Autophagy in periodontal ligament fibroblasts under biomechanical loading

Memmert, Svenja; Damanaki, Anna; Weykopf, Beatrice; Rath-Deschner, Birgit; Nokhbehsaim, Marjan; Götz, Werner; Gölz, Lina; Till, Andreas; Deschner, James; Jäger, Andreas

doi:10.1007/s00441-019-03063-1

Cited by 16 publications

(21 citation statements)

References 32 publications

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“…Most recently, in-vitro cell type verification was increasingly used including several studies on hPDLCs (Marchesan et al, 2011), that were also reported in some of the included studies herein, i.e. flow cytometric analysis of cell surface markers (Wang H. et al, 2019;Wu et al, 2019a), osteogenic potential as reflected by ALP staining and/or Ca 2+ deposition (Jacobs et al, 2018;Wang H. et al, 2019), cell type specific gene expression pattern (Memmert et al, 2019), and immunohistochemical staining of vimentin and cytokeratin (Sun et al, 2017;Yu et al, 2018;.…”

Section: Reasons For Heterogeneity Of Genes/proteins/ Metabolites Regulationmentioning

confidence: 98%

Effect of Tension on Human Periodontal Ligament Cells: Systematic Review and Network Analysis

Sun

Ranković

Folwaczny

et al. 2021

Front. Bioeng. Biotechnol.

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Orthodontic tooth movement is based on the remodeling of tooth-surrounding tissues in response to mechanical stimuli. During this process, human periodontal ligament cells (hPDLCs) play a central role in mechanosensing and mechanotransduction. Various in vitro models have been introduced to investigate the effect of tension on hPDLCs. They provide a valuable body of knowledge on how tension influences relevant genes, proteins, and metabolites. However, no systematic review summarizing these findings has been conducted so far. Aim of this systematic review was to identify all related in vitro studies reporting tension application on hPDLCs and summarize their findings regarding force parameters, including magnitude, frequency and duration. Expression data of genes, proteins, and metabolites was extracted and summarized. Studies’ risk of bias was assessed using tailored risk of bias tools. Signaling pathways were identified by protein-protein interaction (PPI) networks using STRING and GeneAnalytics. According to our results, Flexcell Strain Unit® and other silicone-plate or elastic membrane-based apparatuses were mainly adopted. Frequencies of 0.1 and 0.5 Hz were predominantly applied for dynamic equibiaxial and uniaxial tension, respectively. Magnitudes of 10 and 12% were mostly employed for dynamic tension and 2.5% for static tension. The 10 most commonly investigated genes, proteins and metabolites identified, were mainly involved in osteogenesis, osteoclastogenesis or inflammation. Gene-set enrichment analysis and PPI networks gave deeper insight into the involved signaling pathways. This review represents a brief summary of the massive body of knowledge in this field, and will also provide suggestions for future researches on this topic.

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Section: Reasons For Heterogeneity Of Genes/proteins/ Metabolites Regulationmentioning

confidence: 98%

Effect of Tension on Human Periodontal Ligament Cells: Systematic Review and Network Analysis

Sun

Ranković

Folwaczny

et al. 2021

Front. Bioeng. Biotechnol.

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“…Fibroblasts were treated with F. nucleatum ATCC 25586 (OD 660 : 0.05) for 1 d. The microorganisms had been suspended in phosphate-buffered saline (OD 660 = 1.0, equivalent to 1.2 × 10 9 bacterial cells/mL) and subjected twice to ultra-sonication (160 W for 15 min) before the experiments. Fibroblasts were also subjected to constant tensile strain (CTS) with a cell strain device for 1 d, as in our previous studies (Figure 7a,b) [60][61][62]. In addition, fibroblasts were exposed simultaneously to F. nucleatum and CTS.…”

