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Vagotomy promoted Ly6G + cell infiltration into eWAT. Wild‐type mice were subjected to left cervical vagotomy (VX) or sham surgery and tissues were collected at 7 days following surgery. (A) The percentage of non‐adipocyte nuclei of total nuclei per section was quantified using ImageJ ( n = 4) and right panels show representative images of paraffin sections of eWAT stained with H&E in sham and VX animals. (B) <t>CCL2</t> release from eWAT was analyzed by ELISA. The bar shows the CCL2 levels from sham ( n = 4) or VX ( n = 4) mice normalized to eWAT weight: ng/mL per g ± SEM (unpaired Student's t test). (C) eWAT was collected at 1 ( n = 3), 4 ( n = 4 sham, n = 5 VX), and 7 ( n = 15) days following VX or sham surgery and the eWAT SVCs were analyzed by flow cytometry. The bar shows the % ± SEM of CD11b + Ly6G + cells from CD45 + (one‐way ANOVA, Uncorrected Fisher's LSD). (D) Graphs show representative gating for CD11b + Ly6G + cells in sham and VX eWAT at 7 days (concatenated n = 5–6). (E) Representative immunostaining of Ly6G (red) and Perilipin1 (green) in paraffin sections of eWAT. (F–H) Bone marrow neutrophils after sham ( n = 9) or VX ( n = 5) surgery were isolated using negative magnetic beads and analyzed using bulk RNAseq (DESeq2). Heatmap (F), volcano plot (G) of differentially expressed genes, and GO (Gene Ontology) (H) enrichment bar plot. ns = not significant, * p < 0.05. VX, Vagotomy; eWAT, epididymal white adipose tissue; H&E, hematoxylin–eosin; SVCs, stromal vascular cells.
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Vagotomy promoted Ly6G + cell infiltration into eWAT. Wild‐type mice were subjected to left cervical vagotomy (VX) or sham surgery and tissues were collected at 7 days following surgery. (A) The percentage of non‐adipocyte nuclei of total nuclei per section was quantified using ImageJ ( n = 4) and right panels show representative images of paraffin sections of eWAT stained with H&E in sham and VX animals. (B) <t>CCL2</t> release from eWAT was analyzed by ELISA. The bar shows the CCL2 levels from sham ( n = 4) or VX ( n = 4) mice normalized to eWAT weight: ng/mL per g ± SEM (unpaired Student's t test). (C) eWAT was collected at 1 ( n = 3), 4 ( n = 4 sham, n = 5 VX), and 7 ( n = 15) days following VX or sham surgery and the eWAT SVCs were analyzed by flow cytometry. The bar shows the % ± SEM of CD11b + Ly6G + cells from CD45 + (one‐way ANOVA, Uncorrected Fisher's LSD). (D) Graphs show representative gating for CD11b + Ly6G + cells in sham and VX eWAT at 7 days (concatenated n = 5–6). (E) Representative immunostaining of Ly6G (red) and Perilipin1 (green) in paraffin sections of eWAT. (F–H) Bone marrow neutrophils after sham ( n = 9) or VX ( n = 5) surgery were isolated using negative magnetic beads and analyzed using bulk RNAseq (DESeq2). Heatmap (F), volcano plot (G) of differentially expressed genes, and GO (Gene Ontology) (H) enrichment bar plot. ns = not significant, * p < 0.05. VX, Vagotomy; eWAT, epididymal white adipose tissue; H&E, hematoxylin–eosin; SVCs, stromal vascular cells.
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Vagotomy promoted Ly6G + cell infiltration into eWAT. Wild‐type mice were subjected to left cervical vagotomy (VX) or sham surgery and tissues were collected at 7 days following surgery. (A) The percentage of non‐adipocyte nuclei of total nuclei per section was quantified using ImageJ ( n = 4) and right panels show representative images of paraffin sections of eWAT stained with H&E in sham and VX animals. (B) <t>CCL2</t> release from eWAT was analyzed by ELISA. The bar shows the CCL2 levels from sham ( n = 4) or VX ( n = 4) mice normalized to eWAT weight: ng/mL per g ± SEM (unpaired Student's t test). (C) eWAT was collected at 1 ( n = 3), 4 ( n = 4 sham, n = 5 VX), and 7 ( n = 15) days following VX or sham surgery and the eWAT SVCs were analyzed by flow cytometry. The bar shows the % ± SEM of CD11b + Ly6G + cells from CD45 + (one‐way ANOVA, Uncorrected Fisher's LSD). (D) Graphs show representative gating for CD11b + Ly6G + cells in sham and VX eWAT at 7 days (concatenated n = 5–6). (E) Representative immunostaining of Ly6G (red) and Perilipin1 (green) in paraffin sections of eWAT. (F–H) Bone marrow neutrophils after sham ( n = 9) or VX ( n = 5) surgery were isolated using negative magnetic beads and analyzed using bulk RNAseq (DESeq2). Heatmap (F), volcano plot (G) of differentially expressed genes, and GO (Gene Ontology) (H) enrichment bar plot. ns = not significant, * p < 0.05. VX, Vagotomy; eWAT, epididymal white adipose tissue; H&E, hematoxylin–eosin; SVCs, stromal vascular cells.
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Obesity parameters and metabolic phenotype in male B6 mice. a Body weight (g) measurements over 12 weeks for LFD and HFD-fed male B6 mice ( n = 32-41). b Change in weight (%) (dotted line at 28% represents parameter for LFD and dotted line at 58% represents parameter for HFD). c Fold change in fat mass (g) (dotted line at 1.0 represents parameter for LFD and dotted line at 3.3 represents parameter for obese-HFD). d Pearson correlation analysis showing that the change in weight or fat mass fold change both negatively correlate to trabecular bone loss. e Correlation matrix that shows the change in weight or fat mass fold change both negatively correlate to trabecular bone loss (vertical line and horizontal line represent obesity cutoff). f Glucose tolerance test (GTT) for LFD ( n = 26), obese HFD-fed (OB-HFD; n = 34) and non-obese HFD-fed (NO-HFD; n = 7). g Insulin tolerance test (ITT) for LFD, obese HFD-fed (OB-HFD), and non-obese HFD-fed (NO-HFD). h <t>Serum</t> <t>adiponectin</t> levels ( n = 7). i Serum <t>leptin</t> levels. j Serum procollagen type I N-propeptide (P1NP) levels. k Serum tartrate-resistant acid phosphatase 5b (TRAcP 5b) levels. Analyses for a , f , and g were performed as 2-way ANOVA with Šídák’s multiple comparisons test. Significance for the post-hoc analysis for f , g was defined as: * P < 0.05 LFD vs. OB-HFD, # P < 0.05 LFD vs. NO-HFD-fed, and $ P < 0.05 OB-HFD vs. NO - HFD-fed. Analyses for h , i and k were performed as a Kruskal-Wallis test with Dunn’s multiple comparison. Analysis for j was performed as a One-way ANOVA with Tukey’s multiple comparisons test
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Image Search Results


