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Synthetic mRNA can induce self-repair, regeneration of the infarcted heart

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Posted September 9, 2013
Synthetic mRNA can induce self-repair and regeneration of the infarcted heart

Synthetic mRNA can induce self-repair and regeneration of the infarcted heart
Dr. Kenneth Chien was recently recruited as a researcher to Karolinska Institutet and now share his time between Sweden and the US. Credit: Ulf Sirborn

A team of scientists at Karolinska Institutet and Harvard University has taken a major step towards treatment for heart attack, by instructing the injured heart in mice to heal by expressing a factor that triggers cardiovascular regeneration driven by native heart stem cells. The study, published in Nature Biotechnology, also shows that there was an effect on driving the formation of a small number of new cardiac muscle cells.

“This is the beginning of using the heart as a factory to produce growth factors for specific families of cardiovascular stem cells, and suggests that it may be possible to generate new heart parts without delivering any new cells to the heart itself “, says Kenneth Chien, a Professor at the medical university Karolinska Institutet in Sweden and Harvard University, US, who led the research team behind the new findings.

The study is based upon another recent discovery in the Chien lab, which was published in Cell Research. This study shows that VEGFA, a known growth factor for vascular endothelial cells in the adult heart, can also serve as a switch that converts heart stem cells away from becoming cardiac muscle and towards the formation of the coronary vessels in the fetal heart. To coax the heart to make the VEGFA, the investigators in the Nature Biotechnology study used new technology where synthetic messenger RNA (mRNA) that encodes VEGFA is injected into the muscle cell. Then, heart muscle produces a short pulse of VEGFA. The mRNA is synthetically modified so that it escapes the normal defense system of the body that is known to reject and degrade the non-modified mRNA as a viral invader.

Read more at: Phys.org

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