title: Nemotic human dental pulp fibroblasts promote human dental pulp stem cells migration.
abstract: Dental pulp inflammation has long been perceived as a negative factor leading to pulp disruption. Previous studies have suggested that the inflammatory reaction might be a prerequisite for the burst of progenitors implicated in pulp repair. To investigate the migration of human dental pulp stem cells (hDPSCs) in response to human dental pulp fibroblasts (HDPFs) nemosis, an in vitro model of nemosis-induced inflammation in three-dimensional culture was used in this study. We observed HDPF spheroid formation and that cell-cell adhesion between HDPFs leads to necrosis. Cell death detection and cell counting kit-8 assays showed reduced live cell numbers and increased levels of cell membrane leakage in HDPF spheroids. HDPFs spheroids expressed cyclooxygenase-2 and released an increasing amount of prostaglandin E2 and interleukin-8, indicating inflammation in response to nemosis. The Transwell assays showed that the conditioned medium from HDPFs spheroids significantly induced hDPSCs migration more than the medium from the monolayer. Taken together, these results indicate that HDPFs spheroids induce nemosis and contribute to the migration of hDPSCs. This model might provide a potential research tool for studying interactions between fibroblasts and stem cells, and studies concerning nemosis-targeted stem cells might help treat pulp inflammation.
authors.affiliation: Department of Operative Dentistry and Endodontics, School of Stomatology, Fourth Military Medical University, 145 Changle West Road, Xi'an, Shaanxi 710032, China.
authors.forename: Shafei
authors.initials: S
authors.lastname: Zhai
authors.forename: Yafei
authors.initials: Y
authors.lastname: Wang
authors.forename: Wenkai
authors.initials: W
authors.lastname: Jiang
authors.forename: Qian
authors.initials: Q
authors.lastname: Jia
authors.forename: Jie
authors.initials: J
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Haijing
authors.initials: H
authors.lastname: Wang
authors.forename: Yonglin
authors.initials: Y
authors.lastname: Ding
authors.forename: Ping
authors.initials: P
authors.lastname: Wang
authors.forename: Jun
authors.initials: J
authors.lastname: Liu
authors.forename: Longxing
authors.initials: L
authors.lastname: Ni
mesh_terms: D001641:Bicuspid / Q000378:metabolism / Q000473:pathology; D002448:Cell Adhesion; D002452:Cell Count; D016923:Cell Death; D002462:Cell Membrane / Q000378:metabolism; D002465:Cell Movement; D048430:Cell Shape; D002470:Cell Survival; D017077:Culture Media, Conditioned / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D003782:Dental Pulp / Q000166:cytology / Q000378:metabolism* / Q000648:ultrastructure; D003790:Dental Pulp Necrosis / Q000378:metabolism / Q000473:pathology; D015232:Dinoprostone / Q000235:genetics / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism* / Q000648:ultrastructure; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D046529:Microscopy, Electron, Transmission; D019899:Paracrine Communication; D013234:Stem Cells / Q000378:metabolism*
chemical_list: C508606:CXCL8 protein, human; D017077:Culture Media, Conditioned; D016209:Interleukin-8; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D015232:Dinoprostone