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S100A11-RAGE-NF-κB signaling impairs neural development and migration. In vitro mechanistic validation demonstrated S100A11-mediated neural cell dysfunction in SH-SY5Y cells. A qRT-PCR showing dose-dependent suppression of SOX10, RET, PHOX2B, CACNA1C following S100A11 treatment (50, 200 ng/mL, 48 h; n = 3 with technical triplicates). B Western blot validation of reduced protein levels. C , D Impaired wound healing (32.4% vs. 78.5%, Cohen’s d = 8.76, p < 0.001) and Transwell migration (67 ± 12 vs. 186 ± 23 cells, Cohen’s d = 6.54, p < 0.001) with <t>partial</t> <t>FPS-ZM1</t> rescue. E Western blot in tissue cohort ( n = 15) confirming S100A11 elevation, TLR4 activation, SOX10 suppression, and decreased FOXP3. F Temporal NF-κB activation: IκBα phosphorylation (15 min), degradation (30 min), p65 phosphorylation. G FPS-ZM1 blocked 68.4% of p-p65; TAK-242 reduced 53.7%. H Gene expression at 6 h showing inflammatory upregulation (IL-6, TNF-α, VCAM1, ICAM1, CCL2) and neural marker suppression (SOX10, RET, PHOX2B). Mean ± SEM, n = 3–15 with technical triplicates. One-way ANOVA with Tukey post hoc. ** p < 0.01, *** p < 0.001
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S100A11-RAGE-NF-κB signaling impairs neural development and migration. In vitro mechanistic validation demonstrated S100A11-mediated neural cell dysfunction in SH-SY5Y cells. A qRT-PCR showing dose-dependent suppression of SOX10, RET, PHOX2B, CACNA1C following S100A11 treatment (50, 200 ng/mL, 48 h; n = 3 with technical triplicates). B Western blot validation of reduced protein levels. C , D Impaired wound healing (32.4% vs. 78.5%, Cohen’s d = 8.76, p < 0.001) and Transwell migration (67 ± 12 vs. 186 ± 23 cells, Cohen’s d = 6.54, p < 0.001) with partial FPS-ZM1 rescue. E Western blot in tissue cohort ( n = 15) confirming S100A11 elevation, TLR4 activation, SOX10 suppression, and decreased FOXP3. F Temporal NF-κB activation: IκBα phosphorylation (15 min), degradation (30 min), p65 phosphorylation. G FPS-ZM1 blocked 68.4% of p-p65; TAK-242 reduced 53.7%. H Gene expression at 6 h showing inflammatory upregulation (IL-6, TNF-α, VCAM1, ICAM1, CCL2) and neural marker suppression (SOX10, RET, PHOX2B). Mean ± SEM, n = 3–15 with technical triplicates. One-way ANOVA with Tukey post hoc. ** p < 0.01, *** p < 0.001

Journal: Cell & Bioscience

Article Title: Gordonibacter-associated regulatory T cell dysfunction and S100A11-mediated neural impairment in Hirschsprung’s disease: a microbiota-immune-neural axis

doi: 10.1186/s13578-026-01562-7

Figure Lengend Snippet: S100A11-RAGE-NF-κB signaling impairs neural development and migration. In vitro mechanistic validation demonstrated S100A11-mediated neural cell dysfunction in SH-SY5Y cells. A qRT-PCR showing dose-dependent suppression of SOX10, RET, PHOX2B, CACNA1C following S100A11 treatment (50, 200 ng/mL, 48 h; n = 3 with technical triplicates). B Western blot validation of reduced protein levels. C , D Impaired wound healing (32.4% vs. 78.5%, Cohen’s d = 8.76, p < 0.001) and Transwell migration (67 ± 12 vs. 186 ± 23 cells, Cohen’s d = 6.54, p < 0.001) with partial FPS-ZM1 rescue. E Western blot in tissue cohort ( n = 15) confirming S100A11 elevation, TLR4 activation, SOX10 suppression, and decreased FOXP3. F Temporal NF-κB activation: IκBα phosphorylation (15 min), degradation (30 min), p65 phosphorylation. G FPS-ZM1 blocked 68.4% of p-p65; TAK-242 reduced 53.7%. H Gene expression at 6 h showing inflammatory upregulation (IL-6, TNF-α, VCAM1, ICAM1, CCL2) and neural marker suppression (SOX10, RET, PHOX2B). Mean ± SEM, n = 3–15 with technical triplicates. One-way ANOVA with Tukey post hoc. ** p < 0.01, *** p < 0.001

Article Snippet: Cells were subjected to serum deprivation for 6 h to establish baseline conditions, then treated with recombinant S100A11 (100 ng/mL; Abcam Cat# ab198977) in combination with either RAGE inhibitor FPS-ZM1 (1 μM; MedChemExpress Cat# HY-19370) or TLR4 inhibitor TAK-242 (5 μM; MedChemExpress Cat# HY-11109).

Techniques: Migration, In Vitro, Biomarker Discovery, Quantitative RT-PCR, Western Blot, Activation Assay, Phospho-proteomics, Gene Expression, Marker