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JHU083 suppresses pro‐inflammatory <t>macrophage</t> polarization and improves survival in murine sepsis. (a) Schematic of the RNA‐seq experimental design in CLP‐induced septic mice. (b) Volcano plot showing differentially expressed genes (DEGs) between the CLP group and control group (n = 3 per group). (c) GO enrichment analysis of DEGs identified in septic versus healthy mice. (d) Experimental scheme for glutamate stimulation in macrophages at various concentrations. (e) Flow cytometry analysis of macrophage polarization after 24 h glutamate treatment (n = 3 per group). (f) Primary BMDMs were derived from mouse bone marrow <t>using</t> <t>M‐CSF</t> (10 ng/mL, 7 days), stimulated with LPS (4 h), followed by JHU083 treatment for 24 h prior to RNA‐seq (n = 3 per group). (g) GO enrichment analysis of DEGs between JHU083‐treated and untreated BMDMs. (h) GSEA illustrating key pathways differentially regulated by JHU083 in BMDMs. (i) Kaplan‐Meier survival curves of CLP mice treated with PBS or JHU083 (n = 10 per group). (j) Representative H&E staining images of the ileum and lung tissues from each group. Scale bar, 100 µm. (k) Immunofluorescence staining of NeuN in lung sections. Scale bar, 50 µm. Error bars represent means ± SD. Differences between groups were tested using one‐way ANOVA followed by Tukey's multiple comparisons test, or unpaired Student's t‐test.
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JHU083 suppresses pro‐inflammatory <t>macrophage</t> polarization and improves survival in murine sepsis. (a) Schematic of the RNA‐seq experimental design in CLP‐induced septic mice. (b) Volcano plot showing differentially expressed genes (DEGs) between the CLP group and control group (n = 3 per group). (c) GO enrichment analysis of DEGs identified in septic versus healthy mice. (d) Experimental scheme for glutamate stimulation in macrophages at various concentrations. (e) Flow cytometry analysis of macrophage polarization after 24 h glutamate treatment (n = 3 per group). (f) Primary BMDMs were derived from mouse bone marrow <t>using</t> <t>M‐CSF</t> (10 ng/mL, 7 days), stimulated with LPS (4 h), followed by JHU083 treatment for 24 h prior to RNA‐seq (n = 3 per group). (g) GO enrichment analysis of DEGs between JHU083‐treated and untreated BMDMs. (h) GSEA illustrating key pathways differentially regulated by JHU083 in BMDMs. (i) Kaplan‐Meier survival curves of CLP mice treated with PBS or JHU083 (n = 10 per group). (j) Representative H&E staining images of the ileum and lung tissues from each group. Scale bar, 100 µm. (k) Immunofluorescence staining of NeuN in lung sections. Scale bar, 50 µm. Error bars represent means ± SD. Differences between groups were tested using one‐way ANOVA followed by Tukey's multiple comparisons test, or unpaired Student's t‐test.
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(A) A schematic picture shows the experimental plan for osteoblast viability and mRNA expression study. (B–C) Cell viability of primary osteoblasts after exposure to 1, 10, 100 μM vildagliptin or omarigliptin. mRNA expression of osteoblast‐specific genes, that is, (D–E) Runx2, (F–G) alkaline phosphatase (ALP), (H–I) osteocalcin, and osteoclastogenic factors, that is, (J–K) <t>macrophage‐colony</t> stimulating factor <t>(M‐CSF),</t> (L–M) receptor activator of nuclear factor‐κB ligand (RANKL) in primary osteoblasts after treatment with 1, 10, 100 μM vildagliptin or omarigliptin for 5 days. n = 5–6; * p < 0.05, ** p < 0.01 vs. vehicle‐treated group (Veh) by one‐way analysis of variance (ANOVA) with Dunnett's multiple comparisons test.
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(A) A schematic picture shows the experimental plan for osteoblast viability and mRNA expression study. (B–C) Cell viability of primary osteoblasts after exposure to 1, 10, 100 μM vildagliptin or omarigliptin. mRNA expression of osteoblast‐specific genes, that is, (D–E) Runx2, (F–G) alkaline phosphatase (ALP), (H–I) osteocalcin, and osteoclastogenic factors, that is, (J–K) <t>macrophage‐colony</t> stimulating factor <t>(M‐CSF),</t> (L–M) receptor activator of nuclear factor‐κB ligand (RANKL) in primary osteoblasts after treatment with 1, 10, 100 μM vildagliptin or omarigliptin for 5 days. n = 5–6; * p < 0.05, ** p < 0.01 vs. vehicle‐treated group (Veh) by one‐way analysis of variance (ANOVA) with Dunnett's multiple comparisons test.
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(A) A schematic picture shows the experimental plan for osteoblast viability and mRNA expression study. (B–C) Cell viability of primary osteoblasts after exposure to 1, 10, 100 μM vildagliptin or omarigliptin. mRNA expression of osteoblast‐specific genes, that is, (D–E) Runx2, (F–G) alkaline phosphatase (ALP), (H–I) osteocalcin, and osteoclastogenic factors, that is, (J–K) <t>macrophage‐colony</t> stimulating factor <t>(M‐CSF),</t> (L–M) receptor activator of nuclear factor‐κB ligand (RANKL) in primary osteoblasts after treatment with 1, 10, 100 μM vildagliptin or omarigliptin for 5 days. n = 5–6; * p < 0.05, ** p < 0.01 vs. vehicle‐treated group (Veh) by one‐way analysis of variance (ANOVA) with Dunnett's multiple comparisons test.
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(A) A schematic picture shows the experimental plan for osteoblast viability and mRNA expression study. (B–C) Cell viability of primary osteoblasts after exposure to 1, 10, 100 μM vildagliptin or omarigliptin. mRNA expression of osteoblast‐specific genes, that is, (D–E) Runx2, (F–G) alkaline phosphatase (ALP), (H–I) osteocalcin, and osteoclastogenic factors, that is, (J–K) <t>macrophage‐colony</t> stimulating factor <t>(M‐CSF),</t> (L–M) receptor activator of nuclear factor‐κB ligand (RANKL) in primary osteoblasts after treatment with 1, 10, 100 μM vildagliptin or omarigliptin for 5 days. n = 5–6; * p < 0.05, ** p < 0.01 vs. vehicle‐treated group (Veh) by one‐way analysis of variance (ANOVA) with Dunnett's multiple comparisons test.
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(A) A schematic picture shows the experimental plan for osteoblast viability and mRNA expression study. (B–C) Cell viability of primary osteoblasts after exposure to 1, 10, 100 μM vildagliptin or omarigliptin. mRNA expression of osteoblast‐specific genes, that is, (D–E) Runx2, (F–G) alkaline phosphatase (ALP), (H–I) osteocalcin, and osteoclastogenic factors, that is, (J–K) <t>macrophage‐colony</t> stimulating factor <t>(M‐CSF),</t> (L–M) receptor activator of nuclear factor‐κB ligand (RANKL) in primary osteoblasts after treatment with 1, 10, 100 μM vildagliptin or omarigliptin for 5 days. n = 5–6; * p < 0.05, ** p < 0.01 vs. vehicle‐treated group (Veh) by one‐way analysis of variance (ANOVA) with Dunnett's multiple comparisons test.
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Image Search Results


