Journal: Nature Communications

Article Title: Chronic stress activates a hypothalamic vagal circuit to promote hepatocellular carcinoma progression in male mice

doi: 10.1038/s41467-026-77923-0

Figure Lengend Snippet: a UMAP showing 10 monocyte/macrophage subclusters comprising 12,077 cells. b Selected marker expression across subclusters. c–e CellChat analysis of Epi.c8–monocyte/macrophage communication, highlighting enhanced COLLAGEN signaling and Col1a1/2 – Cd44 interactions between Epi.c8 and Macro_c3 in HCC+CRS. f Col1a1 / Col1a2 expression in Epi.c8 and Cd44 expression in Macro_c3; two-sided Wilcoxon tests with Benjamini–Hochberg correction. g WB showing increased COL1A1/COL1A2 after ACh treatment. h Transwell co-culture system. i WB showing reduced COL1A1/COL1A2 after Chrna9 silencing. j Cxcl1 expression in Macro_c3; two-sided Wilcoxon test with Benjamini–Hochberg correction. k Representative immunostaining and overall survival according to CXCL1 expression (n = 50 cases per group; log-rank test, χ² = 8.17, P = 0.0043). l WB showing increased CXCL1 after ACh treatment. m WB showing reduced ACh-induced CXCL1 after Cd44 silencing. RAW, RAW264.7 macrophages. The western blot experiments in ( g , i , l and m ) were independently repeated three times with similar results. For WB analyses in g and i, the samples derive from the same experiment, but different gels for COL1A1 and COL1A2 were processed in parallel. Data are mean ± SEM. Detailed statistical results for the bioinformatics analyses and experimental data are provided in Supplementary Data and , respectively. Source data are provided as a Source Data file.

Article Snippet: Recombinant mouse CXCL1 (MedChemExpress) was dissolved in sterile PBS containing 0.1% BSA.

Techniques: Marker, Expressing, Analysis, Co-culture Assay, Immunostaining, Western Blot

Journal: Nature Communications

Article Title: Chronic stress activates a hypothalamic vagal circuit to promote hepatocellular carcinoma progression in male mice

doi: 10.1038/s41467-026-77923-0

Figure Lengend Snippet: a Explained variance of plasma cytokine principal components. b PCA separation of Normal, HCC and HCC–CRS groups; ellipses indicate 95% confidence intervals. c PC1 cytokine loadings. d Anti-CXCL1 treatment timeline in HCC–CRS mice. e Behavioral effects of anti-CXCL1 in HCC–CRS mice (n = 10 mice per group; two-sided t tests: OFT, t(10.52) = − 4.73, P < 0.001; EPM, t(10.94) = − 9.75, P < 0.001; FST, t(18) = 6.07, P < 0.001; TST, t(18) = 3.54, P = 0.0024; SPT, t(18) = 3.09, P = 0.0063). f , g Tumor growth ( f ) and PanCK + Ki67 + proliferation index ( g ) after anti-CXCL1 treatment (n = 6 mice per group; two-sided t test: ( f ), t(10) = 6.27, P < 0.001; ( g ), t(7.40) = 4.03, P = 0.0045). Scale bar, 50 μm. h Anti-CXCL1 treatment timeline in HCC–CSDS mice. i) Behavioral effects of anti-CXCL1 in HCC–CSDS mice (n = 10 mice per group; two-sided t tests: OFT, t(11.86) = − 10.60, P < 0.001; EPM, t(10.32) = − 6.11, P < 0.001; FST, t(18) = 6.00, P < 0.001; TST, t(18) = 3.53, P = 0.0024; SPT, t(18) = − 3.49, P = 0.0026; SIT, t(18) = − 6.08, P < 0.001). j , k Tumor growth ( j ) and proliferation index ( k ) after anti-CXCL1 treatment (n = 6 mice per group; two-sided t test: ( j ), t(10) = 4.26, P = 0.0017; ( k ), t(10) = 4.67, P < 0.001). Scale bar, 50 μm. OFT, open field test; EPM, elevated plus maze; FST, forced swimming test; TST, tail suspension test; SPT, sucrose preference test; SIT, social interaction test. Data are mean ± SEM. Detailed statistical results are provided in Supplementary Data . Source data are provided as a Source Data file.

