Human Dental Pulp Stem Cells via the NF-κB Pathway

Gu, Shensheng; Ran, Shujun; Qin, Feng; Cao, Dong; Wang, Jia; Liu, Bin; Ji, Liang

doi:10.1159/000430145

Cited by 13 publications

(7 citation statements)

References 36 publications

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“…Approval for the whole research was obtained from the Ethics Committee of our hospital and the patients provided informed consent. DPSCs were isolated from dental pulp using the outgrowth method, and the cells were subsequently cultured in alpha-minimum essential medium (α-MEM; HyClone, Logan, UT, USA) containing 10% FBS according to a previous study [19, 20]. For DFO and iron treatment, DPSCs were incubated in culture medium containing different concentrations of DFO or DFO with ferric citrate (FC) at the indicated time.…”

Section: Methodsmentioning

confidence: 99%

Deferoxamine-Induced Migration and Odontoblast Differentiation via ROS-Dependent Autophagy in Dental Pulp Stem Cells

Wang

Jiang

et al. 2017

Cell Physiol Biochem

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Background/Aims: As a vital degradation and recycling system, autophagy plays an essential role in regulating the differentiation of stem cells. We previously showed that iron chelator deferoxamine (DFO) could promote the repair ability of dental pulp stem cells (DPSCs). Here, we investigated the effect of DFO in autophagy and the role of autophagy in regulating the migration and odontoblast differentiation of DPSCs. Methods: Transmission electron microscopy, immunofluorescence staining and western blotting were performed to evaluate the autophagic activity of DPSCs. Transmigration assay, alkaline phosphatase staining/activity, alizarin red S staining and quantitative PCR were performed to examine the migration and odontoblast differentiation of DPSCs. Reactive oxygen species (ROS) levels and the effects of ROS scavenger in autophagy induction were also detected. Autophagy inhibitors (3-MA and bafilomycin A1) and lentiviral vectors carrying ATG5 shRNA sequences were used for autophagy inhibition. Results: Early exposure to DFO promoted the mineralization of DPSCs and increased autophagic activity. Autophagy inhibition suppressed DFO-induced DPSC migration and odontoblast differentiation. Furthermore, DFO treatment could induce autophagy partly through hypoxia-inducible factor 1α/B cell lymphoma 2/adenovirus E1B 19K-interacting protein 3 (HIF-1α/BNIP3) pathway in a ROS-dependent manner. Conclusion: DFO increased DPSC migration and differentiation, which might be modulated through ROS-induced autophagy.

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Section: Methodsmentioning

confidence: 99%

Deferoxamine-Induced Migration and Odontoblast Differentiation via ROS-Dependent Autophagy in Dental Pulp Stem Cells

Wang

Jiang

et al. 2017

Cell Physiol Biochem

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“…Moreover, selective targeting of NF-κB signaling could block the receptor activator for nuclear factor κB ligand (RANKL)-induced osteoclastogenesis and prevent osteoporotic bone destruction [19]. In addition, several researchers also demonstrated that estrogen deficiency activates NF-κB pathway, resulting in the inhibition of the odonto/osteogenic differentiation of dental pulp stem cells [20,21]. Thus, the wide involvement of NF-κB in skeletal remodeling and bone homeostasis makes it as a potential therapeutic target to inhibit bone resorption and promote bone formation.…”

mentioning

confidence: 99%

Knockdown of LAP2α inhibits osteogenic differentiation of human adipose-derived stem cells by activating NF-κB

Tang

Zhang

et al. 2020

Stem Cell Res Ther

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Background: Lamina-associated polypeptide 2α (LAP2α) is a nucleoplasmic protein that has been involved in the regulation of the cell cycle, gene transcription, and adult stem cell function. LAP2α down-regulation is linked to age-related osteoporosis and bone deformities; however, the underlying mechanisms remain obscure. The present study aimed to elucidate the function of LAP2α in the osteogenic differentiation of human adipose-derived stem cells (hASCs), which are attractive sources for bone tissue engineering. Methods: The expression of LAP2α during the osteogenic differentiation of hASCs was detected firstly. A loss of function investigation was then carried out to characterize the function of LAP2α in osteogenic differentiation of hASCs both in vitro and in vivo. Moreover, RNA-sequences, western blotting, and confocal analyses were performed to clarify the molecular mechanism of LAP2α-regulated osteogenesis. Results: We found that LAP2α expression was upregulated upon osteogenic induction. Both in vitro and in vivo experiments indicated that LAP2α knockdown resulted in impaired osteogenic differentiation of hASCs. Mechanistically, we revealed that LAP2α deficiency activated nuclear factor kappa B (NF-κB) signaling by controlling the cytoplasmic-nuclear translocation of p65. Conclusions: Collectively, our findings revealed that LAP2α functions as an essential regulator for osteogenesis of hASCs by modulating NF-κB signaling, thus providing novel insights for mesenchymal stem cell-mediated bone tissue engineering.

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“…All patients gave their written informed consent to participate. DPSCs were obtained as described previously 21 . Cells were cultured in alpha‐minimum essential medium (a‐MEM; Hyclone, Logan, UT, USA) supplemented with 10% FBS, 100 U/mL penicillin, and 100 μg/mL streptomycin in a humidified atmosphere of 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Upregulated microRNA‐126 induces apoptosis of dental pulp stem cell via mediating PTEN‐regulated Akt activation

et al. 2020

Clinical Laboratory Analysis

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Introduction Human dental pulp stem cells (DPSCs) have potential applications in regenerative medicine. The molecular mechanisms underlying DPSCs viability and apoptosis are not completely understood. Here, we investigated the role of miR‐126 in DPSCs viability and apoptosis. Material and methods Senescent DPSCs were compared with early passage DPSCs. real‐time PCR and microARRAY were performed to identify the differential expression of miR‐126, and western blot was performed to detect the expression of PTEN. MTT assay was utilized to reveal the proliferative rate of both senescent and early passage DPSCs. Flow cytometry was used to examine the apoptotic rate of DPSCs. Dual‐luciferase reporter assay was carried out to detect the interaction of miR‐126 and PTEN. Results Senescent DPSCs showed a high level of apoptosis. Further study showed that miR‐126 is upregulated in senescent DPSCs and its overexpression in early passaged DPSCs induced apoptosis. Phosphatase and tensin homolog gene (PTEN) was identified as a target of miR‐126. PTEN was downregulated in senescent DPSCs, whereas miR‐126 inhibition upregulated PTEN level, and subsequently activated Akt pathway and suppressed the apoptotic phenotype of senescent DPSCs. In addition, PTEN overexpression rescued apoptosis of DPSCs at later stage. Conclusion Our results demonstrate that the miR‐126‐PTEN‐Akt axis plays a key role in the regulation of DPSCs apoptosis and provide a candidate target to improve the functional and therapeutic potential of DPSCs.

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Human Dental Pulp Stem Cells via the NF-κB Pathway

Cited by 13 publications

References 36 publications

Deferoxamine-Induced Migration and Odontoblast Differentiation via ROS-Dependent Autophagy in Dental Pulp Stem Cells

Deferoxamine-Induced Migration and Odontoblast Differentiation via ROS-Dependent Autophagy in Dental Pulp Stem Cells

Knockdown of LAP2α inhibits osteogenic differentiation of human adipose-derived stem cells by activating NF-κB

Upregulated microRNA‐126 induces apoptosis of dental pulp stem cell via mediating PTEN‐regulated Akt activation

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