Researchers at University of Texas Southwestern Medical Center identified the previously unknown function of the gene, called Meis1, in the heart.
"We found that the activity of the Meis1 gene increases significantly in heart cells soon after birth, right around the time heart muscle cells stop dividing," said Dr Hesham Sadek, assistant professor of internal medicine in the division of cardiology, and senior author of the study.
"Based on this observation we asked a simple question: If the Meis1 gene is deleted from the heart, will heart cells continue to divide through adulthood? The answer is 'yes'," Sadek said.
As the newborn develops, the heart rapidly loses the ability to regenerate and to repair injuries such as heart attacks.
The research team demonstrated that deletion of Meis1 extended the proliferation period in the hearts of newborn mice, and also re-activated the regenerative process in the adult mouse heart without harmful effect on cardiac functions.
The new finding demonstrates that Meis1 is a key factor in the regeneration process, and the understanding of the gene's function may lead to new therapeutic options for adult heart regeneration.
"Meis1 is a transcription factor, which acts like a software programme that has the ability to control the function of other genes. In this case, we found that Meis1 controls several genes that normally act as brakes on cell division," Sadek said.
"As such, Meis1 could possibly be used as an on/off switch for making adult heart cells divide. If done successfully, this ability could introduce a new era in treatment for heart failure," Sadek said.
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