Article Snippet: Recombinant mouse CXCL1 (MedChemExpress) was dissolved in sterile PBS containing 0.1% BSA.

Techniques: Clinical Proteomics, Suspension

Journal: Frontiers in Immunology

Article Title: ANKRD22 contributes to NF-κB-associated inflammatory responses in alveolar type II epithelial cells during PM 2.5 -triggered airway inflammation

doi: 10.3389/fimmu.2026.1894350

Figure Lengend Snippet: ANKRD22 deficiency in murine AT-II cells protected against PM 2.5 -induced airway inflammation. (A) Schematic diagram of PM 2.5 -induced airway inflammation model establishment in AT-II- ANKRD22 △/△ mice and ANKRD22 flox/flox mice. (B) Representative immunofluorescence co-staining images of ANKRD22 (red) and SP-C (green) in paraffin-embedded lung tissue sections from mice. Scale bars: 10 μm (overview), 5 μm (inset). DAPI stained the nuclei; Cell-type marker: SP-C antibody (AT-II cell); Target protein: ANKRD22 antibody (intracellular ANKRD22); Merged images: DAPI + SP-C + ANKRD22 overlay. (C–E) BALF was collected, total leukocyte count (C) , neutrophil percentage (D) and neutrophil count (E) were calculated in BALF. (F, G) Representative HE-stained images of murine lung tissue sections were shown (F) , scale bar = 50 μm. Semi-quantitative analysis of HE staining in murine lung tissues was conducted (G) . (H–K) mRNA expression levels of Il6 (H) , Cxcl1 (I) , Cxcl2 (J) , and Il1b (K) in murine lung tissues were detected by qRT-PCR. (L, M) ELISA detection of IL-6 (L) and CXCL1 (M) protein levels in mouse lung tissue homogenates. BALF differential cell counting and Histological scoring were performed blinded to group allocation. Multiple comparisons were performed using one-way ANOVA followed by Bonferroni’s post hoc test. Experimental data analysis results are expressed as mean ± SEM. Data are representative of three biological replicates with similar results (n = 4 mice in the control group of ANKRD22 flox/flox and AT-II- ANKRD22 △/△ mice, n = 5 mice in the PM 2.5 -treated group of ANKRD22 flox/flox and AT-II- ANKRD22 △/△ mice); * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The levels of IL-6 (RK00008, ABclonal, China) and CXCL1 (RK00038, ABclonal, China) in lung tissues were measured by ELISA according to the manufacturer’s instructions.

Techniques: Immunofluorescence, Staining, Tissue, Marker, Analysis, H&E Stain, Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Cell Counting, Control

Journal: Frontiers in Immunology

Article Title: ANKRD22 contributes to NF-κB-associated inflammatory responses in alveolar type II epithelial cells during PM 2.5 -triggered airway inflammation

doi: 10.3389/fimmu.2026.1894350

Figure Lengend Snippet: ANKRD22 inhibition mitigated PM 2.5 -induced inflammation in A549 cells. (A, B) A549 cells were transfected with ANKRD22 siRNA then stimulated with PM 2.5 , mRNA expression (A) and protein levels (B) of ANKRD22 were determined by qRT-PCR and Western blot. (C–G) mRNA expression levels of IL6 (C) , IL8 (D) , IL1B (E) , CXCL1 (F) , and CXCL2 (G) in A549 cells were detected by qRT-PCR. (H, I) ELISA measurement of IL-6 (H) and IL-8 (I) protein levels in A549 cells culture supernatants. Multiple comparisons were performed using one-way ANOVA followed by Bonferroni’s post hoc test. Experimental data analysis results are expressed as mean ± SEM. Data are representative of three biological replicates with similar results (n = 3 per group) ; * P < 0.05, ** P < 0.01, *** P < 0.001. ns, non-significant.

