Sclerostin inhibits Protein kinase C inhibitor GÖ6976 induced osteogenic differentiation of dental follicle cells.

Human dental follicle cells (DFCs) as multipotent stem cells are currently investigated within the field of regenerative medicine considering their potential for the regeneration of dental tissues, bone defects caused by periodontal or degenerative diseases and the treatment of craniofacial disorders. However, molecular mechanisms of the differentiation into mineralizing cells are still inadequately understood. Previous studies have shown that GÖ6976, an inhibitor of classical isoforms of protein kinase C (PKC), enhanced ostogenic differentiation of DFCs.

Evaluation of Current Studies to Elucidate Processes in Dental Follicle Cells Driving Osteogenic Differentiation.

When research on osteogenic differentiation in dental follicle cells (DFCs) began, projects focused on bone morphogenetic protein (BMP) signaling. The BMP pathway induces the transcription factor DLX3, whichh in turn induces the BMP signaling pathway via a positive feedback mechanism. However, this BMP2/DLX3 signaling pathway only seems to support the early phase of osteogenic differentiation, since simultaneous induction of BMP2 or DLX3 does not further promote differentiation.

Analysis of the phosphoproteome in human dental follicle cells during osteogenic differentiation.

Dental follicle cells (DFCs) are osteogenic progenitor cells and are well suited for molecular studies of differentiation of alveolar osteoblasts. A recent study examined the metabolism in DFCs during osteogenic differentiation and showed that energy metabolism is increased after 14 days of differentiation (mid phase). However, previous studies have examined proteomes at early (2 h, 24 h) or very late (28 days) stages of differentiation, but not during the phase of increased metabolic activity.

Dental stem cells for tooth regeneration: how far have we come and where next?

Introduction: Human dental stem cells are promising for tooth repair because of their differentiation potential. In 2018, this journal published a report on dental stem cell treatment options that had been attempted since the early 2000s. Although it is very difficult to follow every trend since then, new achievements have been made in the last 5 years.

DNA protein kinase promotes cellular senescence in dental follicle cells.

Objective: Short telomeres and genomic DNA damage are causes of cellular senescence in dental follicle cells (DFCs).

Design: This study examined the role of the DNA damage response (DDR) during cellular senescence of DFCs by β-galactosidase activity and DNA damage by comet assay. Expression of genes/proteins was determined by Western Blots and reverse transcription-quantitative polymerase chain reaction, while glycolysis was enzymatically estimated.

Changes in AMPK activity induces cellular senescence in human dental follicle cells.

Dental Follicle Cells (DFCs) are somatic stem cells with a limited lifespan, but little is known about a possible mechanism of cellular senescence. Previous studies have shown that cellular senescence is associated with increased demand of glycolsis or the "glycolytic metabotype", which can be induced by activation of 5' adenosine monophosphate-activated protein kinase (AMPK), and decreased autophagy. This study examined the role of AMPK in inducing senescence in DFCs.

Peripheral Nerve Regeneration-Adipose-Tissue-Derived Stem Cells Differentiated by a Three-Step Protocol Promote Neurite Elongation via NGF Secretion.

The lack of supportive Schwann cells in segmental nerve lesions seems to be one cornerstone for the problem of insufficient nerve regeneration. Lately, adipose-tissue-derived stem cells (ASCs) differentiated towards SC (Schwann cell)-like cells seem to fulfill some of the needs for ameliorated nerve recovery. In this study, three differentiation protocols were investigated for their ability to differentiate ASCs from rats into specialized SC phenotypes.

Energy Metabolism and Lipidome Are Highly Regulated during Osteogenic Differentiation of Dental Follicle Cells.

Dental follicle cells (DFCs) are stem/progenitor cells of the periodontium and give rise to alveolar osteoblasts. However, understanding of the molecular mechanisms of osteogenic differentiation, which is required for cell-based therapies, is delimited. This study is aimed at analyzing the energy metabolism during the osteogenic differentiation of DFCs.

Mechanisms during Osteogenic Differentiation in Human Dental Follicle Cells.

Human dental follicle cells (DFCs) as periodontal progenitor cells are used for studies and research in regenerative medicine and not only in dentistry. Even if innovative regenerative therapies in medicine are often considered the main research area for dental stem cells, these cells are also very useful in basic research and here, for example, for the elucidation of molecular processes in the differentiation into mineralizing cells. This article summarizes the molecular mechanisms driving osteogenic differentiation of DFCs.

Protein kinase A is activated during bone morphogenetic protein 2-induced osteogenic differentiation of dental follicle stem cells via endogenous parathyroid hormone-related protein.

Objective: The aim of this study was to investigate the mechanisms of how protein kinase A (PKA) is activated during bone morphogenetic protein 2 (BMP2)-induced osteogenic differentiation in dental follicle stem cells.

Design: Human dental follicle stem cells were cultured and treated with a BMP2-containing osteogenic differentiation medium or differentiation medium without BMP2. Specific siRNAs and substances/proteins were used to modulate pathways.

Classical isoforms of protein kinase C (PKC) and Akt regulate the osteogenic differentiation of human dental follicle cells via both β-catenin and NF-κB.

Background: Human dental follicle cells (DFCs) are the precursor cells of the periodontium with a high potential for regenerative therapies of (alveolar) bone. However, the molecular mechanisms of osteogenic differentiation are inadequately understood. Classical isoforms of protein kinase C (PKC) are reported to inhibit osteogenesis of stem/precursor cells.

AMP-activated protein kinase and the down-stream activated process of autophagy regulate the osteogenic differentiation of human dental follicle cells.

