The latest research led by Robert Tsai, M.D., Ph.D., associate professor in the Texas A&M Health Science Center (TAMHSC) Institute of Biosciences and Technology (IBT) Center for Cancer and Stem Cell Biology, has revealed a new mechanism preventing DNA damage at cell division in the liver. The new finding could improve the recovery time of injured adult tissues and organs such as the brain and muscles.
Dr. Milton J. Finegold of Texas Children’s Hospital and Baylor College of Medicine, together with researchers from China Medical University, also participated in the research. The study has appeared online and in the December issue of the journal Hepatology.
“Stem cells and cancer cells have the unique ability to maintain an extended reproductive lifespan compared to most other cells in the body,” said Tsai. “We applied this understanding to adult tissue regeneration to discover why this proliferating trait is not present in all tissue.”
The liver is one of the few organs with a remarkable ability to regenerate lost tissue. When the liver reproduces new tissue, it undergoes rapid cell division that could cause an increased in DNA misprinting.
Tsai’s team previously discovered a protein called nucleostemin, which prevents genetic misprinting during neural stem cell replication. Nucleostemin was detected at a much higher level in livers damaged by toxin or surgery. Encouraged by these discoveries, they examined the effect of the nucleostemin presence in the injured liver for the tissue recovery process. In nucleostemin-deficient mouse models, significantly increased genetic mistakes in new liver tissues were detected, and the models showed eventual liver cell death, slow regeneration of new cells and impaired liver function.
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“Our findings prove this mechanism is critical for the adult liver when undergoing the regeneration process,” said Tsai. “The adult liver is typically mitotically quiescent – or inactive – but under certain circumstances, such as toxin-induced injury or surgical removal of liver mass, the hepatocytes re-enter the cell cycle and become proliferative. Essentially, the mechanism we discovered plays a crucial role in allowing these cells to regenerate without incurring damage to their genome.”