| Literature DB >> 26585691 |
Dmitriy Sheyn1, Galina Shapiro2, Wafa Tawackoli3, Douk Soo Jun4, Youngdo Koh4, Kyu Bok Kang4, Susan Su1, Xiaoyu Da5, Shiran Ben-David1, Maxim Bez2, Eran Yalon2, Ben Antebi2, Pablo Avalos6, Tomer Stern7, Elazar Zelzer7, Edward M Schwarz8, Zulma Gazit9, Gadi Pelled9, Hyun M Bae4, Dan Gazit10.
Abstract
Osteoporosis affects more than 200 million people worldwide leading to more than 2 million fractures in the United States alone. Unfortunately, surgical treatment is limited in patients with low bone mass. Parathyroid hormone (PTH) was shown to induce fracture repair in animals by activating mesenchymal stem cells (MSCs). However, it would be less effective in patients with fewer and/or dysfunctional MSCs due to aging and comorbidities. To address this, we evaluated the efficacy of combination i.v. MSC and PTH therapy versus monotherapy and untreated controls, in a rat model of osteoporotic vertebral bone defects. The results demonstrated that combination therapy significantly increased new bone formation versus monotherapies and no treatment by 2 weeks (P < 0.05). Mechanistically, we found that PTH significantly enhanced MSC migration to the lumbar region, where the MSCs differentiated into bone-forming cells. Finally, we used allogeneic porcine MSCs and observed similar findings in a clinically relevant minipig model of vertebral defects. Collectively, these results demonstrate that in addition to its anabolic effects, PTH functions as an adjuvant to i.v. MSC therapy by enhancing migration to heal bone loss. This systemic approach could be attractive for various fragility fractures, especially using allogeneic cells that do not require invasive tissue harvest.Entities:
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Year: 2015 PMID: 26585691 PMCID: PMC4817819 DOI: 10.1038/mt.2015.211
Source DB: PubMed Journal: Mol Ther ISSN: 1525-0016 Impact factor: 11.454