TNF‐α and LPS activate angiogenesis via VEGF and SIRT1 signalling in human dental pulp cells

Shin, Mee-Ran; Kang, Soo‐Kyung; Kim, Y. S.; Lee, S. Y.; Hong, Seon-Pyo; Kim, E.-C.

doi:10.1111/iej.12396

Cited by 52 publications

(39 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The activation of the JNK, PI3K/ AKT/mTOR, p38 MAPK, MAPK/ERK and NF-jb pathways in the presence of TNF-a has also been Table 1. reported (Goda et al 2015, Shin et al 2015. Cytokines and chemokines are produced in response to NF-jb signalling and are able to regulate the immune and inflammatory responses by binding to their specific receptors .…”

Section: Molecular Events Involved In Inflammatory Responsesmentioning

confidence: 99%

“…Main effects p38 MAPK Pathway (p38 Mitogen-Activated Protein Kinases) Implicated in cell differentiation and proliferation, odontoblast secretory activity and inflammatory response , Cooper et al 2014, Shin et al 2015, Cvikl et al 2016). TGFb-Smad Signalling Pathway (Transforming Growth Factor/Small Mother Against Decapentaplegic Pathway) Implicated in cell differentiation and proliferation (Chang et al 2015) and odontoblast secretory activity (Lucchini et al 2002, He et al 2004).…”

Section: Pathwaymentioning

confidence: 99%

“…cell differentiation(Kim et al 2011), odontoblast secretory activity and inflammatory response(Shin et al 2015). Wnt/b-catenin Signalling Pathway Implicated in odontoblast differentiation and proliferation(Wang et al 2012a, Yoshida et al 2016).…”

mentioning

confidence: 99%

“…Wnt/b-catenin Signalling Pathway Implicated in odontoblast differentiation and proliferation(Wang et al 2012a, Yoshida et al 2016). NF-kb Pathway (key Nuclear Factor kappa b Pathway) Implicated in inflammatory responses, innate and adaptive immunity and stress responses(Chang et al 2005, Shin et al 2015, Cvikl et al 2016). MAPK/ERK Pathway (Mitogen-Activated Protein Kinase/ Extracellular signal-Regulated Kinase Pathway) Implicated in cell differentiation and proliferation(Bento et al 2013, Wang et al 2016b, odontoblast secretory activity and inflammatory responses(Botero et al 2010, Shin et al 2015, Cvikl et al 2016.…”

mentioning

confidence: 99%

“…NF-kb Pathway (key Nuclear Factor kappa b Pathway) Implicated in inflammatory responses, innate and adaptive immunity and stress responses(Chang et al 2005, Shin et al 2015, Cvikl et al 2016). MAPK/ERK Pathway (Mitogen-Activated Protein Kinase/ Extracellular signal-Regulated Kinase Pathway) Implicated in cell differentiation and proliferation(Bento et al 2013, Wang et al 2016b, odontoblast secretory activity and inflammatory responses(Botero et al 2010, Shin et al 2015, Cvikl et al 2016. JNK Pathway (c-Jun N-terminal Kinase Pathway) Implicated in cell differentiation, odontoblast secretory activity and inflammatory responses(Goda et al 2015, Shin et al 2015.…”

mentioning

confidence: 99%

See 4 more Smart Citations

Disclosing the physiology of pulp tissue for vital pulp therapy

2018

View full text Add to dashboard Cite

The discovery that dentine is a reservoir of bioactive molecules that can be recruited on demand has attracted efforts to develop new protocols and materials for vital pulp therapy (VPT). The noncollagenous proteins (NCPs) present in the dentine extracellular matrix (ECM) include growth factors (TGF-β1, BMP-7, FGF-2, IGF-1 and IGF-2, NGF and GDNF), extracellular matrix molecules (DSP, DPP, BSP, DMP-1 and DSPP) and both anti-inflammatory and pro-inflammatory chemokines and cytokines (TNF-α, IL-1, IL-6 and IL-10). Molecules such as DSP and DPP are mainly expressed by odontoblasts, and they are cleaved products from dentine sialophosphoprotein (DSPP). Some molecules, such as TGF-β1, specifically interact with decorin/biglycan in dentine. Although TGF-β1 increases the expression and secretion of NGF in human pulp cells, NGF induces mineralization and increases the expression of DSPP and DMP-1. Furthermore, GDNF may act as a cell survival factor and mitogen during tooth injury and repair. Pulp capping materials, such as MTA and calcium hydroxide, can solubilize bioactive dentine molecules (TGF-β1, NGF and GDNF) that stimulate tertiary dentinogenesis. The binding of these signalling molecules leads to activation of several signalling transduction pathways involved in dentinogenesis, odontoblast differentiation and inflammatory responses, such as the p38 MAPK, NF-kβ and Wnt/β-catenin signalling pathways. Understanding the cascade of cellular and molecular events underlying the repair and regeneration processes provides a reasonable new approach to VPT through a targeted interaction between tooth tissue and bioactive molecules.

show abstract

Section: Molecular Events Involved In Inflammatory Responsesmentioning

confidence: 99%

Section: Pathwaymentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Disclosing the physiology of pulp tissue for vital pulp therapy

