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Stem Cells Programmed to Survive Within Harsh Post MI Environments

June 23rd, 2015 Medgadget Editors News

stem-cell-patch

Immunofluorescence image showing expression of cardiomyocyte marker α-sarcomeric actinin (green color); Nuclei (blue color); and Aligned nanofiber (red Color) in the cardiac patch in vitro.

While stem cells for healing diseased cardiac tissue have shown some promise, their inability to wow us may be due to the low rate of survival of these cells once they are inside the myocardium, especially if it’s scarred by the previous infarction. In addition to a low perfusion environment, unbalance of signalling molecules inside the scarred heart is partially responsible for early apoptosis of stem cells.

A microRNA molecule called miR-133a has been noted to be in abnormally low quantities in patients following a heart attack. Researchers at Ohio State University thought that if they prime stem cells with high levels of miR-133a, as though they are in a healthy environment, once implanted into a diseased area they won’t be as susceptible to low levels of miR-133a that’s telling them it’s time to begin apostosis.

The team used a specialty molecule that was able to induce mesenchymal stem cells to produce their own miR-133a. They tested these stem cells within rat hearts that suffered a myocardial infarction, showing that the cells made to produce the regulating microRNA survived in considerably larger quantities compared to untreated stem cels. Sounds like it may be possible to go over previously conducted studies applying the new technique to see whether their efficacy could be significantly improved.

Study in Cardiovascular Pharmacology: MicroRNA-133a Engineered Mesenchymal Stem Cells Augment Cardiac Function and Cell Survival in the Infarct Heart…

Medgadget Editors

Medical technologies transform the world! Join us and see the progress in real time. At Medgadget, we report the latest technology news, interview leaders in the field, and file dispatches from medical events around the world since 2004.

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