Jagged1 inhibits <scp>osteoprotegerin</scp> expression by human periodontal ligament cells

Manokawinchoke, Jeeranan; Sumrejkanchanakij, Piyamas; Subbalekha, Keskanya; Pavasant, Prasit; Osathanon, Thanaphum

doi:10.1111/jre.12357

Cited by 22 publications

(19 citation statements)

References 35 publications

(86 reference statements)

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“…It should be noted that NOTCH3 mRNA levels were also upregulated under intermittent compressive stress. However, a previous report demonstrated that the mRNA baseline expression of NOTCH2 was the highest among the four Notch receptor types (Manokawinchoke et al, ). The role of NOTCH3 in this regulatory mechanism could not be excluded.…”

Section: Discussionmentioning

confidence: 92%

“…However, there is limited information regarding the function of Notch signaling in hPDLs. The function of Notch signaling may be dependent on cell type, differentiation stage, or microenvironment (Osathanon et al, ,; Zhu et al, ; Ashley et al, ; Manokawinchoke et al, ). As previously mentioned, mechanical stimuli alters the expression of Notch signaling pathway components, leading to changes in cell behavior.…”

Section: Discussionmentioning

confidence: 99%

“…Bars indicate a significant difference compared with the control (P 0.05). differentiation stage, or microenvironment (Osathanon et al, 2013a,b;Zhu et al, 2013;Ashley et al, 2015;Manokawinchoke et al, 2016). As previously mentioned, mechanical stimuli alters the expression of Notch signaling pathway components, leading to changes in cell behavior.…”

Section: Discussionmentioning

confidence: 99%

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Notch Signaling Participates in TGF‐β‐Induced SOST Expression Under Intermittent Compressive Stress

Manokawinchoke

Sumrejkanchanakij

Pavasant

et al. 2017

Journal Cellular Physiology

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Notch signaling is regulated by mechanical stimuli in various cell types. It has previously been reported that intermittent compressive stimuli enhanced sclerostin (SOST) expression in human periodontal ligament cells (hPDLs) by regulating transforming growth factor-β (TGF-β) expression. The aim of the present study was to determine the involvement of Notch signaling in the TGF-β-induced SOST expression in hPDLs. Cells were treated with intermittent compressive stress in a computer-controlled apparatus for 24 h. The mRNA and protein expression of the cells were determined by real-time polymerase chain reaction and Western blot analysis, respectively. In some experiments, the target signaling pathway was impeded by the addition of a TGF-β receptor kinase inhibitor (SB431542) or a γ-secretase inhibitor (DAPT). The results demonstrated that hPDLs under intermittent compressive stress exhibited significantly higher NOTCH2, NOTCH3, HES1, and HEY1 mRNA expression compared with control, indicating that mechanical stress induced Notch signaling. DAPT pretreatment markedly reduced the intermittent stress-induced SOST expression. The expression of NOTCH2, NOTCH3, HES1, and HEY1 mRNA under compressive stress was significantly reduced after pretreatment with SB431542, coinciding with a reduction in SOST expression. Recombinant human TGF-β1 enhanced SOST, Notch receptor, and target gene expression in hPDLs. Further, DAPT treatment attenuated rhTGF-β1-induced SOST expression. In summary, intermittent compressive stress regulates Notch receptor and target gene expression via the TGF-β signaling pathway. In addition, Notch signaling participates in TGF-β-induced SOST expression in hPDLs. J. Cell. Physiol. 232: 2221-2230, 2017. © 2016 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Notch Signaling Participates in TGF‐β‐Induced SOST Expression Under Intermittent Compressive Stress

Manokawinchoke

Sumrejkanchanakij

Pavasant

et al. 2017

Journal Cellular Physiology

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“…Osteolysis is principally attributed to bone resorption regulators, i.e. receptor activator of nuclear factor kappa B ligand (RANKL), its cellular receptor RANK and the decoy receptor osteoprotegerin (OPG) . Increased RANKL/OPG ratio induces osteoclasts differentiation and promotes bone resorption.…”

Section: Introductionmentioning

confidence: 99%

The down‐regulation of Notch 1 signaling contributes to the severity of bone loss in aggressive periodontitis

