11 research outputs found

    Iron Administration before Stem Cell Harvest Enables MR Imaging Tracking after Transplantation

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    PURPOSE: To determine whether intravenous ferumoxytol can be used to effectively label mesenchymal stem cells (MSCs) in vivo and can be used for tracking of stem cell transplants. MATERIALS AND METHODS: This study was approved by the institutional animal care and use committee. Sprague-Dawley rats (6–8 weeks old) were injected with ferumoxytol 48 hours prior to extraction of MSCs from bone marrow. Ferumoxytol uptake by these MSCs was evaluated with fluorescence, confocal, and electron microscopy and compared with results of traditional ex vivo–labeling procedures. The in vivo–labeled cells were subsequently transplanted in osteochondral defects of 14 knees of seven athymic rats and were evaluated with magnetic resonance (MR) imaging up to 4 weeks after transplantation. T2 relaxation times of in vivo–labeled MSC transplants and unlabeled control transplants were compared by using t tests. MR data were correlated with histopathologic results. RESULTS: In vivo–labeled MSCs demonstrated significantly higher ferumoxytol uptake compared with ex vivo–labeled cells. With electron microscopy, iron oxide nanoparticles were localized in secondary lysosomes. In vivo–labeled cells demonstrated significant T2 shortening effects in vitro and in vivo when they were compared with unlabeled control cells (T2 in vivo, 15.4 vs 24.4 msec; P < .05) and could be tracked in osteochondral defects for 4 weeks. Histologic examination confirmed the presence of iron in labeled transplants and defect remodeling. CONCLUSION: Intravenous ferumoxytol can be used to effectively label MSCs in vivo and can be used for tracking of stem cell transplants with MR imaging. This method eliminates risks of contamination and biologic alteration of MSCs associated with ex vivo–labeling procedures. © RSNA, 2013 Supplemental material: http://radiology.rsna.org/lookup/suppl/doi:10.1148/radiol.13130858/-/DC

    The Epigenome at the Crossroad Between Social Factors, Inflammation, and Osteoporosis Risk

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    Both genetic and environmental factors are involved in the pathogenesis of osteoporosis and other skeletal disorders. Epidemiological studies have revealed an influence of a variety of social factors, including socioeconomic status (SES) on the risk of osteoporosis. The mechanisms involved are complex and still incompletely elucidated. Nevertheless, a variety of clinical risk factors known to influence skeletal homeostasis have been reported as being socially patterned, including nutrition, exercise, and other lifestyles, among others. These factors may impact the skeleton through a variety of mechanisms. Among them, there is increasing evidence for a role of DNA methylation and other epigenetic mechanisms. Indeed, several studies of human cohorts and experimental models showed that social deprivation is associated with changes in the methylation pattern of a number of genes, including some involved in stress and inflammatory responses. The influence of socioeconomic factors may be important not only during postnatal life but also in utero and may be transmitted to future generations by its direct effect on peripheral and target tissues and perhaps through epigenetic inheritance. Although the exact relevance of these pathways in humans has not been fully elucidated yet, they bring attention to the influences of social factors on the skeletal health of the individuals and their descendants. Therefore, they also bring forward our responsibility for both present and future generations
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