Vagotomy promoted Ly6G + cell infiltration into eWAT. Wild‐type mice were subjected to left cervical vagotomy (VX) or sham surgery and tissues were collected at 7 days following surgery. (A) The percentage of non‐adipocyte nuclei of total nuclei per section was quantified using ImageJ ( n = 4) and right panels show representative images of paraffin sections of eWAT stained with H&E in sham and VX animals. (B) CCL2 release from eWAT was analyzed by ELISA. The bar shows the CCL2 levels from sham ( n = 4) or VX ( n = 4) mice normalized to eWAT weight: ng/mL per g ± SEM (unpaired Student's t test). (C) eWAT was collected at 1 ( n = 3), 4 ( n = 4 sham, n = 5 VX), and 7 ( n = 15) days following VX or sham surgery and the eWAT SVCs were analyzed by flow cytometry. The bar shows the % ± SEM of CD11b + Ly6G + cells from CD45 + (one‐way ANOVA, Uncorrected Fisher's LSD). (D) Graphs show representative gating for CD11b + Ly6G + cells in sham and VX eWAT at 7 days (concatenated n = 5–6). (E) Representative immunostaining of Ly6G (red) and Perilipin1 (green) in paraffin sections of eWAT. (F–H) Bone marrow neutrophils after sham ( n = 9) or VX ( n = 5) surgery were isolated using negative magnetic beads and analyzed using bulk RNAseq (DESeq2). Heatmap (F), volcano plot (G) of differentially expressed genes, and GO (Gene Ontology) (H) enrichment bar plot. ns = not significant, * p < 0.05. VX, Vagotomy; eWAT, epididymal white adipose tissue; H&E, hematoxylin–eosin; SVCs, stromal vascular cells.

