Journal: Periodontology 2000

Article Title: Periodontal pathogens and cancer development

doi: 10.1111/prd.12590

Figure Lengend Snippet: Peiodontal pathogens and cancer: Summary of mechanistic evidence.

Article Snippet: , PC , Animal model , PG‐LPS (lipopolysaccharide from P. gingivalis ATCC 33277) was prepared in physiological saline and intraperitoneally administered to C57BL/J mice , The upregulated expression levels of Reg3A and G might play a key role in PG‐LPS‐related pancreatic cancer in mouse , Hiraki et al. .

Techniques: In Vitro, Activation Assay, Protein-Protein interactions, Animal Model, Infection, Migration, In Vivo, Phospho-proteomics, Expressing, Membrane, Transplantation Assay, Stable Transfection, Injection, Saline, Bacteria, Binding Assay, Activity Assay, Biomarker Discovery, Transformation Assay

Journal: Brain, behavior, and immunity

Article Title: GSK3β is involved in promoting Alzheimer's disease pathologies following chronic systemic exposure to Porphyromonas gingivalis lipopolysaccharide in amyloid precursor protein NL-F/NL-F knock-in mice.

doi: 10.1016/j.bbi.2021.08.213

Figure Lengend Snippet: Fig. 6. Chronic systemic exposure to PgLPS increases GSK3β activation in both microglia and neurons in 10-month old APPNL-F/NL-F mice. (A) The immunoblots showing the p-GSK3β and GSK3β expression in the cortex of APPNL-F/NL-F mice with or without PgLPS injection. (B) The quantitative analyses of the ratio of p-GSK3β to GSK3β immunoblots in (A). Each column and bar represent the mean ± SEM (n = 3, each group). The asterisks indicate significant differences between values (**p < 0.01, student’s t test). (C) The correlation between p-GSK3β relative immunoreactivity and T231 relative immunoreactivity in the cortex of saline and PgLPS- injected APPNL-F/NL-F mice. (D) The correlation between PSD95 relative immunoreactivity and T231 relative immunoreactivity in the cortex of saline and PgLPS- injected APPNL-F/NL-F mice. Each circle represents single individual and each line represents linear approximation (N = 3, each group). The Pearson correlation coefficient (r) was used to analyze the strength of the association between the two variables (0.7 ≤| r | < 1 is a highly linear correlation; The Pearson correlation coefficient. (E) Immunofluorescent CLMS images of p-GSK3β (green) and Iba1 (red, left) or Nissl (red, right) in the cortex of APPNL-F/NL-F mice. Scale bar, 20 μm. (F) Mean relative intensity of p-GSK3β in the microglia (Iba1) images of (E). (G) Mean relative intensity of p-GSK3β in the neuron (Nissl) images of (E). Each column and vertical bar represent the mean ± SEM (n = 4, each group). The asterisks indicate significant differences from the saline group (***p < 0.001, student’s t test).

Article Snippet: The cultured cells were stimulated with PgLPS (1 μg/ml; InvivoGen) or were stimulated with PgLPS pretreated with TWS119 (GSK3β inhibitor; 5 μM; Selleckchem) for 1 h. The MG6 conditioned medium was harvested 48 h after PgLPS stimulation or PgLPS stimulation pretreated with TNF-α inhibitor (1 μM; sigma) for 1 h.

Techniques: Activation Assay, Western Blot, Expressing, Injection, Saline

Journal: Brain, behavior, and immunity

Article Title: GSK3β is involved in promoting Alzheimer's disease pathologies following chronic systemic exposure to Porphyromonas gingivalis lipopolysaccharide in amyloid precursor protein NL-F/NL-F knock-in mice.

