Researchers from the University of Cambridge‘s Department of Pharmacology have inadvertently discovered a gene that triggers heart cell regeneration, which could one day lead to a way to heal damaged hearts.
This will have major implications for treatments of heart disease explains Dr. Catherine Wilson who led the team’s research recently published in Nature Communications:
This is really exciting because scientists have been trying to make heart cells proliferate for a long time. None of the current heart disease treatments are able to reverse [the] degeneration of the heart tissue – they only slow progression of the disease. Now we’ve found a way to do it in a mouse model.
The team was trying to find a way to “turn off” the Myc gene that is overactive in cancer patients. The Myc gene plays a vital role in cancer cells’ ability to replicate themselves uncontrollably. When scientists try to stop a certain gene, they will also ramp up or increase that gene to make sure that it is indeed what is causing a problem.
What happened next was a complete surprise to the team. When they administered the ramped up Myc in a study on mice with cancer, the cancer was regenerating and spreading in areas like the liver and the lungs. However, the heart was unaffected, at first, and this led the team to switch their focus from a cancer study to a heart study.
The researchers discovered that for the Myc gene activity to work in the heart it is critically dependant on a protein called Cyclin T1 that is made by a different gene called Ccnt1. When these two genes are used together, the heart cells begin to replicate causing regeneration.
Dr. Wilson talks about the team’s findings:
When these two genes were overexpressed together in the heart muscle cells of adult mice we saw extensive cell replication, leading to a large increase in the number of heart muscle cells.
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They were able to watch this regeneration by ChIP, a next-generation sequencing technology that provides images of the Myc gene within the heart cells. By producing a protein called a transcription factor, Myc can activate gene expression thereby binding the DNA in specific cells. Despite this, the heart cells did not start to replicate themselves until the team added the Cyclin T1 gene. Dr. Wilson explains:
None of the current treatment options can reverse the degeneration of heart tissue. The inability of the heart to regenerate itself is a significant unmet clinical need. We found that even when Myc is switched on in a heart, the other tools aren’t there to make it work, which may be one of the reasons heart cancer is so extremely rare. Now we know what’s missing, we can add it and make the cells replicate.
Dr. Wilson and her team focused mainly on the heart and the liver after this discovery was made. However, they stated that their findings could offer insights into both regenerative medicine and cancer susceptibility.
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