Human Dental Pulp Stem Cells Differentiate into Neural Crest-Derived Melanocytes and Have Label-Retaining and Sphere-Forming Abilities

Stevens, Angelique; Zuliani, Thomas; Olejnik, Cécile; LeRoy, Helene; Obriot, Hélène; Kerr–Conte, Julie; Formstecher, Pierre; Bailliez, Yves; Polakowska, Renata

doi:10.1089/scd.2008.0012

Cited by 147 publications

(121 citation statements)

References 38 publications

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“…The primary DPC cultures used in our experiments expressed 86.4% -6.02 and 81.03% -8.11 of CD166 and CD105 DPSC markers, respectively, but consistent with our previous study [13], only a very few cells expressed CD271 (0.23 -0.2) and CD57 (1.39 -1.5) neural crest stem cell markers. Since the expression of surface markers is condition dependent, we did not relay on them in defining SCs and used a vital DiI dyebased functional assay to distinguish quiescent LRCs from the cycling population.…”

Section: Igf-1r and P38 Mapk Inhibitors Decrease The Pool Of Quiescensupporting

confidence: 92%

“…First reported in 2000 [8], the existence of DPSCs has been confirmed by many laboratories, including ours [13]; however, the exact area of the dental pulp in which they are located is still not well established. A recent study by Martens et al [14] confirmed earlier findings [4,12,15,16] that DPSCs occupy the prevascular niche and, in developing teeth, the cervical niche located near the cementum/dentin zone.…”

Section: Introductionmentioning

confidence: 76%

“…DPSCs, which are normally quiescent, enter the cell cycle in response to odontoblast injury in vivo [4] and can proliferate and differentiate in vitro [12,13,71]. The actual factors that regulate the transition of DPSCs from the quiescent to the active state, however, are not well defined, and we have a limited understanding of how the self-renewal and differentiation of these cells is regulated.…”

Section: Discussionmentioning

confidence: 99%

“…The solvents in which the inhibitors were dissolved were added at the same concentrations to the control cultures. Colony-forming units (CFUs) and sphere-forming units (SFUs) were calculated as the percentage of the colonies or spheres of, respectively, 200 and 4,000 seeded live cells formed, as described previously [13]. Cell proliferation was monitored on 96-well plates using IncuCyte 2011A Kinetic Imaging System and software (Essen BioScience).…”

Section: Tissue Samples and Cell Culturesmentioning

confidence: 99%

“…To detect mineralization, cells were incubated in the odontoblast growth medium supplemented with 10 mM b-glycerol phosphate (bGP) for the indicated times, fixed in PAF for 10 min, and stained as described previously [13].…”

Section: Immunohistochemistrymentioning

confidence: 99%

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Insulin-Like Growth Factor 1 Receptor and p38 Mitogen-Activated Protein Kinase Signals Inversely Regulate Signal Transducer and Activator of Transcription 3 Activity to Control Human Dental Pulp Stem Cell Quiescence, Propagation, and Differentiation

Vandomme

Touil

Ostyn

et al. 2014

Stem Cells and Development

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Dental pulp stem cells (DPSCs) remain quiescent until activated in response to severe dental pulp damage. Once activated, they exit quiescence and enter regenerative odontogenesis, producing reparative dentin. The factors and signaling molecules that control the quiescence/activation and commitment to differentiation of human DPSCs are not known. In this study, we determined that the inhibition of insulin-like growth factor 1 receptor (IGF-1R) and p38 mitogen-activated protein kinase (p38 MAPK) signaling commonly activates DPSCs and promotes their exit from the G0 phase of the cell cycle as well as from the pyronin Y low stem cell compartment. The inhibition of these two pathways, however, inversely determines DPSC fate. In contrast to p38 MAPK inhibitors, IGF-1R inhibitors enhance dental pulp cell sphere-forming capacity and reduce the cells' colony-forming capacity without inducing cell death. The inverse cellular changes initiated by IGF-1R and p38 MAPK inhibitors were accompanied by inverse changes in the levels of active signal transducer and activator of transcription 3 (STAT3) factor, inactive glycogen synthase kinase 3, and matrix extracellular phosphoglycoprotein, a marker of early odontoblast differentiation. Our data suggest that there is cross talk between the IGF-1R and p38 MAPK signaling pathways in DPSCs and that the signals provided by these pathways converge at STAT3 and inversely regulate its activity to maintain quiescence or to promote self-renewal and differentiation of the cells. We propose a working model that explains the possible interactions between IGF-1R and p38 MAPK at the molecular level and describes the cellular consequences of these interactions. This model may inspire further fundamental study and stimulate research on the clinical applications of DPSC in cellular therapy and tissue regeneration.

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Section: Igf-1r and P38 Mapk Inhibitors Decrease The Pool Of Quiescensupporting

confidence: 92%