Journal: Frontiers in Molecular Biosciences

Article Title: Transcriptomic profiling of chlorogenic acid and taurine treatment in human skin cells provides insights into cellular senescence mechanisms

doi: 10.3389/fmolb.2026.1748185

Figure Lengend Snippet: Inferred transcriptomic architecture of antioxidant-responsive DEGs. (A) , Number of identified antioxidant-responsive DEGs in each human skin cell type. Bar heights indicate the number of DEGs identified under each treatment condition, with values labeled above each bar. Dark-colored segments represent the subset of AR-DEGs among the antioxidant-responsive DEGs. Bar colors correspond to different treatment conditions. (B) , Regulatory network of DEGs inferred using DoRothEA. Circles represent genes with directed edges from transcription factors to their predicted targets based on the DoRothEA regulon. Nodes are colored by log 2 FC from differential expression analysis in epidermal keratinocytes (above) and melanocytes (below). Gene symbols and log 2 FC values are labeled on each node. Genes with |log 2 FC| ≤ 0.585 are shown with lighter colors and gray text. Aging-related DEGs are marked with an asterisk next to the gene names. (C) , Antioxidative and anti-inflammatory pathways associated with DEGs. Each bar represents a pathway or GO term ( y -axis) identified in this study, with the corresponding −log 10 adjusted P -values from gprofiler2 ( x -axis). The vertical dashed line indicates the significance threshold of adjusted P -value = 0.05. (D) , A selected molecular model illustrates interaction between treatment of CGA and taurine and genes related with anti-aging mechanisms. Abbreviations: CGA, chlorogenic acid; CGA + Tau, combined treatment of chlorogenic acid and taurine; log 2 FC, Bayesian shrinkage estimator for log 2 fold change.

Article Snippet: Normal Human Epidermal Keratinocytes (Cat. no. PCS-200–010; ATCC, Manassas, VA, United States) were cultured in Keratinocyte Growth Medium (Lonza, KGMTM Gold, Cat. no. 00192060; BS, Switzerland) supplemented with 10% fetal bovine serum (Gibco, Waltham, MA, United States), 100 U/mL penicillin, and 100 μg/mL streptomycin (Gibco).

Techniques: Labeling, Quantitative Proteomics

Journal: The Journal of Clinical Investigation

Article Title: Staphylococcus aureus accessory gene regulator quorum-sensing system inhibits keratinocyte lipid enzymes and delays wound repair

doi: 10.1172/JCI190411

Figure Lengend Snippet: ( A ) Representative images of murine wounds 7 days after infection with indicated S . aureus mutants. ( B ) Bacteria recovered from day 7 murine wounds infected with S . aureus mutants. ( C ) Quantification of closure on day 7 of murine wounds infected with S . aureus mutants. ( D ) LDH release from scratch-wounded primary NHEKs 24 hours after treatment with CM of S . aureus mutants (3 × 10 7 CFU/mL equivalent). ( E ) Scratch-wounded NHEK migration after 24-hour treatment with CM of S . aureus mutants (3 × 10 7 CFU/mL equivalent). ( F ) Proliferation measured with MTT assay of NHEKs after 24-hour treatment with CM of S . aureus mutants (3 × 10 7 CFU/mL equivalent). ( G ) KI67 gene expression in proliferating NHEKs treated for 24 hours with CM of S . aureus mutants (3 × 10 7 CFU/mL equivalent). One-way ANOVA followed by Bonferroni’s multiple-comparison adjustment for more than 2 groups ( B – G ). Experiments were performed at least twice. Data represent mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: Primary NHEKs (ATCC, PCS-200-010) were cultured in EpiLife medium containing 60 μM CaCl 2 (Gibco, MEPI500CA) supplemented with Human Keratinocyte Growth Supplement (Gibco, S0015) and antibiotic-antimycotic (penicillin 100 U/mL, streptomycin 100 U/mL, and amphotericin B 250 ng/mL; Gibco, 15240062) at 37°C, 5% CO 2 .

Techniques: Infection, Bacteria, Migration, MTT Assay, Gene Expression, Comparison