2018

View full text Add to dashboard Cite

show abstract

Robust expression of SIRT6 inhibits pulpitis via activation of the TRPV1 channel

Chen

Qiu

et al. 2020

Cell Biochemistry & Function

View full text Add to dashboard Cite

Invasion of dentinal tubules and pulp tissue by pathogenic bacteria may cause infection leading to pulpitis. Sirtuin 6 (SIRT6) is a NAD‐dependent protein deacetylase encoded by the SIRT6 gene. The effect of SIRT6 on lipopolysaccharide (LPS)‐induced pulpitis and its mechanism of action were discussed in this study. Dental pulp cells (DPCs) were extracted from human teeth and injected with LPS to induce inflammation. The cells injected with LPS showed substantially decreased expression of SIRT6. The overexpression of SIRT6, induced by plasmid‐transfection of DPCs with SIRT6 overexpressing vector, led to a marked decrease in proinflammatory cytokines (IL‐6, IL‐1β, and TNF‐α) and deactivation of NF kappa B pathway. Additionally, dentin matrix protein‐1 (DMP1), a promoter of inflammation in dental pulp tissues, was downregulated. Further investigation revealed that SIRT6 promotes ubiquitination of the transient receptor potential vanilloid 1 (TRPV1) channel, leading to its degradation and deactivation. The role of TRPV1 in the anti‐inflammatory effects of SIRT6 was determined through incubation of SIRT6‐expressing dental pulp stem cells (DPSCs) with capsaicin. This incubation counteracted the effect of SIRT6 on cytokines and DMP1. The injection of lentivirus‐SIRT6 attenuated LPS‐induced pulpitis in vivo by suppressing TRPV1 activity. Thus, SIRT6 inhibits the TRPV1 channel during LPS‐induced inflammation of dental pulp.Significance of the StudyThis study discussed the effect of sirtuin 6 (SIRT6) on lipopolysaccharide (LPS)‐induced pulpitis as well as its mechanism of action and found that SIRT6 may be a negative regulator of pulpitis. Additionally, low expression of SIRT6 and high expression of transient receptor potential vanilloid 1 (TRPV1) in LPS‐treated human dental pulp cells are closely associated with proinflammatory cytokines, dentin matrix protein 1 expression, and activation of the NF‐κB pathway, which indicated that TRPV1 may be a biomarker for pulpitis and the SIRT6‐TRPV1‐CGRP axis maybe a clinical target due to their role regulating inflammation and neuropathic pain.

show abstract

Investigation of Cardioprotective Activity of Silybin: Network Pharmacology, Molecular Docking, and In Vivo Studies

Kumar Pasala,

Donakonda,

Dintakurthi

et al. 2023

ChemistrySelect

View full text Add to dashboard Cite

The abundant health benefits of silybin are known to benefit people with myocardial infarction (MI). However, their mechanisms of action are not precise. To address this problem, network pharmacology was used to identify the various components that can be utilized to treat this condition, and an in vivo study was conducted to evaluate the cardioprotective effect in MI rats. Genes associated with silybin and MI targets were extracted, and overlapping genes between silybin‐associated genes and MI targets were identified using Venn diagrams. Using Cytoscape, we built, visualized, and analyzed a network of compounds and genes with pathways. Protein‐protein interaction network (PPI), gene ontology (GO) function enrichment, and Kyoto Encyclopedia of Genes, and Genomes (KEGG) pathway enrichment analyses of the core targets were performed to predict its mechanism. A molecular docking study assessed the affinity between silybin and the top three genes. ECG pattern, serum CK‐MB, LDH, serum and heart tissue antioxidants, SOD and catalase in isoproterenol‐induced MI rats were used to test the cardioprotective effect of silybin. Silybin‐related genes (114) and MI‐related genes (1800) were identified, and 74 genes overlapped, in which the degrees of AKT1, TNF‐α and IL‐6 were higher than those of other targets are the disease target precisely. The enrichment of the gene set‐based indicated that the PI3K‐Akt, TNF‐α, IL‐17, VEGF, and HIF‐1 signaling pathways were significantly involved in the mechanisms of silybin against MI. The QRS complex of the ECG of silybin‐treated MI rats was restored to normal ECG and significantly increased serum (p<0.0001***) and heart tissue (p<0.0001***) SOD and serum (p<0.001**) and heart tissue (p<0.001**) catalase compared to MI rats. This study embodies the complex network relationship of multi‐target and multiple pathways of silybin in the treatment of MI and provides a novel method for further research on the mechanism of silybin. It has been suggested that silybin alleviates the symptoms of MI by improving antioxidant levels through the PI3K‐Akt/HIF‐1 pathway.

show abstract

TNF‐α and LPS activate angiogenesis via VEGF and SIRT1 signalling in human dental pulp cells

Cited by 52 publications

References 70 publications

Disclosing the physiology of pulp tissue for vital pulp therapy

Disclosing the physiology of pulp tissue for vital pulp therapy

Robust expression of SIRT6 inhibits pulpitis via activation of the TRPV1 channel

Investigation of Cardioprotective Activity of Silybin: Network Pharmacology, Molecular Docking, and In Vivo Studies

Contact Info

Product

Resources

About