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Dental pulp stem cells (DPSCs) are a type of mesenchymal stem cells (MSCs) characterised by self-renewal and multi-lineage differentiation, including chondrocytes, adipocytes, neural cells and osteoblasts, which make it an attractive choice for tissue engineering purposes. Tumour necrosis factor α (TNF-α) had the positive effect on the mineralisation of bone marrow MSCs and stromal cells derived from human adipose tissue. However, the effect of TNF-α on DPSCs is unclear. We found that TNF-α activated the NF-κB pathway during the osteogenic differentiation of DPSCs. TNF-α also increased mineralisation and the expression of bone morphogenetic protein 2 (BMP2), alkaline phosphatase (ALP), runt-related transcription factor 2 (RUNX2) and collagen type I (COL I) during this process. PDTC, an NF-κB inhibitor, blocked the osteogenic differentiation induced by TNF-α. No effect of TNF-α on proliferation of DPSCs or cell cycle was detected. In summary, TNF-α promotes mineralisation and mineralisation-related gene expression through the NF-κB signalling pathway in DPSCs, which may provide a foundation for autologous transplantation of DPSCs.

T1DM (type 1 diabetes mellitus) is an autoimmune disease characterized by T-cell-mediated damage of islet β-cells. The pathology of NOD (non-obese diabetic) mouse involves the insulitis induced by infiltration of T-cells, a similar pathogenic mechanism in T1DM patient. BM-MSCs (bone marrow mesenchymal stem cells) are multipotent progenitor cells that can be isolated from a number of sources. Recent studies have shown that transplantation of MSCs to the NOD mice could prevent the process and have the therapeutic effects on T1DM. In our studies, we have found that migration and adhesion of BM-MSCs from NOD mice were suppressed compared with the BM-MSCs from ICR (imprinting control region) mice, accompanying with the abnormal distribution of FAK (focal adhesion kinase) and F-actin (filamentous actin). Further, we have found that the activation of PI3K (phosphoinositide 3-kinase)-Akt pathway was suppressed in BM-MSCs from NOD mice. When the PI3K-Akt pathway was inhibited by LY294002, the adhesion and migration of BM-MSCs from ICR mice were suppressed as well. These results indicated that the suppression of PI3K-Akt pathway is involved in the decreased adhesion and migration of BM-MSCs from NOD mice.