The viral vectors used in human gene therapy were combined with the methods by which injured hearts in zebrafish are mended in the hopes of one-day treating humans suffering from heart disorders.
A group of Duke University scientists studying how animals heal damaged tissues has made substantial progress toward precisely manipulating at least one component of the regenerative mechanism, as reported in a press release.
Gene Activity
Researchers demonstrated that gene activity may be modulated in response to injury so that it occurs in a small area of tissue and for a limited amount of time rather than throughout an entire organ.
They isolated a TREE (tissue regeneration enhancer element), a member of a family of enhancers found across the genome that tells genes to repair a specific region of the body when it senses injury.
During the reparative process, these enhancers can also silence genes. Duke University researchers said that these regulatory components have been found in mice, worms, and fruit flies in addition to zebrafish.
Researchers began their six-year study by inserting several TREE variants from zebrafish into the genomes of mouse embryos.
About half of the enhancers were found to work as expected, with the desired blue coloration of tissues occurring in response to injury detection in transgenic mammals.
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Mouse Samples For Gene Therapy Studies
The next step was to determine if the enhancer elements could be integrated explicitly into an adult mouse using an adeno-associated virus, a standard gene therapy approach for delivering gene sequences into cells.
Using mouse models of heart attacks, researchers showed that injecting the animals with viruses harboring a TREE one week before injury would cause the enhancer to activate in response to the onset of damage.
The researchers found that administering the drug a few days after the incident had the desired effect on the animal.
Using a mutant YAP controlled by a TREE, researchers examined the possibility of a mouse recovering from a heart attack with healthy muscle growth. After a few weeks, the TREE reportedly shut down the expression of a mutant YAP at the site of the injury.
The mouse’s heart was fully functional a few weeks after treatment, though it had developed some slight scarring. After the treatment, muscle cells also started to divide.
Moreover, the next step for the researchers is to hone their targeting skills and gain a deeper understanding of the roles and locations of the molecules that connect to the enhancers in the human genome.
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