Differential effects of p38 and Erk1/2 on the chondrogenic and osteogenic differentiation of dental pulp stem cells

Ba, Pengfei; Duan, Xiaoyu; Fu, Guo; Lv, Shuyan; Yang, Pishan; Qi-zhong, Sun

doi:10.3892/mmr.2017.6563

Cited by 26 publications

(19 citation statements)

References 25 publications

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“…Such mechanisms include, among others, methylation of cartilage-specific promoter genes, or acetylation, methylation, phosphorylation and SUMOylation of histones, which depending on the case, are able of promoting or repressing the transcriptional activation of chondrogenic genes such as SOX9 (see [49] for a review). In fact, in contrast to the observations in this paper, ERK1/2 signaling pathway has shown able to facilitate chondrogenic differentiation in the dental pulp stem cells (DPSCs) [50], what indicates that MAPK pathway activation might play distinct roles in the differentiation of stem cells from different lineages. As epigenetic mechanisms play a pivotal role in the stem cell fate commitment, it is possible that epigenetic factors are involved in the herein reported effects of CRET on the chondrogenic differentiation of ADSC.…”

Section: Discussioncontrasting

confidence: 99%

Chondrogenic Differentiation of Adipose-Derived Stem Cells by Radiofrequency Electric Stimulation

Hernández-Bule¹,

Trillo²,

Martínez‐García³

et al. 2017

J Stem Cell Res Ther

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Objective: Although capacitive-resistive electric transfer (CRET) therapies, based on transdermal application of electrothermal radiofrequency currents, have shown promising therapeutic effectiveness in regeneration of traumatic or degenerative tissue lesions, their potential effects on tissues like cartilage, having poor regenerative capabilities, have not been studied sufficiently. Here we investigate the effects of the exposure to a 448 kHz current typically used in CRET therapy, on the early chondrogenic differentiation of human, adipose-derived stem cells (ADSC). Materials and methods: Stem cells obtained from healthy donors were differentiated in chondrogenic medium for 16 days. During the last 2 days of incubation the cultures were intermittently exposed or sham-exposed to a 448-kHz, sine wave current, administered at a 50 µA/mm 2 subthermal density. The cellular response was assessed by: XTT proliferation assay, glycosaminoglycans (GAG) and collagen quantification (image analysis, Blyscan assay and immunoblot) and analysis of the expression of chondrogenic factors Sox5 and Sox6, and of the transcription factor ERK1/2 and its active form p-ERK1/2 (immunoflorescence, immunoblot and RT-PCR). Results: The electric stimulus significantly increased the levels of both, cartilage-specific collagen type II and GAG in the extracellular matrix of the differentiating cultures. Although no changes were observed in the expression of the SOX genes at the end of the 48-hour treatment, the stimulus did induce significant overexpression of transcription factors L-Sox5, Sox6 and p-ERK1/2. Since these proteins are crucial regulators of the synthesis of the extracellular matrix during chondrogenic differentiation, it is likely that their overexpression is involved in the observed increases in the content of extracellular collagen and GAG. Conclusion: The present data set provides support to the hypothesis that the electric component of the electrothermal treatment applied in CRET therapies could stimulate cartilage repair by promoting chondrogenic differentiation. These data, coupled with previously reported results that in vitro treatment with the same type of subthermal electric signal promotes proliferation of undifferentiated ADSC, identify molecular phenomena underlying the potential repairing and regenerative effects of such radiofrequency currents.

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Section: Discussioncontrasting

confidence: 99%

Chondrogenic Differentiation of Adipose-Derived Stem Cells by Radiofrequency Electric Stimulation

Hernández-Bule¹,

Trillo²,

Martínez‐García³

et al. 2017

J Stem Cell Res Ther

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“…Dental pulp stem cells which are closely related to SCAPs, also depend on growth factor-activated p38 for osteogenic differentiation 65 . Interestingly, ERK1/2 MAPK inhibits osteogenesis, while p38 MAPK promotes osteogenic differentiation of human DPSCs 66 . Our results suggest that bacterial triggering of p38-induced pro-inflammatory activation supersedes growth factor-activated p38-driven osteogenesis.…”

