Molecular Mechanism Found That May Improve Ability Of Stem Cells To Fight Disease
Adult stem cell transplantation offers great therapeutic potential for a variety of diseases due to their ability to replenish diseased cells and tissue. While they are unique in this ability, it remains a challenge to effectively treat disease long-term with stem cells because of our inability to grow them in the laboratory. Defining the molecular switch in the stem cell replication process, or cell cycle, is a key step to stimulating their growth for broader clinical use. In the May issue of Nature Cell Biology, Tao Cheng, M.D., assistant professor, department of radiation oncology, University of Pittsburgh School of Medicine, and colleagues report the discovery of a molecular mechanism in the cell cycle that appears to impact the replicating ability of stem cells from bone marrow and blood to fight disease. They found that blood stem cells from mice missing a gene called p18 were much better able to multiply and grow. p18 is a molecule in a class of so-called "cyclin-dependent kinase inhibitors" that are critical inhibitors of cell cycle control. In the study, Dr. Cheng and his team isolated p18-deficient stem cells from mice and found that these cells were much more efficient at repopulating injured bone marrow tissue. As a result, they concluded that blocking the function of p18 may be a productive way to enhance the efficacy of stem cell transplantation as a treatment for diseases.