Objective: Dental follicle cells (DFCs) are progenitors of alveolar osteoblasts. AMP-activated protein kinase (AMPK) and the down-stream activated autophagy process play a key role in cellular energy and metabolic homeostasis and are involved in many biological processes including differentiation. Previous studies showed ambiguous results about the role of AMPK and autophagy in osteogenic differentiation of various osteogenic progenitors, but the role of AMPK and autophagy in DFCs is unknown.

Effects of Cellular Senescence on Dental Follicle Cells.

The dental follicle is part of the tooth germ, and isolated stem cells from this tissue (dental follicle cells; DFCs) are considered, for example, for regenerative medicine and immunotherapies. However somatic stem cells can also improve pharmaceutical research. Cell proliferation is limited by the induction of senescence, which, while reducing the therapeutic potential of DFCs for cell therapy, can also be used to study aging processes at the cellular level that can be used to test anti-aging pharmaceuticals.

High endogenous expression of parathyroid hormone-related protein (PTHrP) supports osteogenic differentiation in human dental follicle cells.

Dental follicle cells (DFCs) are progenitor cells for mineralizing cells such as alveolar osteoblasts, but little is known about the mechanisms of the differentiation. Interestingly, different cell lines sometimes have different potentials to differentiate into mineralizing cells. In this study, we compared two different DFC lines, with one cell line (DFC_B) showing a high alkaline phosphatase (ALP) activity in long-term cultures with standard medium and a reliable mineralizing potential.

p53 inhibits the osteogenic differentiation but does not induce senescence in human dental follicle cells.

Replicative senescence causes a reduced osteogenic differentiation potential of senescent dental follicle cells (DFCs). The transcription factor p53 is often involved in the induction of cellular senescence, but little is known about its role in DFCs. This study examined for the first time the role of p53 compared to its pro-proliferative antagonist E2F-1 in terms of osteogenic differentiation potential and induction of senescence.

Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells.

Background: Dental follicle cells (DFCs) are dental stem cells and interesting options for regenerative therapies in dentistry. However, DFCs acquire replicative senescence in long-term cultures, but little is known about molecular processes. In previous studies, we observed that DFC cell lines become senescent at different rates.

Extent of Inflammation and Foreign Body Reaction to Porous Polyethylene and .

Background/aim: High-density porous polyethylene (PP) offers possibilities for reconstruction in craniofacial surgery. The purpose of this study was to evaluate the extent of inflammation and foreign body reactions to PP in vitro and in vivo.

Materials And Methods: Cell attachment, proliferation and expression of inflammatory cytokines were assessed using murine macrophages (RAW 264.

Cellular senescence in dental pulp stem cells.

Objective: This short review summarizes our current knowledge about dental stem cell aging and about possible targets for the regulation of cellular senescence.

Design: A literature search was performed using a combination of keywords, e.g.

WNT5A supports viability of senescent human dental follicle cells.

The osteogenic differentiation of dental follicle cells (DFCs) is inhibited by the onset of cellular senescence, but the cause for this is largely unknown. Recently it was shown that WNT5a, which is an inductor of the non-canonical WNT pathway, stimulates both cellular senescence and osteogenic differentiation of different cell types. In this study, we investigated the role of WNT5a for viability and osteogenic differentiation in human DFCs after the induction of cellular senescence.

Dental stem cells in tooth regeneration and repair in the future.

Introduction: Human dental stem cells can be obtained from postnatal teeth, extracted wisdom teeth or exfoliated deciduous teeth. Due to their differentiation potential, these mesenchymal stem cells are promising for tooth repair. Therefore, the development of dental tissue regeneration represents a suitable but challenging, target for dental stem cell therapies.

The cell cycle regulator protein P16 and the cellular senescence of dental follicle cells.

Cellular senescence is a restricting factor for regenerative therapies with somatic stem cells. We showed previously that the onset of cellular senescence inhibits the osteogenic differentiation in stem cells of the dental follicle (DFCs), although the mechanism remains elusive. Two different pathways are involved in the induction of the cellular senescence, which are driven either by the cell cycle protein P21 or by the cell cycle protein P16.

The dexamethasone induced osteogenic differentiation of dental follicle cells.

Mesenchymal stem cells are excellent for in vitro studies about biological processes during the differentiation of osteogenic progenitor cells into mineralizing cells such as osteoblasts. Human dental follicle cells (DFCs) are dental mesenchymal stem cells and they can be isolated from third molar teeth. Because DFCs are the genuine progenitor cells of periodontal tissue cells, they have been used for the evaluation of molecular mechanisms during the differentiation of undifferentiated stem cells into alveolar osteoblasts and cementoblasts.

Flightless-I governs cell fate by recruiting the SUMO isopeptidase SENP3 to distinct genes.

Background: Despite recent studies on the role of ubiquitin-related SUMO modifier in cell fate decisions, our understanding on precise molecular mechanisms of these processes is limited. Previously, we established that the SUMO isopeptidase SENP3 regulates chromatin assembly of the MLL1/2 histone methyltransferase complex at distinct genes, including the osteogenic master regulator . A comprehensive mechanism that regulates SENP3 transcriptional function was not understood.

miRNA-101 supports the osteogenic differentiation in human dental follicle cells.

Objective: Human dental follicle cells (DFCs) are genuine precursor cells of cementoblasts and alveolar bone osteoblasts. MicroRNAs (miRNAs) represent a class of non-coding endogenous RNAs that silence gene expression post-transcriptionally. miRNA101 actively regulates the osteogenic differentiation of periodontal ligament cells.