Inflammation can influence multipotency and self-renewal of mesenchymal stem cells (MSCs), resulting in their awakened bone-regeneration ability. Human periodontal ligament tissue-derived MSCs (PDLSCs) have been isolated, and their differentiation potential was found to be defective due to β-catenin signaling indirectly regulated by inflammatory microenvironments. Nuclear factor-κB (NF-κB) is well studied in inflammation by many different groups. The role of NF-κB needs to be studied in PDLSCs, although genetic evidences have recently shown that NF-κB inhibits osteoblastic bone formation in mice. However, the mechanism as to how inflammation leads to the modulation of β-catenin and NF-κB signaling remains unclear. In this study, we investigated β-catenin and NF-κB signaling through regulation of glycogen synthase kinase 3β activity (GSK-3β, which modulates β-catenin and NF-κB signaling) using a specific inhibitor LiCl and a phosphatidylinositol 3-kinase (PI3K) inhibitor LY 294002. We identified that NF-κB signaling might be more important for the regulation of osteogenesis in PDLSCs from periodontitis compared with β-catenin. BAY 11-7082 (an inhibitor of NF-κB) could inhibit phosphorylation of p65 and partly rescue the differentiation potential of PDLSCs in inflammation. Our data indicate that NF-κB has a central role in regulating osteogenic differentiation of PDLSCs in inflammatory microenvironments. Given the molecular mechanisms of NF-κB in osteogenic differentiation governed by inflammation, it can be said that NF-κB helps in improving stem cell-mediated inflammatory bone disease therapy.

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In this study the relation between lysophosphatidic acid (LPA) and myocardial infarction was investigated, the typical and simplified methods for measuring serum LPA concentration by dot immunogold filtration assay (DIFA) based on a polyclonal antibody to LPA were developed, and serum LPA concentrations were measured in 31 patients with acute myocardial infarction (AMI) and 12 controls (blood donors) by DIFA. Serum LPA levels were raised more than twofold 8 h after the onset of AMI. Maximal elevation (10.43 mg/L) was found at 48-72 h following onset and remained higher than the control concentration (1.66 mg/L) 7 days after AMI. The rise in serum LPA concentration in AMI patients suggests that LPA might be involved in AMI-related pathophysiology in the cardiovascular system. The simplified DIFA developed in the present study for measuring serum LPA concentration is convenient and highly sensitive.