Expression Pattern of Basal Markers in Human Dental Pulp Stem Cells and Tissue

Martens, Wendy; Wolfs, Esther; Struys, Tom; Politis, Constantinus; Bronckaers, Annelies; Lambrichts, Ivo

doi:10.1159/000338654

Cited by 78 publications

(54 citation statements)

References 58 publications

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“…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. A study based on the mRNA expression levels of DPSC markers, including CD166, CD146, and CD105, concluded that in rat molars, ''coronal pulp harbors more SCs than the other regions'' [17].…”

Section: Introductionsupporting

confidence: 69%

“…Representative images from these ex vivo studies ( Table S1; Supplementary Data are available online at www.liebertpub .com/scd), indicating that the inactivation of IGF-1R and p38 MAPK selectively stimulates the division of some quiescent DPCs. Interestingly, most of the cells that entered the cell cycle were located near or within CD271-or p75 neurotrophin receptor (p75 NTR )-positive nerve bundles penetrated by blood vessels where the niche for multipotent DPSCs was found [14,15,55].…”

Section: Inactivation Of Igf-1r and P38 Mapk Induces Cycling Of Quiesmentioning

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: Introductionsupporting

confidence: 69%

Section: Inactivation Of Igf-1r and P38 Mapk Induces Cycling Of Quiesmentioning

confidence: 99%

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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“…Of note, the expression of c-MYC, that is not modulated to maintain the stemness-like state in BM-MSC (Roson-Burgo et al, 2014), was unaffected by a low pHe. As DPSC originate from the cranial-derived neural crest cells, we also investigated the expression of the neuronal stem-related markers nestin and p75/NGFR (Mitsiadis et al, 2015;Martens et al, 2012) after exposure to acidic conditions. Similarly to the other mentioned stemrelated markers, these genes were induced by pHe 6.5.…”

Section: Discussionmentioning

confidence: 99%

The effect of extracellular acidosis on the behaviour of mesenchymal stem cells in vitro

Massa

Perut

Chano

et al. 2017

eCM

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The stem cell fraction of a cell population is finely tuned by stimuli from the external microenvironment. Among these stimuli, a decrease of extracellular pH (pHe) may occur in a variety of physiological and pathological conditions, including hypoxia and inflammation. In this study, by using bone marrow stem cells and dental pulp stem cells, we provided evidence that extracellular acidosis endows the maintenance of stemness in mesenchymal cells. Indeed, continuous exposure for 21 d to low pHe (6.5-6.8) conditions impaired the osteogenic differentiation of both cell types. Moreover, the exposure to low pHe, for 1 and up to 7 d, induced the expression of stemness-related genes and proteins, drove cells to reside in the quiescent G0 alert state and enhanced their ability to form floating spheres. The pre-conditioning with extracellular acidosis for 7 d did not affect the differentiation potential of dental pulp stem cells since, when the cells were cultured again at physiological pHe, their multilineage potential was almost unmodified.Our data provided evidence of the role of extracellular acidosis as a modulator of the stemness of mesenchymal cells. This condition is commonly found both in systemic and local bone conditions, hence underlining the relevance of this phenomenon for a better comprehension of bone healing and regeneration.

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“…Therefore, there are non-vascular DPSCs niches. Since cultured DPSCs express neural markers in high percentage (nestin: 92.7 %, NF-H: 42.3 %, GalC: 92.3 %, and βIII-tubulin: 95.9 %) [22], they were used to locate stem cell niches in the pulp of young permanent teeth. Nestin was found to be expressed throughout the tissue and βIII-tubulin was in the subodontoblast zone [23].…”

Section: Cd146mentioning

confidence: 99%