Stem cells may stop osteoporosis, promote bone growthMarch 5th, 2009 - 1:37 pm ICT by ANI
Washington, Mar 5 (ANI): A new study has shown that tweaking a certain group of multipotent stem cells-mesenchymal stem cells-with a hormone called interferon (IFN) in our bodies, might stop osteoporosis and promote bone growth.
Scientists from the Research Institute of the McGill University Health Centre say that IFN holds great promise to repair bones affected by osteoporosis.
“We have identified a new pathway, centered on IFN gamma, that controls the bone remodelling process both in-vivo and in-vitro. More studies are required to describe it more precisely, but we are hopeful that it could lead to a better understanding of the underlying causes of osteoporosis, as well as to innovative treatments,” said Dr. Richard Kremer, the study’’s lead author and co-director of the Musculoskeletal Axis of the McGill University Health Centre.
He added: “First, we stimulated cultured mesenchymal stem cells to turn into bone cells (osteoblasts) in-vitro. We realised that this differentiation process involved IFN gamma-related genes, but also that these bone cells precursors could both be stimulated by IFN gamma and produced IFN gamma.”
In the next step, the researchers focussed on an animal model where IFN gamma effect is blocked by inactivating its receptor-a model called IFN gamma receptor knock-out.
They later conducted bone density tests, comparable to those used to diagnose people with osteoporosis.
The results revealed that the animals had significantly lower bone mass than their healthy counterparts, and also the mesenchymal stem cells were found to have a decreased ability to make bone.
“These findings confirm that IFN gamma is an integral factor for mesenchymal stem cells” differentiation into osteoblasts also in-vivo,” said Kremer.
Both in-vitro and in-vivo results proved that IFN gamma was key to the differentiation of mesenchymal cells into bone cells, and to growth process of the bone.
The findings provide hope that IFN gamma itself, or another molecule involved in its pathway, could soon become efficient drug-target for an antidote for osteoporosis.
The study has been published in the journal Stem Cells. (ANI)
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