The binding of TNF-α to its receptors results in the activation of multiple signaling pathways, which actively interact with each other to regulate the differentiation, proliferation, survival and apoptosis of MSCs.

Preterm birth is suggested to play an important role in the development of diabetes. However, results have been inconsistent. We conducted a systematic review and meta-analysis to clarify the relationship between preterm birth and type 1 and type 2 diabetes. PubMed, Embase and ISI Web of Science were searched. A total of 18 studies (including 2,176,480 participants and 22,073 cases) for type 1 diabetes and five studies (including 31,478 participants and 1,898 cases) for type 2 diabetes were included in the current meta-analyses. We calculated pooled odds ratio (OR) and 95% confidence interval (CI) using fixed-effects model to evaluate the relations between preterm birth and type 1 and type 2 diabetes. The results suggested that preterm birth was significantly associated with increased risk of type 1 diabetes (OR = 1.18, 95% CI = 1.11-1.25), with no evidence of between-study heterogeneity (I(2) = 13.2%, P = 0.296). Preterm birth was also significantly associated with increased risk of type 2 diabetes (OR = 1.51, 95% CI = 1.32-1.72), with no evidence of (I(2) = 0.0%, P = 0.557). Subgroup analyses suggested that there was significant association in both case-control studies (OR = 1.16, 95% CI = 1.06-1.26) and cohort studies (relative risk = 1.20, 95% CI = 1.11-1.29) for type 1 diabetes, and similar results were found for type 2 diabetes. The results suggested that preterm birth was a significant and independent risk factor for both type 1 and type 2 diabetes.

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Multipotent DFCs can be induced to differentiate towards osteoblasts, adipocytes or chondrocytes in vitro. Runx2 over-expression up-regulated expression levels of osteoblast/cementoblast-related genes and in vitro enhanced osteogenic differentiation of DFCs. In addition, mutant Runx2-induced changes in DFCs were more prominent than those induced by full-length Runx2.