Article Snippet: The levels of IL-6 (RK00008, ABclonal, China) and CXCL1 (RK00038, ABclonal, China) in lung tissues were measured by ELISA according to the manufacturer’s instructions.

Techniques: Inhibition, Transfection, Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Analysis

Journal: Bioactive Materials

Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming

doi: 10.1016/j.bioactmat.2025.11.039

Figure Lengend Snippet: SCS suppresses senescence cascade amplification by attenuating secondary spread from GC-induced primary senescent adipocytes. ( A ) Schematic illustration of SCS intervention exclusively during the fully developed senescent phase of MPS-induced bone marrow. ( B ) qPCR analysis of senescence-associated markers ( Cdkn1b , Cdkn1a , and Cdkn2c ) in bone tissues at 4 weeks following combined SCS and MPS treatment. n = 3 biological replicates. ( C ) ELISA analysis of bone marrow senescence-associated factors (IL-1β, IL-18, TNF-α, IL-6, CXCL1, and CCL3) after 4 weeks of combined treatment with SCS and MPS. n = 4 biological replicates. ( D ) Quantification of the maximal compressive load of the isolated distal femur and femoral diaphysis. n = 6 biological replicates. ( E ) Schematic diagram depicting isolation of bone marrow adipocytes from mice treated with SCS and MPS for 14 days using mature adipocyte-specific fast centrifugation and construction of a senescence propagation model in vitro . ( F and G ) Representative flow cytometry plots (D) and quantification (E) of EdU-positive (proliferating) CD45 − Ter119 − CD31 − LepR + MSCs cultured for 3 days with adipocyte conditioned medium (CM). n = 6 biological replicates. ( H and I ) Representative ALP staining images (F) and corresponding quantification of ALP activity (G) in CD45 − Ter119 − CD31 − LepR + MSCs cultured with SCS-induced adipocyte CM. n = 6 biological replicates. (Scale bars, 50 μm and 30 μm) ( J and K ) Representative Oil Red O staining (H) and quantification (I) of adipogenic differentiation in MSCs cultured with SCS-induced adipocyte CM. n = 6 biological replicates. (Scale bars, 50 μm and 25 μm) ( L and M ) Representative images (J) and quantification (K) of crystal violet-stained fibroblast colony-forming units (CFU-F) in MSCs cultured with various adipocyte CMs. n = 6 biological replicates. (Scale bars, 400 μm) ( N ) qPCR analysis of senescence-related markers ( Cdkn2a and Cdkn1a ) in MSCs treated with different adipocyte CMs. n = 3 biological replicates. ( O and P ) Representative immunofluorescence-FISH images (M) and quantification (N) showing colocalization of γ-H2A.X with telomere-associated foci (TAF) in MSCs cultured with different adipocyte CMs. n = 6 biological replicates. (Scale bars, 7 μm and 1 μm) ( Q and R ) Representative images (O) and quantification (P) of 2D tube formation assays in HUVECs cultured for 3 days with various adipocyte CMs. n = 6 biological replicates. (Scale bars, 100 μm and 25 μm) ( S and T ) Representative images (Q) and quantification (R) of SA-β-Gal–positive HUVECs (green) following 3-day treatment with different adipocyte CMs. n = 6 biological replicates. (Scale bars, 100 μm and 25 μm) ( U ) qPCR analysis of the senescence-related gene LMNB1 in HUVECs treated with various adipocyte CMs. n = 3 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using an unpaired two-tailed Student's t -test ( B, C, D, G, I, K, M, N, R, T and U ).

Article Snippet: In addition, ELISA analyses of senescence-associated inflammatory factors (IL-1β, IL-18, TNF-α, CCL3 (Neobioscience, EMC010a.96), CXCL1 (R&D Systems, MKC00B-1), and IL-6 (Neobioscience, EMC004.96)) were conducted on day 28 following combined treatment with SCS and rapamycin and/or T0070907.

Techniques: Amplification, Enzyme-linked Immunosorbent Assay, Isolation, Centrifugation, In Vitro, Flow Cytometry, Cell Culture, Staining, Activity Assay, Immunofluorescence, Two Tailed Test