Section: Discussionmentioning

confidence: 97%

Secreted products of oral bacteria and biofilms impede mineralization of apical papilla stem cells in TLR-, species-, and culture-dependent fashion

Petridis

Sluis

Dijkstra

et al. 2018

Sci Rep

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Regenerative endodontics exploits the mineralization potential of stem cells from the apical papilla (SCAPs) in order to promote root maturation of permanent immature teeth. SCAPs may encounter post-disinfection residual bacteria either in planktonic or in biofilm growth mode. Bacterial components bind to Toll-like receptors (TLRs) and trigger pro-inflammatory responses. We hypothesized that biofilm-triggered TLR activation affects the mineralization potential of human SCAPs. SCAPs were challenged with conditioned media derived from standardized dual-species biofilms and planktonic bacterial cultures and their inflammatory status and mineralization capacity were studied. Bacterial products from both growth modes (planktonic vs. biofilm) compromised cell viability, proliferation and mineralization capacity of SCAPs, but in a species- and growth mode-dependent fashion. While TLR4 expression remained unaffected, TLR2 expression was upregulated coinciding with a pro-inflammatory activation of SCAPs. Moreover, TLR and its downstream TGF-β-associated kinase (TAK1) appeared to be blocking mineralization, as inhibition of these factors restored it. In conclusion, bacterial products promoted the pro-inflammatory status and inhibited mineralization of human SCAPs in a TLR-, species-, and culture-dependent fashion. TLR2 emerged as the pivotal mediator of these responses and further research is warranted towards the judicious manipulation of SCAPs in order to modify the untoward events of TLR-priming and signaling.

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“…As an essential member in the MAPK superfamily, p38 MAPK pathway has been proved to participate in various cytokines’ and molecules’ regulation process of cell physiological activities in different cells (Ba et al, 2017; Kornasio et al, 2009; Luo et al, 2005). In this study, we found that the activity of p38 MAPK pathway was enhanced transiently but distinctly under irisin stimulation.…”

Section: Discussionmentioning

confidence: 99%

Irisin promotes cementoblast differentiation via p38 MAPK pathway

et al. 2020

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Objective Irisin is a newly identified exercise‐induced myokine which can affect glucose metabolism and cortical bone mass and strength. However, the influence of irisin on cementoblasts remains largely unknown. Material and methods An immortalized mouse cementoblast cell line OCCM‐30 was used in this study. Cementoblast differentiation markers and PGC‐1α in cells cultured with mineral induction medium were evaluated by qRT‐PCR. Cementoblast mineralization was evaluated by alizarin red staining. Differentiation markers and the activity of p38 MAPK pathway under irisin stimulation were assessed by qRT‐PCR or Western blot analysis. p38 MAPK pathway inhibitor SB203580 or p38 siRNA was used to further identify the regulatory mechanism. Cell proliferation treated with irisin was examined by CCK‐8 method. Results The expression of Runx2, osterix, ALP, and PGC‐1α was up‐regulated consistently under mineral induction. The formation of mineralized nodules was increased by irisin. Runx2, osterix, ALP, and osteocalcin were obviously up‐regulated under irisin stimulation as well as the activity of p38 MAPK pathway. When pretreated with SB203580 or p38 siRNA before irisin stimulation, the irisin‐induced differentiation was distinctly suppressed. OCCM‐30 cell proliferation was enhanced when treated with high‐dose irisin for long time. Conclusion Irisin can promote the differentiation of cementoblasts via p38 MAPK pathway.

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Differential effects of p38 and Erk1/2 on the chondrogenic and osteogenic differentiation of dental pulp stem cells

Cited by 26 publications

References 25 publications

Chondrogenic Differentiation of Adipose-Derived Stem Cells by Radiofrequency Electric Stimulation

Chondrogenic Differentiation of Adipose-Derived Stem Cells by Radiofrequency Electric Stimulation

Secreted products of oral bacteria and biofilms impede mineralization of apical papilla stem cells in TLR-, species-, and culture-dependent fashion

Irisin promotes cementoblast differentiation via p38 MAPK pathway

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