Section: Culture and Treatment Of Human Periodontal Fibroblastsmentioning

confidence: 99%

Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues

Rath-Deschner

Nogueira

Memmert

et al. 2021

IJMS

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The aim of the study was to clarify whether orthodontic forces and periodontitis interact with respect to the anti-apoptotic molecules superoxide dismutase 2 (SOD2) and baculoviral IAP repeat-containing protein 3 (BIRC3). SOD2, BIRC3, and the apoptotic markers caspases 3 (CASP3) and 9 (CASP9) were analyzed in gingiva from periodontally healthy and periodontitis subjects by real-time PCR and immunohistochemistry. SOD2 and BIRC3 were also studied in gingiva from rats with experimental periodontitis and/or orthodontic tooth movement. Additionally, SOD2 and BIRC3 levels were examined in human periodontal fibroblasts incubated with Fusobacterium nucleatum and/or subjected to mechanical forces. Gingiva from periodontitis patients showed significantly higher SOD2, BIRC3, CASP3, and CASP9 levels than periodontally healthy gingiva. SOD2 and BIRC3 expressions were also significantly increased in the gingiva from rats with experimental periodontitis, but the upregulation of both molecules was significantly diminished in the concomitant presence of orthodontic tooth movement. In vitro, SOD2 and BIRC3 levels were significantly increased by F. nucleatum, but this stimulatory effect was also significantly inhibited by mechanical forces. Our study suggests that SOD2 and BIRC3 are produced in periodontal infection as a protective mechanism against exaggerated apoptosis. In the concomitant presence of orthodontic forces, this protective anti-apoptotic mechanism may get lost.

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“…It has been highlighted that β-catenin signaling regulates cementum homeostasis, and a down-regulation of WNT causes root resorptions ( Lim et al, 2014 ). Mechanical compression of the periodontium is one of the numerous conditions occurring during orthodontic tooth movement ( Memmert et al, 2019 ). As part of the periodontium, the cementum is often compressed through orthodontic force application.…”

Section: Introductionmentioning

confidence: 99%

Adiponectin as Well as Compressive Forces Regulate in vitro β-Catenin Expression on Cementoblasts via Mitogen-Activated Protein Kinase Signaling Activation

Yong

Bremen

Ruiz‐Heiland

et al. 2021

Front. Cell Dev. Biol.

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We aimed to investigate the molecular effect that adiponectin exerts on cementoblasts especially in the presence of compressive forces. OCCM-30 cells (M. Somerman, NIH, NIDCR, United States) were used. Real-time reverse transcriptase–polymerase chain reaction (RT-PCR) and western blots were employed to verify if the mRNA and protein levels of adiponectin receptors (AdipoRs), mitogen-activated protein kinase (MAPK), and β-catenin signaling were influenced by compressive forces or adiponectin. Moreover, siRNAs targeting P38α, JNK1, ERK1, ERK2, and AdipoRs as well as pharmacological MAPK inhibition were performed. We found that compressive forces increase the expression of AdipoRs. Adiponectin and compression up-regulate P38α,JNK1, ERK1, and ERK2 as well as β-catenin gene expression. Western blots showed that co-stimuli activate the MAPK and β-catenin signaling pathways. MAPK inhibition alters the compression-induced β-catenin activation and the siRNAs targeting AdipoRs, P38α, and JNK1, showing the interaction of single MAPK molecules and β-catenin signaling in response to compression or adiponectin. Silencing by a dominantly negative version of P38α and JNK1 attenuates adiponectin-induced TCF/LEF reporter activation. Together, we found that light compressive forces activate β-catenin and MAPK signaling pathways. Adiponectin regulates β-catenin signaling principally by inactivating the GSK-3β kinase activity. β-Catenin expression was partially inhibited by MAPK blockade, indicating that MAPK plays a crucial role regulating β-catenin during cementogenesis. Moreover, adiponectin modulates GSK-3β and β-catenin mostly through AdipoR1. P38α is a key connector between β-catenin, TCF/LEF transcription, and MAPK signaling pathway.

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Autophagy in periodontal ligament fibroblasts under biomechanical loading

Cited by 16 publications

References 32 publications

Effect of Tension on Human Periodontal Ligament Cells: Systematic Review and Network Analysis

Effect of Tension on Human Periodontal Ligament Cells: Systematic Review and Network Analysis

Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues

Adiponectin as Well as Compressive Forces Regulate in vitro β-Catenin Expression on Cementoblasts via Mitogen-Activated Protein Kinase Signaling Activation

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