Study Shows Unmodified Stem Cells Might Stop Osteoporosis Caused by Autoimmune Drugs
Durham, NC (PRWEB) August 18, 2016 -- An infusion of a healthy donor’s unmodified stem cells might one day be used to prevent a type of osteoporosis caused by glucocorticoid therapy, according to a study published this month in STEM CELLS Translational Medicine. Osteoporosis is among the most significant side effects of glucocorticoid therapy, which is used for the management of inflammatory and auto-immune diseases.
A previous study by Lien, et al., showed the promise of gene-modified mesenchymal stem cells (MSCs) to relieve glucocorticoid therapy-induced osteoporosis (GIOP). Other studies involving unmodified MSCs did the same for osteoporosis not brought on by glucocorticoid drugs. This led researchers at the Fourth Military Medical University in Shaanxi, China, to wonder whether unmodified MSCs might be a therapy for GIOP, too. MSCs, adult stem cells traditionally found in the bone marrow, are attractive to researchers because they can be coaxed into differentiating into a variety of cell types.
“We hypothesized that it might prevent the reduction of bone mass and strength in GIOP through maintaining bone formation by inhabiting and functioning in recipient bone marrow,” said the study’s lead investigator, Yan Jin, M.D., Ph.D., of the university’s Center for Tissue Engineering.
Allogeneic – that is, the healthy donor’s – bone marrow-derived MSCs were isolated, identified and systemically infused into mice that had been given an excessive dose of a glucocorticoid (dexamethasone) to induce GIOP.
Dr. Jin said, “We found the MSC infusions prevented the reduction of both bone mass and bone strength in the glucocorticoid-treated mice by maintaining the bone formation. Our results also uncovered previously unrecognized MSC behaviors following a homing event (the phenomenon whereby stem cells migrate to the organ of their origin and engraft or establish residence there – thus providing greater regenerative effect). They indicated that minimizing the time of cell culture in the lab offers an advantage for increasing transplanted MSCs to the targeted organ to promote therapeutic effects.
“Future steps may involve the application of autologous – that is, the recipient’s own – MSCs in GIOP,” he added.
“Although preliminary, this study provides some promising data for the therapeutic potential of allogeneic MSCs in glucocorticoid therapy-induced osteoporosis,” said Anthony Atala, M.D., Editor-in-Chief of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine.
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The full article, “Allogeneic mesenchymal stem cell therapy promotes osteoblastogenesis and prevents glucocorticoid-induced osteoporosis,” can be accessed at http://stemcellstm.alphamedpress.org/content/early/2016/06/30/sctm.2015-0347.abstract?sid=5f249f7d-698f-42cb-8dd6-35bffb9fef5f.
About STEM CELLS Translational Medicine: STEM CELLS Translational Medicine (SCTM), published by AlphaMed Press, is a monthly peer-reviewed publication dedicated to significantly advancing the clinical utilization of stem cell molecular and cellular biology. By bridging stem cell research and clinical trials, SCTM will help move applications of these critical investigations closer to accepted best practices.
About AlphaMed Press: Established in 1983, AlphaMed Press with offices in Durham, NC, San Francisco, CA, and Belfast, Northern Ireland, publishes two other internationally renowned peer-reviewed journals: STEM CELLS® (http://www.StemCells.com), celebrating its 34th year, is the world's first journal devoted to this fast paced field of research. The Oncologist® (http://www.TheOncologist.com), also a monthly peer-reviewed publication, entering its 21st year, is devoted to community and hospital-based oncologists and physicians entrusted with cancer patient care. All three journals are premier periodicals with globally recognized editorial boards dedicated to advancing knowledge and education in their focused disciplines.
Chelsea Kekahuna, AlphaMed Press, +1 (919) 680-0011, [email protected]
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