AIM: To evaluate the impact of activated platelets on the mitogenic expansion of human dental pulp-derived cells (DPC) in vitro. METHODOLOGY: The effect of supernatants released from activated platelets (PRS) and the corresponding platelet membranes (MEM) on proliferation and protein synthesis of DPC was evaluated. The contributions of the phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) pathways to the response of DPC were assessed using kinase inhibitors. Also examined was whether the presence of calcium hydroxide or the inflammatory mediators tumour necrosis factor alpha, interleukin-1, interleukin-6 and lipopolysaccharide of Escherichia coli modulated the expansion of DPC. RESULTS: Physiologic concentrations of PRS and MEM stimulated proliferation and protein synthesis by 18.4-fold (P < 0.01) and 2.9-fold (P < 0.01), respectively. This mitogenic expansion was paralleled by activation of AKT and the MAP kinases extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38. Inhibitor studies revealed that the mitogenic response of DPC involved PI3K/AKT, JNK and p38 signalling (P < 0.05). Calcium hydroxide and inflammatory factors did not significantly modulate the mitogenic response of DPC to PRS and MEM. CONCLUSION: Supernatants released from activated platelets and the corresponding platelet membranes stimulated DPC proliferation and protein synthesis involving PI3K/AKT and MAPK signalling. These findings may serve as a basis for preclinical studies that address the role of activated platelets in dental pulp repair.
AIM: To evaluate the impact of activated platelets on the mitogenic expansion of human dental pulp-derived cells (DPC) in vitro. METHODOLOGY: The effect of supernatants released from activated platelets (PRS) and the corresponding platelet membranes (MEM) on proliferation and protein synthesis of DPC was evaluated. The contributions of the phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) pathways to the response of DPC were assessed using kinase inhibitors. Also examined was whether the presence of calcium hydroxide or the inflammatory mediators tumour necrosis factor alpha, interleukin-1, interleukin-6 and lipopolysaccharide of Escherichia coli modulated the expansion of DPC. RESULTS: Physiologic concentrations of PRS and MEM stimulated proliferation and protein synthesis by 18.4-fold (P < 0.01) and 2.9-fold (P < 0.01), respectively. This mitogenic expansion was paralleled by activation of AKT and the MAP kinases extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38. Inhibitor studies revealed that the mitogenic response of DPC involved PI3K/AKT, JNK and p38 signalling (P < 0.05). Calcium hydroxide and inflammatory factors did not significantly modulate the mitogenic response of DPC to PRS and MEM. CONCLUSION: Supernatants released from activated platelets and the corresponding platelet membranes stimulated DPC proliferation and protein synthesis involving PI3K/AKT and MAPK signalling. These findings may serve as a basis for preclinical studies that address the role of activated platelets in dental pulp repair.
Authors: Eva-Maria Mozgan; Michael Edelmayer; Klara Janjić; Manuela Pensch; Michael B Fischer; Andreas Moritz; Hermann Agis Journal: BMC Oral Health Date: 2017-03-21 Impact factor: 2.757