Entity

Time filter

Source Type


Grassi F.,Laboratorio Istituto Ortopedico Rizzoli Bologna Italy | Cattini L.,boratorio Of Immunoreumatologia generazione Tissutale Istituto Ortopedico Rizzoli Bologna Italy | Gambari L.,boratorio Of Immunoreumatologia generazione Tissutale Istituto Ortopedico Rizzoli Bologna Italy | Manferdini C.,boratorio Of Immunoreumatologia generazione Tissutale Istituto Ortopedico Rizzoli Bologna Italy | And 4 more authors.
Journal of Tissue Engineering and Regenerative Medicine | Year: 2013

T lymphocytes play a key role in the regulation of bone homeostasis and bone healing. The inflammatory response at the site of bone injury is essential to the initiation of the bone repair program; however, an uncontrolled exposure to inflammatory environment has a negative effect on tissue regeneration - indeed, activated T cells were shown to inhibit osteogenic differentiation on human mesenchymal stromal cells (MSCs). Whether resting T cells can induce osteogenic differentiation of MSCs and what role specific T cells subset play in this process is still elusive. In this study, we sought to analyse the osteogenic gene expression profile of whole T cells, CD4 and CD8 T cells isolated from healthy donors and investigated whether secreted factors from each group modulate osteogenic differentiation of human MSCs. Gene expression profiling identified a pool of 51 genes involved at various stages in bone growth which are expressed above detectable levels in CD4 and CD8 T cells. Most genes of this pool were expressed at higher levels in the CD4 subset. In vitro mineralization assays revealed that conditioned medium from CD4 T cells, but not from CD8 cells, significantly increased mineralization in osteogenic cultures of human MSCs; furthermore, mRNA expression of Runt-related transcription factor 2 (RUNX-2), osteocalcin (OC), bone sialoprotein (BSP) and alkaline phosphatase (ALP) in MSCs was significantly upregulated in the presence of CD4-conditioned medium but not with that obtained from CD8. The results show a differential role for CD4 and CD8 T cells in supporting bone formation and identify an osteogenic gene signature of each subset. © 2013 John Wiley & Sons, Ltd. Source


Manferdini C.,Science Laboratorio Of Immunoreumatologia generazione Tissutale Istituto Ortopedico Rizzoli Bologna Italy | Cavallo C.,Laboratorio Istituto Ortopedico Rizzoli Bologna Italy | Grigolo B.,Science Laboratorio Of Immunoreumatologia generazione Tissutale Istituto Ortopedico Rizzoli Bologna Italy | Fiorini M.,Fin Ceramica Faenza SpA Faenza | And 6 more authors.
Journal of Tissue Engineering and Regenerative Medicine | Year: 2013

Osteochondral lesions require treatment to restore the biology and functionality of the joint. A novel nanostructured biomimetic gradient scaffold was developed to mimic the biochemical and biophysical properties of the different layers of native osteochondral structure. The present results show that the scaffold presents important physicochemical characteristics and can support the growth and differentiation of mesenchymal stromal cells (h-MSCs), which adhere and penetrate into the cartilaginous and bony layers. H-MSCs grown in chondrogenic or osteogenic medium decreased their proliferation during days 14-52 on both scaffold layers and in medium without inducing factors used as controls. Both chondrogenic and osteogenic differentiation of h-MSCs occurred from day 28 and were increased on day 52, but not in the control medium. Safranin O staining and collagen type II and proteoglycans immunostaining confirmed that chondrogenic differentiation was specifically induced only in the cartilaginous layer. Conversely, von Kossa staining, osteocalcin and osteopontin immunostaining confirmed that osteogenic differentiation occurred on both layers. This study shows the specific potential of each layer of the biomimetic scaffold to induce chondrogenic or osteogenic differentiation of h-MSCs. These processes depended mainly on the media used but not the biomaterial itself, suggesting that the local milieu is fundamental for guiding cell differentiation. © 2013 John Wiley & Sons, Ltd. Source

Discover hidden collaborations