Journal: The FASEB Journal

Article Title: Lymphocyte Antigen 6G Mediates Vagotomy‐Associated Reduction in Body Weight

doi: 10.1096/fj.202600151RR

Figure Lengend Snippet: Vagotomy promoted Ly6G + cell infiltration into eWAT. Wild‐type mice were subjected to left cervical vagotomy (VX) or sham surgery and tissues were collected at 7 days following surgery. (A) The percentage of non‐adipocyte nuclei of total nuclei per section was quantified using ImageJ ( n = 4) and right panels show representative images of paraffin sections of eWAT stained with H&E in sham and VX animals. (B) CCL2 release from eWAT was analyzed by ELISA. The bar shows the CCL2 levels from sham ( n = 4) or VX ( n = 4) mice normalized to eWAT weight: ng/mL per g ± SEM (unpaired Student's t test). (C) eWAT was collected at 1 ( n = 3), 4 ( n = 4 sham, n = 5 VX), and 7 ( n = 15) days following VX or sham surgery and the eWAT SVCs were analyzed by flow cytometry. The bar shows the % ± SEM of CD11b + Ly6G + cells from CD45 + (one‐way ANOVA, Uncorrected Fisher's LSD). (D) Graphs show representative gating for CD11b + Ly6G + cells in sham and VX eWAT at 7 days (concatenated n = 5–6). (E) Representative immunostaining of Ly6G (red) and Perilipin1 (green) in paraffin sections of eWAT. (F–H) Bone marrow neutrophils after sham ( n = 9) or VX ( n = 5) surgery were isolated using negative magnetic beads and analyzed using bulk RNAseq (DESeq2). Heatmap (F), volcano plot (G) of differentially expressed genes, and GO (Gene Ontology) (H) enrichment bar plot. ns = not significant, * p < 0.05. VX, Vagotomy; eWAT, epididymal white adipose tissue; H&E, hematoxylin–eosin; SVCs, stromal vascular cells.

Article Snippet: In vitro release rate was calculated as mg NEFAs per mg eWAT tissue per hour. (2) CCL2 levels were quantified using a mouse CCL2 ELISA kit (R&D Systems, #DY497‐05), according to the manufacturer's instructions ( n = 1 experiment).

Techniques: Staining, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Immunostaining, Isolation, Magnetic Beads, RNA sequencing

