Following blood flow restriction resulting from a heart attack there is mass cell death in the heart tissue of the sufferer. If the factors that direct the cycle from cell growth to cell death can be controlled in this instance, harm to heart attack victims could be significantly reduced. PhD, Keith Jones and his colleagues have carried out research in the field of “Gene Regulatory Therapy” as a way to reduce and prevent heart damage at the university of Cincinatti.
Cell death is a process controlled by transcription factors. The transcription factors are proteins that bind to specific parts of DNA and are part of a system that controls the transfer of genetic information from DNA to RNA to protein; the cycle from cell growth to cell death. Keith Jones and his colleagues have identified the role of an important group of interacting transcription factors. The genes that the identified transcription factors regulate are specific genes found to determine whether a cell survives or dies following heart trauma.
Using this information the researchers have developed new non-viral delivery systems designed to repress activation of specific transcription factors in the heart. The non-viral delivery method is carried out by vehicles that flood the cells with nucleic acids, including transcription factor decoys. The job of the decoys is to trick the transcription factors in to binding to the decoys rather than the target genes. These target genes when activated are the genes believed to code for cell death.
The benefits of the investigated non-viral method are that it can be used to block a factor at any point in time and is reversible. Current viral methods cannot directly address the effects of gene regulation in disease and can have significant adverse outcomes. The method is looking very promising having been used successfully in animal models and the focus is now set on clinical trials.
REFERENCE:
University of Cincinnati (2008, June 24). New Ways To Regulate Genes, Reduce Heart Damage Identified. ScienceDaily. Retrieved April 18, 2009, from http://www.sciencedaily.com/releases/2008/06/080620195513.htm
Alexandra Kirkwood
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