| First Author | Fujioka K | Year | 2015 |
| Journal | Biochem Biophys Res Commun | Volume | 456 |
| Issue | 3 | Pages | 785-91 |
| PubMed ID | 25514036 | Mgi Jnum | J:220365 |
| Mgi Id | MGI:5634262 | Doi | 10.1016/j.bbrc.2014.12.040 |
| Citation | Fujioka K, et al. (2015) Inhibition of osteoclastogenesis by osteoblast-like cells genetically engineered to produce interleukin-10. Biochem Biophys Res Commun 456(3):785-91 |
| abstractText | Bone destruction at inflamed joints is an important complication associated with rheumatoid arthritis (RA). Interleukin-10 (IL-10) may suppress not only inflammation but also induction of osteoclasts that play key roles in the bone destruction. If IL-10-producing osteoblast-like cells are induced from patient somatic cells and transplanted back into the destructive bone lesion, such therapy may promote bone remodeling by the cooperative effects of IL-10 and osteoblasts. We transduced mouse fibroblasts with genes for IL-10 and Runx2 that is a crucial transcription factor for osteoblast differentiation. The IL-10-producing induced osteoblast-like cells (IL-10-iOBs) strongly expressed osteoblast-specific genes and massively produced bone matrix that were mineralized by calcium phosphate in vitro and in vivo. Culture supernatant of IL-10-iOBs significantly suppressed induction of osteoclast from RANKL-stimulated Raw264.7 cells as well as LPS-induced production of inflammatory cytokine by macrophages. The IL-10-iOBs may be applicable to novel cell-based therapy against bone destruction associated with RA. |
