Journal: Cell Death & Disease

Article Title: Inflammation reprograms fibro-adipogenic progenitors to sustain immunopathogenic niches in myositis

doi: 10.1038/s41419-026-08966-w

Figure Lengend Snippet: A NichNet analysis of the cell-to-cell communication. Lymphocytes were set as the sender cell type and FAPs as the receiver cell type. Analysis was performed for each IIM subtype, as indicated, compared to NDC. Results are shown for the 20 ligands best predicting the FAP transcriptome, ranked by the Pearson correlation coefficient, indicating the ability of each ligand to predict target genes. The second column indicated the log fold change (LFC) for each gene in the lymphocyte cell cluster comparing each IIM subtype to NDC as indicated. The ligand–target matrix indicates the regulatory potential between ligands and target genes from the FAP transcriptome. B Feature plot indicating the expression of EGF in each group. The normalized gene expression is shown. C Representative immunofluorescence image of an IBM muscle biopsy. The target proteins are indicated. The scale bar shows 20 µm. ASYS anti-synthetase syndrome, FAP fibro-adipogenic progenitor, IBM inclusion body myositis, IMNM immune-mediated necrotizing myopathy, NDC non-diseased control, NOVA1 RNA-binding protein Nova1, EGF epidermal growth factor, TGF transforming growth factor.

Article Snippet: After reaching a confluence of 70 to 80%, the medium was supplemented with 10 ng/μL EGF (#130-093-825, Miltenyi Biotec) and 5 ng/μL TGF-β1 (#130-095-066, Miltenyi Biotec).

Techniques: Expressing, Gene Expression, Immunofluorescence, Control, RNA Binding Assay

Journal: Cell Death & Disease

Article Title: Inflammation reprograms fibro-adipogenic progenitors to sustain immunopathogenic niches in myositis

doi: 10.1038/s41419-026-08966-w

Figure Lengend Snippet: A Two-sample ATAC-seq scatterplot. Each dot is a union peak (N = 139,260). Axes show log10(CPM + 1) for Control (x) and EGF + TGF-β (y). CPMs were derived from fragment counts per peak divided by library size, then log-transformed with a + 1 offset. Peaks were considered significant if the log2 fold change was ≥0.58. Three biological replicates were pooled per group. B Volcano plot indicating the transcription factor binding sites (TFBS) comparing EGF + TGF-β (treated) to vehicle (control). The x-axis is the effect size calculated as the change in the TFBS between groups. The y-axis is −log10( p value). The full list of results is in Suppl. File . C qPCR time-course for CCL2 and CXCL2. Mean ± SD of normalized expression over time for Control (blue), Primed (EGF + TGF-β; red), and Primed + SR11302 (gray). FAPs were exposed to EGF + TGF-β or vehicle at day 0 to 10 (priming) and 21 to 27 (re-challenge). N = 3 per group. CPM counts per million, EGF epidermal growth factor, TGF-β transforming growth factor beta.

Article Snippet: After reaching a confluence of 70 to 80%, the medium was supplemented with 10 ng/μL EGF (#130-093-825, Miltenyi Biotec) and 5 ng/μL TGF-β1 (#130-095-066, Miltenyi Biotec).

Techniques: Control, Derivative Assay, Transformation Assay, Binding Assay, Expressing

Journal: Science Advances

Article Title: Renoprotective effects of tubular glucagon receptor activation mediated by V-ATPase

doi: 10.1126/sciadv.aeg2534

Figure Lengend Snippet: ( A ) Representative LysoSensor Yellow/Blue DND-160 fluorescence images showing lysosomal pH in Ctrl and cKO primary RTECs treated with HG + PA, with quantification. ( B ) Calculated lysosomal pH values in indicated group, derived from the LysoSensor Yellow/Blue fluorescence ratio using a calibration curve. ( C ) Measurement of lysosomal phospholipase A 2 (PLA 2 ), phospholipase C (PLC), and phospholipase D (PLD) activities in indicated group. ( D ) Immunoblot analysis of EGFR degradation following EGF stimulation in Ctrl and cKO primary RTECs under HG + PA conditions, with quantification. ( E and F ) Immunoblotting of cathepsin B (CTSB) maturation (E) and LC3 and p62 (F) in HG + PA-treated Ctrl and cKO RTECs, with quantification. ( G ) Cell viability assay of HG + PA-treated Ctrl and cKO RTECs. ( H ) Calculated lysosomal pH measurement in HG + PA-treated Ctrl and cKO RTECs following Forskolin treatment with or without BafA1. ( I and J ) Measurement of lysosomal phospholipase A2 activities (I) and cathepsin activities (J) in HG + PA-treated Ctrl and cKO RTECs following Forskolin treatment with or without BafA1. ( K and L ) Immunofluorescence staining of Nile Red (K) or LipidTOX (L) (red) together with LAMP1 (green) in HG + PA-treated Ctrl and cKO RTECs following Forskolin treatment with or without BafA1, with corresponding quantitative analyses. ( M ) Cell viability analysis of HG + PA-treated Ctrl and cKO RTECs following Forskolin treatment with or without BafA1. Data are presented as mean ± SEM. P values were determined by unpaired two-tailed Student’s t test for (A) to (G) and by one-way ANOVA followed by Tukey’s multiple-comparisons test for (H) to (M). Scale bar: 10 μm in (A), (K), and (L). n = 6 for (A), (K), and (L), n = 4 for (B) and (H), n = 3 for (C) to (F), (I), (J), and (M), n = 5 for (G). * P < 0.05, ** P < 0.01, *** P < 0.001; ns, not significant.

Article Snippet: RTECs were serum-starved for 4 hours and stimulated with recombinant human EGF (100 ng/ml, MCE HY-P7109) for 0–120 min at 37°C.

Techniques: Fluorescence, Derivative Assay, Western Blot, Viability Assay, Immunofluorescence, Staining, Two Tailed Test