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Exosomes with Highly Angiogenic Potential for Possible Use in Pulp Regeneration.
Journal of Endodontics 2018 May
INTRODUCTION: Angiogenesis is critical for pulp regeneration. Exosomes, a key component of paracrine secretion, have emerged as important players in the modulation of angiogenesis. The role of dental pulp cell-derived exosomes (DPC-Exos) in angiogenesis has rarely been reported. The proangiogenic properties of DPC-Exos in human umbilical vein endothelial cells (HUVECs) are investigated in the current study.
METHODS: Exosomes were isolated from dental pulp cell (DPC) culture supernatants by ultracentrifugation and were characterized by transmission electron microscopy, Western blotting, and nanoparticle tracking analysis. Their roles in HUVEC proliferation, proangiogenic factor expression, and tube formation were examined in vitro.
RESULTS: We isolated and characterized exosomes from DPCs and showed that DPC-Exos promoted HUVEC proliferation, proangiogenic factor expression, and tube formation. Furthermore, we found that p38 mitogen-activated protein kinase (MAPK) signaling inhibition enhances DPC-Exos-induced tube formation.
CONCLUSIONS: Taken together, these results suggest that DPC-Exos have vital roles in angiogenesis, and p38 MAPK signaling inhibition enhances tubular morphogenesis.
METHODS: Exosomes were isolated from dental pulp cell (DPC) culture supernatants by ultracentrifugation and were characterized by transmission electron microscopy, Western blotting, and nanoparticle tracking analysis. Their roles in HUVEC proliferation, proangiogenic factor expression, and tube formation were examined in vitro.
RESULTS: We isolated and characterized exosomes from DPCs and showed that DPC-Exos promoted HUVEC proliferation, proangiogenic factor expression, and tube formation. Furthermore, we found that p38 mitogen-activated protein kinase (MAPK) signaling inhibition enhances DPC-Exos-induced tube formation.
CONCLUSIONS: Taken together, these results suggest that DPC-Exos have vital roles in angiogenesis, and p38 MAPK signaling inhibition enhances tubular morphogenesis.
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