Journal: Frontiers in Cell and Developmental Biology

Article Title: Integrated re-analysis of bulk and single-cell transcriptomic data reveals limited ferroptosis and neuroinflammation signatures after sevoflurane exposure in the aged rat hippocampus and human prefrontal cortex cells

doi: 10.3389/fcell.2026.1938601

Figure Lengend Snippet: qRT-PCR analysis of ferroptosis-related gene expression after sevoflurane and H 2 O 2 exposure. Relative expression of GPX4, SLC7A11, ACSL4, and PTGS2 in Control, Sevo (3.3% for 6 h), H 2 O 2 (200 μM for 24 h), and Sevo + H 2 O 2 groups in C6 glioma cells and HA astrocytes. *P < 0.05 versus Control; significant comparisons are displayed with a single asterisk. Data represent mean ± SEM from three independent experiments. Two-way ANOVA (sevoflurane × H 2 O 2 ) was followed by Dunnett’s multiple-comparisons test against Control.

Article Snippet: To examine regulation of key ferroptosis-related genes identified in the transcriptomic analyses, quantitative RT-PCR was performed in C6 rat glioma cells (ATCC CRL-2309) and HA human astrocytes (ATCC CRL-3050).

Techniques: Quantitative RT-PCR, Analysis, Gene Expression, Expressing, Control

Journal: eBioMedicine

Article Title: Parvimonas micra exacerbates periodontitis by infiltrating host cells through TmpC and circumventing lysosomal elimination via AppA

doi: 10.1016/j.ebiom.2026.106187

Figure Lengend Snippet: P. micra interacts with PDLSCs through TmpC-integrin α v β 3 axis. ( A ) Schematic representation of His pull-down. ( B ) Co-IP assay showing the interaction between purified His-TmpC and integrin α v β 3 of PDLSCs. ( C ) Sensorgrams of integrin α v β 3 binding to immobilised TmpC and K D value. ( D ) The interaction between TmpC (blue), integrin α v (green) and integrin β 3 (red), as predicted by molecular docking. ( E–F ) Bacterial attachment assay revealing altered bacterial recovery rate in PDLSCs treated with siIntegrin α v+ β 3 ( E ) or Cyclo ( F ). ( G–H ) Flow cytometry showing the percentages of invaded PDLSCs treated with siIntegrin α v+ β 3 ( G ) or Cyclo ( H ). ( I ) Knockdown of integrin α v β 3 altered downstream pFAK and the activation of NF-κB and ERK1/2 signalling pathways triggered by P. micra . β-actin was set as control. ( J ) Western blot showing altered activation of NF-κB and ERK1/2 signalling pathways triggered by P. micra in PDLSCs pretreated with Cyclo. β-actin was set as control. ( K ) Representative image and quantification of ALP staining in Cyclo-pretreated PDLSCs infected with P. micra WT or P. micra ΔtmpC . ( L ) Representative image and quantification of ARS staining of PDLSCs with blocked TmpC-integrin α v β 3 interaction. ( M ) Western blot of Col1, ALPL, Runx2 in Cyclo-pretreated PDLSCs infected with P. micra WT or P. micra ΔtmpC . GAPDH was set as control. ( N ) Flow cytometric analysis of FDAA-labelled P. micra internalisation in Cyclo-pretreated PDLSCs. ( O ) Schematic diagram showing the experimental design and timeline of rat models infected with P. micra and/or treated with Cyclo. ( P ) Quantitative analyses of CEJ-ABC, BV/TV, BMD and Tb.Sp. of the alveolar bone. Data are represented as the mean ± SD of three independent experiments ( n = 3) in (E–N) and six independent experiments ( n = 6) in (P). P values were determined by two-tailed unpaired Student's t -test in (E–H) and one-way ANOVA test in (I–N, P). ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001; ns, not significant.

Article Snippet: Commercially available integrin α v β 3 (R&D Systems, 3050-AV-050) was diluted in sodium acetate (pH 5.0) and passed over the sensor chip in various concentrations from 0 μM to 160 μM, with the 5 μM concentration as internal control.

Techniques: Co-Immunoprecipitation Assay, Purification, Binding Assay, Flow Cytometry, Knockdown, Activation Assay, Control, Western Blot, Staining, Infection, Two Tailed Test