Abstract
SDF-1 (stromal cell derived factor-1) has been found to be widely expressed during dental pulp inflammation, while hDPSCs (human dental pulp stem cells) contribute to the repair of dental pulp. We showed that the migration of hDPSCs was induced by SDF-1 in a concentration-dependent manner and could be inhibited with siCXCR4 (C-X-C chemokine receptor type 4) and siCDC42 (cell division control protein 42), as well as drug inhibitors such as AMD3100 (antagonist of CXCR4), LY294002 (inhibitor of PI3K) and PF573228 (inhibitor of FAK). It was also confirmed that SDF-1 regulated the phosphorylation of FAK (focal adhesion kinases) on cell membranes and the translocation of β-catenin into the cell nucleus. Subsequent experiments confirmed that the expression of CXCR4 and β-catenin and the phosphorylation of FAK, PI3K (phosphoinositide 3-kinase), Akt and GSK3β (glycogen synthase kinase-3β) were altered significantly with SDF-1 stimulation. FAK and PI3K worked in coordination during this process. Our findings provide direct evidence that SDF-1/CXCR4 axis induces hDPSCs migration through FAK/PI3K/Akt and GSK3β/β-catenin pathways, implicating a novel mechanism of dental pulp repair and a possible application of SDF-1 for the treatment of pulpitis.
Highlights
SDF-1 has been found to be widely expressed during dental pulp inflammation, while human dental pulp stem cells (hDPSCs) contribute to the repair of dental pulp
To investigate the signal transition induced by SDF-1 in hDPSCs, we examined the phosphorylated protein level changes of focal adhesion kinase (FAK), phosphoinositide 3-kinase (PI3K), Akt and GSK3β, as well as the protein level alterations of β-catenin after cells were stimulated by the indicated concentration of SDF-1 (30, 50, or 100 ng/ml) for 2 hours (Fig. 2A)
Since the function of SDF-1 depends on the activation of CXCR4, we investigated whether downregulation of CXCR4 by siRNA transfection could affect the migration of hDPSCs as we had observed with AMD3100 inhibition
Summary
SDF-1 (stromal cell derived factor-1) has been found to be widely expressed during dental pulp inflammation, while hDPSCs (human dental pulp stem cells) contribute to the repair of dental pulp. Subsequent experiments confirmed that the expression of CXCR4 and β-catenin and the phosphorylation of FAK, PI3K (phosphoinositide 3-kinase), Akt and GSK3β (glycogen synthase kinase-3β) were altered significantly with SDF-1 stimulation. Our findings provide direct evidence that SDF-1/CXCR4 axis induces hDPSCs migration through FAK/PI3K/Akt and GSK3β/β-catenin pathways, implicating a novel mechanism of dental pulp repair and a possible application of SDF-1 for the treatment of pulpitis. At the late stage of caries, inflammation will emerge at the dental pulp under the caries and induce apoptosis of odontoblasts This process can be partially repaired under the effect of human dental pulp stem cells (hDPSCs). Previous reports demonstrated that GSK3βinhibition could augment the expression of β-catenin[22]
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