Lipoteichoic acid promotes nuclear accumulation of β-catenin via AKT in human gingival fibroblasts

Gutiérrez-Venegas, Gloria; Cardoso-Jiménez, Patricia

doi:10.1016/j.intimp.2011.04.008

Cited by 9 publications

(12 citation statements)

References 36 publications

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“…Periodontitis is a progressive disease that affects the dentition-supporting tissues, including the gums, periodontal ligaments and alveolar bone [1][2][3]. The principal result of advanced periodontitis is tooth loss.…”

Section: Introductionmentioning

confidence: 99%

Myricetin blocks lipoteichoic acid-induced COX-2 expression in human gingival fibroblasts

Gutiérrez-Venegas

Luna

Arreguín-Cano

et al. 2014

Cellular and Molecular Biology Letters

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Abstract:Periodontitis is an infectious disease caused by microorganisms present in dental bacterial plaque. Lipoteichoic acid (LTA) is a component of the external membrane of Gram-positive bacteria. It causes septic shock. Ingested flavonoids have been reported to directly affect the regulation of cyclooxygenase-2 (COX-2) expression induced by bacterial toxins. In this study, we examined the effects of four flavonoids (luteolin, fisetin, morin and myricetin) on the activation of ERK1/2, p38 and AKT, and on the synthesis of COX-2 in human gingival fibroblasts treated with LTA from Streptococcus sanguinis. We found that luteolin and myricetin blocked AKT and p38 activation and that myricetin blocked LTA-induced COX-2 expression. The results of our study are important for elucidating the mechanism of action of flavonoid regulation of inflammatory responses.

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Section: Introductionmentioning

confidence: 99%

Myricetin blocks lipoteichoic acid-induced COX-2 expression in human gingival fibroblasts

Gutiérrez-Venegas

Luna

Arreguín-Cano

et al. 2014

Cellular and Molecular Biology Letters

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“…Treatment of human gingival fibroblasts (HGFs) with LTA activated Akt which in turn inactivated GSK-3 and promoted the accumulation of β-catenin, resulting in an increase of connexin43 expression [32]. Given that the interaction of β-catenin with NF-κB leads to a decrease of the NF-κB ability to bind DNA and induce gene expression [7,33], it is likely that the accumulation of β-catenin in LTA-stimulated HGFs causes a negative regulation of the NF-κB activity and that this gives rise to a decrease of the pro-inflammatory cytokines production [32]. It is also likely that GSK-3β inactivation might be able to modulate the transcription of specific pro-inflammatory genes containing a T-cell factor/lymphoid enhancer-binding factor (TCF/LEF) binding site in their promoter.…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, inactivation of GSK3β by phosphorylation at Ser9 in macrophages occurred in the absence of MyD88 [32]. In this case, GSK3β activity was a critical component of the regulatory mechanism that controlled the levels of IFNβ in TLR4-stimulated cells both in vitro and in vivo [37].…”

Section: Introductionmentioning

confidence: 99%

Role of glycogen synthase kinase-3 beta in the inflammatory response caused by bacterial pathogens

et al. 2012

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Glycogen synthase kinase 3β (GSK3β) plays a fundamental role during the inflammatory response induced by bacteria. Depending on the pathogen and its virulence factors, the type of cell and probably the context in which the interaction between host cells and bacteria takes place, GSK3β may promote or inhibit inflammation. The goal of this review is to discuss recent findings on the role of the inhibition or activation of GSK3β and its modulation of the inflammatory signaling in monocytes/macrophages and epithelial cells at the transcriptional level, mainly through the regulation of nuclear factor-kappaB (NF-κB) activity. Also included is a brief overview on the importance of GSK3 in non-inflammatory processes during bacterial infection.

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“…This component is found in both Gram positive and negative bacteria. On the other hand, LTA is the major component of the cell wall of Gram positive bacteria [5], [6]. It is composed of a backbone of repeating glycerophosphate units with D-alanine or N-acetyl glucosamine substituent and a lipophilic anchor [7].…”

Section: Reviewmentioning

confidence: 99%

Studies of Infective Endocarditis in Cardiomyoblasts H9c2 Cell Line

Gloria¹

2016

ICPJL

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Infective endocarditis (IE) is a condition that could possibly be induced by poor oral hygiene. Peptidoglycan (PGN) and lipoteichoic acid (LTA) promote cytokine expression and nitric oxide (NO) production by binding toll-like receptor (TLR)-2, considered the innate immune response initiator. Some studies have indicated that flavonoids possess antioxidant and anti-inflammatory properties. The aim of this review consisted in describe in vitro studies related to PGN and LTA in IE in H9c2 cell line.

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Lipoteichoic acid promotes nuclear accumulation of β-catenin via AKT in human gingival fibroblasts

Cited by 9 publications

References 36 publications

Myricetin blocks lipoteichoic acid-induced COX-2 expression in human gingival fibroblasts

Myricetin blocks lipoteichoic acid-induced COX-2 expression in human gingival fibroblasts

Role of glycogen synthase kinase-3 beta in the inflammatory response caused by bacterial pathogens

Studies of Infective Endocarditis in Cardiomyoblasts H9c2 Cell Line

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