Peroxisome proliferator‐activated receptor δ inhibits <i>Porphyromonas gingivalis</i> lipopolysaccharide‐induced activation of matrix metalloproteinase‐2 by downregulating <scp>NADPH</scp> oxidase 4 in human gingival fibroblasts

Yoo, Taesik; Ham, Sun Ah; Hwang, Jae Joon; Lee, Won Jin; Paek, Kyung Shin; Oh, Jae-Wook; Kim, Jin‐Hoi; Tae, Jeong; Han, Chang Woo; Seo, Han Geuk

doi:10.1111/omi.12137

Cited by 17 publications

(15 citation statements)

References 47 publications

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“…The results indicated that the LPS-induced increase in MMP-2 activity may be suppressed by PDTC and FTS. Similarly, a previous study demonstrated that inhibitors of RhoA and NF-kB inhibited LPS-induced increase of MMP-2 activity (28). In addition, the results of the present study demonstrated that LPS-induced increased expression levels of p-RhoA and p-MEK1/2 were significantly suppressed by curcumin treatment.…”

Section: Discussionsupporting

confidence: 87%

Curcumin prevents lipopolysaccharide-induced matrix metalloproteinase-2 activity via the Ras/MEK1/2 signaling pathway in rat vascular smooth muscle cells

Zhong

Feng

et al. 2017

Molecular Medicine Reports

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The aim of the present study was to examine the effect of curcumin treatment on lipopolysaccharide (LPS)-induced matrix metalloproteinase‑2 (MMP‑2) activity, and assess whether the effects are mediated by the Ras/mitogen‑activated protein kinase kinase 1/2 (MEK1/2) signaling pathway in vascular smooth muscle cells (VSMCs). VSMCs were isolated from male Sprague‑Dawley rats. Protein expression levels were analyzed by western blotting. The activity of MMP‑2 was measured with gelatin zymography, and an electrophoretic mobility shift assay was used to detect the DNA binding activity of nuclear factor‑κB (NF‑κB). Curcumin treatment was demonstrated to inhibit LPS‑induced MMP‑2 activity in rat VSMCs. This inhibitory effect was partially blocked by ammonium pyrrolidinedithiocarbamate, an inhibitor of NF‑κB activation, and farnesylthiosalicylic acid, an inhibitor of Ras. In addition, the results of the present study indicated that LPS‑induced phosphorylation of Ras homolog family member A and MEK1/2 was significantly decreased by curcumin. Furthermore, NF‑κB p65 expression in the nucleus and the DNA binding activity of NF‑κB in rat LPS‑exposed VSMCs was decreased by curcumin. Taken together, these findings suggest that curcumin prevents of LPS‑induced MMP‑2 activity through Ras/MEK1/2 and NF‑κB signaling.

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Section: Discussionsupporting

confidence: 87%

Curcumin prevents lipopolysaccharide-induced matrix metalloproteinase-2 activity via the Ras/MEK1/2 signaling pathway in rat vascular smooth muscle cells

Zhong

Feng

et al. 2017

Molecular Medicine Reports

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“…Cell viability was determined as previously described (Yoo et al, ). Briefly, ARPE‐19 cells (0.5 × 10 5 cells/well) were seeded in 24‐well plates and exposed to various concentrations of lutein for 24 hr in low (5.6 mM) or high (30 mM) glucose conditions.…”

Section: Methodsmentioning

confidence: 99%

Lutein suppresses hyperglycemia-induced premature senescence of retinal pigment epithelial cells by upregulating SIRT1

et al. 2018

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Hyperglycemia contributes to the pathogenesis of diabetic complications, such as diabetic retinopathy, by affecting cellular redox state. In this study, we investigated the effects of lutein on hyperglycemia-induced premature senescence in retinal pigment epithelium (RPE) cells. In ARPE-19 cells, a spontaneously immortalized cell line derived from human RPE, lutein treatment significantly inhibited high glucose-triggered premature senescence and production of reactive oxygen species (ROS). Notably, lutein treatment increased SIRT1 mRNA and protein levels, suggesting that lutein exerted its beneficial effects in these cells by upregulating SIRT1 expression.Resveratrol, an activator of SIRT1, mimicked the inhibitory effects of lutein on high glucoseinduced premature senescence and ROS generation, whereas sirtinol, a specific inhibitor of SIRT1, blocked these effects of lutein. Collectively, these observations indicate that lutein interferes with hyperglycemia-induced RPE senescence by modulating SIRT1 signaling. Practical applicationsLutein, a xanthophyll carotenoid present in green leafy vegetables and eggs, has been consumed as a dietary supplement to improve eye health. Lutein exhibited anti-senescent properties by suppressing ROS generation through SIRT1 upregulation in RPE cells exposed to hyperglycemia mimicking diabetic conditions. Thus, we propose that lutein could be applied to therapeutic interventions aimed at treating hyperglycemia-induced retinal disorders. K E Y W O R D S hyperglycemia, lutein, premature senescence, reactive oxygen species, retinal pigment epithelium, SIRT1 J Food Biochem. 2018;42:e12495.

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“…Accumulating evidence suggests that peroxisome proliferator‐activated receptor activation may have protective effects in periodontitis. The activation of peroxisome proliferator‐activated receptor delta (also known as peroxisome proliferator‐activated receptor beta, and hence often designated peroxisome proliferator‐activated receptor beta/delta) was shown to suppress the ability of P. gingivalis lipopolysaccharide to activate matrix metalloproteinase‐2 in human gingival fibroblasts . Mechanistically, peroxisome proliferator‐activated receptor beta/delta signaling – triggered by the selective agonist GW501516 – inhibited transcription of mRNA and protein expression of NADPH oxidase 4, thereby attenuating the production of reactive oxygen species that would, in turn, induce matrix metalloproteinase‐2 activation.…”

Section: Nuclear Metabolic Receptor Agonistsmentioning

confidence: 99%

Current understanding of periodontal disease pathogenesis and targets for host‐modulation therapy

Hajishengallis

Chavakis

Lambris

2020

Periodontology 2000

266

165

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Recent advances indicate that periodontitis is driven by reciprocally reinforced interactions between a dysbiotic microbiome and dysregulated inflammation. Inflammation is not only a consequence of dysbiosis but, via mediating tissue dysfunction and damage, fuels further growth of selectively dysbiotic communities of bacteria (inflammophiles), thereby generating a self‐sustained feed‐forward loop that perpetuates the disease. These considerations provide a strong rationale for developing adjunctive host‐modulation therapies for the treatment of periodontitis. Such host‐modulation approaches aim to inhibit harmful inflammation and promote its resolution or to interfere directly with downstream effectors of connective tissue and bone destruction. This paper reviews diverse strategies targeted to modulate the host periodontal response and discusses their mechanisms of action, perceived safety, and potential for clinical application.

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Peroxisome proliferator‐activated receptor δ inhibits Porphyromonas gingivalis lipopolysaccharide‐induced activation of matrix metalloproteinase‐2 by downregulating NADPH oxidase 4 in human gingival fibroblasts

Cited by 17 publications

References 47 publications

Curcumin prevents lipopolysaccharide-induced matrix metalloproteinase-2 activity via the Ras/MEK1/2 signaling pathway in rat vascular smooth muscle cells

Curcumin prevents lipopolysaccharide-induced matrix metalloproteinase-2 activity via the Ras/MEK1/2 signaling pathway in rat vascular smooth muscle cells

Lutein suppresses hyperglycemia-induced premature senescence of retinal pigment epithelial cells by upregulating SIRT1

Current understanding of periodontal disease pathogenesis and targets for host‐modulation therapy

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