What's more, through further experiments the researchers found that instead of using the mutated gene to induce the transformation, they could incubate endothelial cells with either one of two specific proteins (growth factors TGF-beta2 and BMP4) whose cellular interactions mimicked the effects of the mutated gene, providing a more efficient way to reprogram the cells.
Afterwards, Medici was able to take these reprogrammed cells and, in both culture dishes and animal models, coax them into developing into a group of related tissue types.
"It's important to clarify that these new cells are not exactly the same as mesenchymal stem cells from bone marrow," says Medici. "There are some important differences. However, they appear to have all the potential and plasticity of mesenchymal stem cells."
"The power of this system is that we are simply repeating and honing a process that occurs in nature," says Olsen. "In that sense, it's less artificial than other current methods for reprogramming cells."
According to study collaborator Frederick Kaplan, Isaac & Rose Nassau Professor of Orthopaedic Molecular Medicine at the University of Pennsylvania School of Medicine and a world expert on FOP, "While we want to use this knowledge to stop the renegade bone formation of FOP, these new findings provide the first glimpse of how to recruit and harness the process to build extra bone for those who desperately need it."
Medici and Olsen echo this, stating that the most direct application for these findings is the field of tissue engineering and personalized medicine. It is conceivable that transplant patients may one day have some of their own endothelial cells extracted, reprogrammed, and then grown into the desired tissue type for implantation. Host rejection would not be an issue.
|Contact: David Cameron|
Harvard Medical School