doi: 10.1016/j.bbi.2021.08.213

Figure Lengend Snippet: Fig. 8. PgLPS-induced TNF-α secreted by microglia contributes to tau hyperphosphorylation in cultured neurons. (A) The immunoblots showing S202, T231, S396 and tau5 expression in neurons after treatment with microglia condition medium, PgLPS-primed microglia condition medium or PgLPS-primed microglia condition medium pretreated with TNF-α inhibitor for 48 h. (B, C, D) The quantitative analyses of the ratio of S202, T231, S396 to tau5 immunoblots in (A). Each column and bar represent the mean ± SEM (n = 3, each group). The asterisks indicate a statistically significant difference from the control group (FS202(3, 8) = 234.8, FT231(3, 8) = 702.5, FS396(3, 8) = 1577, ***p < 0.001 versus control group, one-way ANOVA test). The daggers indicate a significant difference from PgLPS-primed microglia condition medium group (yyp < 0.01, yyyp < 0.001 versus P-MCM group, one-way ANOVA test). (E) Immunofluorescent CLMS images of MAP2 (red) and T231S396 (green) in primary neuron after treatment with PgLPS, PgLPS-primed microglia condition medium or PgLPS-primed microglia condition medium pretreated with TNF- α inhibitor for 48 h. (F, G) Mean relative intensity of T231 and S396 in the CLSM images of (E). The asterisks indicate a statistically significant difference from the control group (FT231(3, 12) = 154.8, FS396(3, 12) = 2876, ***p < 0.001 versus control group, one-way ANOVA test). The daggers indicate a significant difference from PgLPS-primed microglia condition medium group (yyp < 0.01, yyyp < 0.001 versus P-MCM group, one-way ANOVA test). (H) The immunoblots showing the expression of p-AKT, AKT, p-GSK3β and GSK3β after treatment with microglia condition medium, PgLPS-primed microglia condition medium or PgLPS-primed microglia condition medium pretreated with TNF-α inhibitor for 48 h. (I, J) The quantitative analyses of the ratio of p-AKT to AKT and p-GSK3β to GSK3β im munoblots in (H). Each column and bar represent the mean ± SEM (n = 3, each group). The asterisks indicate a statistically significant difference from the control group (Fp-AKT (3, 8) = 14.53, Fp-GSK3β (3, 8) = 46.49, **p < 0.01, ***p < 0.001 versus MCM group, one-way ANOVA test). The daggers indicate a significant difference from PgLPS-primed microglia condition medium group (yp < 0.05, yyp < 0.01 versus P-MCM, one-way ANOVA test).

Article Snippet: The cultured cells were stimulated with PgLPS (1 μg/ml; InvivoGen) or were stimulated with PgLPS pretreated with TWS119 (GSK3β inhibitor; 5 μM; Selleckchem) for 1 h. The MG6 conditioned medium was harvested 48 h after PgLPS stimulation or PgLPS stimulation pretreated with TNF-α inhibitor (1 μM; sigma) for 1 h.

Techniques: Cell Culture, Western Blot, Expressing, Control

Journal: Brain, behavior, and immunity

Article Title: GSK3β is involved in promoting Alzheimer's disease pathologies following chronic systemic exposure to Porphyromonas gingivalis lipopolysaccharide in amyloid precursor protein NL-F/NL-F knock-in mice.

doi: 10.1016/j.bbi.2021.08.213

Figure Lengend Snippet: Fig. 9. A schematic representation of the critical roles performed by microglia in promoting tau hyperphosphorylation of neurons in an Aβ-rich environment during chronic systemic exposure to PgLPS. In microglia, PgLPS induces TNF-α production though the activation of GSK3β/NFκB signaling. In contrast, the effects of PgLPS on neurons are microglia-dependent. In neurons, the microglia-released TNF-α is involved in tau hyperphosphorylation through the activation of AKT/ GSK3β signaling.

Article Snippet: The cultured cells were stimulated with PgLPS (1 μg/ml; InvivoGen) or were stimulated with PgLPS pretreated with TWS119 (GSK3β inhibitor; 5 μM; Selleckchem) for 1 h. The MG6 conditioned medium was harvested 48 h after PgLPS stimulation or PgLPS stimulation pretreated with TNF-α inhibitor (1 μM; sigma) for 1 h.

Techniques: Activation Assay