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Researchers' interest in human embryonic stem cells has abated since the discovery in 2007 by the Japanese biologist Dr. Shinya Yamanaka that the mature cells of the body can be reprogrammed to the embryonic state.
This led to restoration of dystrophin protein expression in cells from Duchenne patients, including skeletal myoblasts and dermal fibroblasts that were reprogrammed to the myogenic lineage by MyoD.
Research recently has revealed not only that monocytes are part of inflammation and inflammatory disease, but also can be reprogrammed to the opposite, namely to cells that are highly anti-inflammatory and contribute to resolution of inflammation.
Additionally, the metabolism of host organism was reprogrammed to the desired biochemical product by the clustered regularly interspaced short palindromic repeats interference system, resulted in a final MCFA production of 3.8 g/L.
If the HEF genome was reprogrammed to the state of a CD34+ hFL cell, then the hybrid cells should have retained the multi-lineage potential of hFL cells.
These results suggest that fibroblasts are reprogrammed to the blood program, at least in part, through multipotential hematopoietic progenitor cells.
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Although the cells lost the capacity to switch identity when the animals were just three days of age, it may be possible to extend the period of reprogramming to the mature brain.
Their intermediate state between adult and embryonic stem cells makes them an ideal candidate for reprogramming to the pluripotent status.
The TGF- β-dependent reprogramming to the M2 phenotype is under the SMAD7 control.
These observations suggested that Lif responsiveness might be limiting for reprogramming to the pluripotent ground state.
They develop by an initial macrophage-like differentiation, followed by reprogramming to the osteoclast lineage and fusion of preosteoclasts to mature multinucleated osteoclasts [ 1, 4].
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