Obesity parameters and metabolic phenotype in male B6 mice. a Body weight (g) measurements over 12 weeks for LFD and HFD-fed male B6 mice ( n = 32-41). b Change in weight (%) (dotted line at 28% represents parameter for LFD and dotted line at 58% represents parameter for HFD). c Fold change in fat mass (g) (dotted line at 1.0 represents parameter for LFD and dotted line at 3.3 represents parameter for obese-HFD). d Pearson correlation analysis showing that the change in weight or fat mass fold change both negatively correlate to trabecular bone loss. e Correlation matrix that shows the change in weight or fat mass fold change both negatively correlate to trabecular bone loss (vertical line and horizontal line represent obesity cutoff). f Glucose tolerance test (GTT) for LFD ( n = 26), obese HFD-fed (OB-HFD; n = 34) and non-obese HFD-fed (NO-HFD; n = 7). g Insulin tolerance test (ITT) for LFD, obese HFD-fed (OB-HFD), and non-obese HFD-fed (NO-HFD). h Serum adiponectin levels ( n = 7). i Serum leptin levels. j Serum procollagen type I N-propeptide (P1NP) levels. k Serum tartrate-resistant acid phosphatase 5b (TRAcP 5b) levels. Analyses for a , f , and g were performed as 2-way ANOVA with Šídák’s multiple comparisons test. Significance for the post-hoc analysis for f , g was defined as: * P < 0.05 LFD vs. OB-HFD, # P < 0.05 LFD vs. NO-HFD-fed, and $ P < 0.05 OB-HFD vs. NO - HFD-fed. Analyses for h , i and k were performed as a Kruskal-Wallis test with Dunn’s multiple comparison. Analysis for j was performed as a One-way ANOVA with Tukey’s multiple comparisons test

Journal: Bone Research

Article Title: Expansion of bone marrow adipocytes in obese mice leads to PD-L1-driven bone marrow immunosuppression and osteoclastogenesis

doi: 10.1038/s41413-026-00509-5

Figure Lengend Snippet: Obesity parameters and metabolic phenotype in male B6 mice. a Body weight (g) measurements over 12 weeks for LFD and HFD-fed male B6 mice ( n = 32-41). b Change in weight (%) (dotted line at 28% represents parameter for LFD and dotted line at 58% represents parameter for HFD). c Fold change in fat mass (g) (dotted line at 1.0 represents parameter for LFD and dotted line at 3.3 represents parameter for obese-HFD). d Pearson correlation analysis showing that the change in weight or fat mass fold change both negatively correlate to trabecular bone loss. e Correlation matrix that shows the change in weight or fat mass fold change both negatively correlate to trabecular bone loss (vertical line and horizontal line represent obesity cutoff). f Glucose tolerance test (GTT) for LFD ( n = 26), obese HFD-fed (OB-HFD; n = 34) and non-obese HFD-fed (NO-HFD; n = 7). g Insulin tolerance test (ITT) for LFD, obese HFD-fed (OB-HFD), and non-obese HFD-fed (NO-HFD). h Serum adiponectin levels ( n = 7). i Serum leptin levels. j Serum procollagen type I N-propeptide (P1NP) levels. k Serum tartrate-resistant acid phosphatase 5b (TRAcP 5b) levels. Analyses for a , f , and g were performed as 2-way ANOVA with Šídák’s multiple comparisons test. Significance for the post-hoc analysis for f , g was defined as: * P < 0.05 LFD vs. OB-HFD, # P < 0.05 LFD vs. NO-HFD-fed, and $ P < 0.05 OB-HFD vs. NO - HFD-fed. Analyses for h , i and k were performed as a Kruskal-Wallis test with Dunn’s multiple comparison. Analysis for j was performed as a One-way ANOVA with Tukey’s multiple comparisons test

Article Snippet: Serum protein analysis of adiponectin (Mouse Adiponectin/Acrp30 Quantikine ELISA, R&D Systems MRP300), leptin (Mouse/Rat Leptin Quantikine ELISA, R&D Systems MOB00B), TRAP (Mousetrap TRAcP 5b ELISA, Immunodiagnostic Systems SB-TR103), CTX-1 (Mouse CTX ELISA Kit, Immunodiagnostic Systems AC-06F1), and P1NP (Rat/Mouse P1NP EIA, Immunodiagnostic Systems AC-33F1) were measured by ELISA according to manufacturer’s instructions.

Techniques: Comparison