case Western Reserve research associate and lead author on the study, Dr. Yongyou Zhang.

“It has been a pleasure to be involved in another example of a collaborative, multi-disciplinary team advancing the results of a high throughput, chemical library screen toward a therapeutic possibility for an unmet medical need,” said Associate Professor of Biochemistry at UT Southwestern, member of the Simmons Cancer Center, and study’s co-author, Dr. Bruce Posner.

The researchers aim to continue testing their findings in further clinical trials.

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