2015
DOI: 10.1155/2016/1908365
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The Modulatory Effects of Mesenchymal Stem Cells on Osteoclastogenesis

Abstract: The effect of mesenchymal stem cells (MSCs) on bone formation has been extensively demonstrated through several in vitro and in vivo studies. However, few studies addressed the effect of MSCs on osteoclastogenesis and bone resorption. Under physiological conditions, MSCs support osteoclastogenesis through producing the main osteoclastogenic cytokines, RANKL and M-CSF. However, during inflammation, MSCs suppress osteoclast formation and activity, partly via secretion of the key anti-osteoclastogenic factor, ost… Show more

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Cited by 42 publications
(42 citation statements)
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References 158 publications
(200 reference statements)
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“…We also found that the presence of macrophages reduced the secretion of OPG, the decoy RANKL receptor. OPG is known to be secreted by both macrophages and MSCs, so it is surprising that OPG protein in the supernatant was most dramatically reduced in the polarized macrophage (M1 and M2) co‐cultures with greater than 60% reduction compared to MSCs grown alone and a statistically significant reduction compared to undifferentiated M0‐MSCs . These findings suggest that the inflammatory environment mediated by macrophages negatively regulate OPG secretion in our co‐culture system and thus may affect osteoclast activity along the OPG‐RANKL axis.…”
Section: Discussionmentioning
confidence: 85%
“…We also found that the presence of macrophages reduced the secretion of OPG, the decoy RANKL receptor. OPG is known to be secreted by both macrophages and MSCs, so it is surprising that OPG protein in the supernatant was most dramatically reduced in the polarized macrophage (M1 and M2) co‐cultures with greater than 60% reduction compared to MSCs grown alone and a statistically significant reduction compared to undifferentiated M0‐MSCs . These findings suggest that the inflammatory environment mediated by macrophages negatively regulate OPG secretion in our co‐culture system and thus may affect osteoclast activity along the OPG‐RANKL axis.…”
Section: Discussionmentioning
confidence: 85%
“…Quantitative reverse transcriptase‐polymerase chain reaction revealed an increased expression of the RANKL, also known as tumor necrosis factor ligand superfamily member 11 (TNFSF11) with an FC (Log2) of 4.36 and FC 4.87 at days 21 and 40, respectively. During the process of the physiological bone remodeling RANKL, the main osteoclastic effector, is expressed in a membrane‐bound form on many mesenchymal cells including MSCs, osteoblasts, osteocytes, and chondrocytes . To maintain normal bone homeostasis, RANKL signaling must be properly regulated .…”
Section: Discussionmentioning
confidence: 99%
“…43 To maintain normal bone homeostasis, RANKL signaling must be properly regulated. 43 Downregulated genes were those that encode for (i) cell-to-cell adhesion, such as VCAM1 and COMP, In hASCs grown on biomaterial CLEC3B protein was found to be expressed up to day 40. CLEC3B protein, which binds Ca 2+ , was investigated because of its potential involvement in the bone mineral metabolism.…”
Section: Discussionmentioning
confidence: 99%
“…Similarly, the effects of MSCs on osteoclast also depends on the dose of the surrounding biomolecules as well as the concentration of the inflammatory condition [75]. Osteoclast formation was enhanced when cocultured with BM-MSCs in the presence of 10 -9 M 1α,25(OH)2D3.…”
Section: Effects Of Oral Mscs Onmentioning
confidence: 99%