Mijailović

Nikolic

Djinic

et al. 2019

Journal of Periodontology

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Background:The exact mechanisms of bone resorption in periodontitis have not been fully elucidated. The aims of this study were to analyze the expression of Notch signaling molecules, bone remodeling mediators, and pro-inflammatory cytokines in periodontitis patients and to determine their potential correlations. Methods:The study included 130 individuals: 40 with aggressive periodontitis (AP group), 40 with chronic periodontitis (CP group), and 50 periodontally healthy controls. Total RNA was extracted from gingival crevicular fluid samples and relative gene expression of investigated molecules (Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1, TNF-, IL-17, RANKL, and OPG) was determined by reverse transcriptase -realtime polymerase chain reaction (RT-qPCR). Results:In AP group, a significant increase of Notch 2, TNF-, IL-17 and RANKL and a significant decrease of Notch 1 and Jagged 1 expression were observed compared to control group (P = 0.023, P = 0.005, P = 0.030, and P = 0.001 P = 0.031 and P = 0.029, respectively). Notch 2 and RANKL were also overexpressed in CP group compared to controls (P = 0.001 and P = 0.011). Significant correlations were observed in AP group between expression levels of the analyzed genes. Conclusion:The present findings implicate Notch 2 overexpression in the ethiopathogenesis of bone resorption in aggressive and chronic periodontitis. The downregulation of Notch 1 and Jagged 1 and loss of their osteoprotective function might cause a more excessive osteoclast formation and contribute to greater osteolysis in aggressive periodontitis. K E Y W O R D Saggressive periodontitis, bone remodeling, gene expression, periodontitis 554

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“…The role of the Notch signaling pathway in osteogenesis is conflicting. Previous reports demonstrated that activation of Notch signaling could lead to decreased or increased osteogenic differentiation, osteoporosis, or increased radiodensity (Dishowitz et al, 2014;Engin et al, 2008;Hilton et al, 2008;Manokawinchoke, Sumrejkanchanakij, Subbalekha, Pavasant, & Osathanon, 2016;Tian et al, 2017;Tu et al, 2012). Several scholars found that the effect of Notch signaling was associated with osteoclast maturation stage.…”

Section: Histological Analysismentioning

confidence: 99%

The implication of the notch signaling pathway in biphasic calcium phosphate ceramic‐induced ectopic bone formation: A preliminary experiment

Guo

Jiang

Zong

et al. 2020

J Biomedical Materials Res

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Calcium phosphate (BCP) ceramic is a promising material in bone regeneration because it was proved biocompatible, osteoconductive, osteoinductive, and effective. Although it manifests favorable characteristics in critical‐sized bone defects repair, the mechanism of its osteoinduction is still unclear. In the present study, we studied the mechanism of ectopic bone formation, with interest in the Notch signaling pathway. BCP ceramics with or without Notch signaling inhibitor RO4929097 were cocultured with bone marrow‐derived stem cells in vitro. The expression of osteogenesis (OPN/Col/Runx2) and Notch signaling pathway‐related genes (Hes1/Jagged/Notch1) were increased in the BCP group compared with the control group without BCP but significantly decreased after adding RO4929097. Furthermore, a higher level of alkaline phosphatase activity was observed in the BCP group compared with RO4929097 and control group separately. For further confirmation, the intramuscularly ectopic implantation models of Beagle dogs were used. Quantitative real‐time polymerase chain reaction showed a similar trend with the in vitro experiment. Histological and histomorphometric analysis indicated that bone formation was delayed by RO4929097. These findings illustrated that the Notch signaling pathway plays a pivotal role in bone formation induced by BCP; Notch signaling pathway may positively influence ectopic bone formation by promoting BMSCs to differentiate toward osteoblasts.

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Jagged1 inhibits osteoprotegerin expression by human periodontal ligament cells

Abstract: These results suggest that Jagged1 activates Notch signaling in hPDL cells, leading to decreased OPG expression. This may imply an indirect role of Jagged1 on the regulation of osteoclast differentiation via hPDL cells.

Cited by 22 publications

References 35 publications

Notch Signaling Participates in TGF‐β‐Induced SOST Expression Under Intermittent Compressive Stress

Notch Signaling Participates in TGF‐β‐Induced SOST Expression Under Intermittent Compressive Stress

The down‐regulation of Notch 1 signaling contributes to the severity of bone loss in aggressive periodontitis

The implication of the notch signaling pathway in biphasic calcium phosphate ceramic‐induced ectopic bone formation: A preliminary experiment

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