JHU083 suppresses pro‐inflammatory macrophage polarization and improves survival in murine sepsis. (a) Schematic of the RNA‐seq experimental design in CLP‐induced septic mice. (b) Volcano plot showing differentially expressed genes (DEGs) between the CLP group and control group (n = 3 per group). (c) GO enrichment analysis of DEGs identified in septic versus healthy mice. (d) Experimental scheme for glutamate stimulation in macrophages at various concentrations. (e) Flow cytometry analysis of macrophage polarization after 24 h glutamate treatment (n = 3 per group). (f) Primary BMDMs were derived from mouse bone marrow using M‐CSF (10 ng/mL, 7 days), stimulated with LPS (4 h), followed by JHU083 treatment for 24 h prior to RNA‐seq (n = 3 per group). (g) GO enrichment analysis of DEGs between JHU083‐treated and untreated BMDMs. (h) GSEA illustrating key pathways differentially regulated by JHU083 in BMDMs. (i) Kaplan‐Meier survival curves of CLP mice treated with PBS or JHU083 (n = 10 per group). (j) Representative H&E staining images of the ileum and lung tissues from each group. Scale bar, 100 µm. (k) Immunofluorescence staining of NeuN in lung sections. Scale bar, 50 µm. Error bars represent means ± SD. Differences between groups were tested using one‐way ANOVA followed by Tukey's multiple comparisons test, or unpaired Student's t‐test.

Journal: Advanced Science

Article Title: Nanotherapeutic Macrophage‐Neuro Reprogramming Through Immunometabolic Crosstalk Mitigates Sepsis‐Induced Lung Injury and Neurologic Damage

doi: 10.1002/advs.202520665

Figure Lengend Snippet: JHU083 suppresses pro‐inflammatory macrophage polarization and improves survival in murine sepsis. (a) Schematic of the RNA‐seq experimental design in CLP‐induced septic mice. (b) Volcano plot showing differentially expressed genes (DEGs) between the CLP group and control group (n = 3 per group). (c) GO enrichment analysis of DEGs identified in septic versus healthy mice. (d) Experimental scheme for glutamate stimulation in macrophages at various concentrations. (e) Flow cytometry analysis of macrophage polarization after 24 h glutamate treatment (n = 3 per group). (f) Primary BMDMs were derived from mouse bone marrow using M‐CSF (10 ng/mL, 7 days), stimulated with LPS (4 h), followed by JHU083 treatment for 24 h prior to RNA‐seq (n = 3 per group). (g) GO enrichment analysis of DEGs between JHU083‐treated and untreated BMDMs. (h) GSEA illustrating key pathways differentially regulated by JHU083 in BMDMs. (i) Kaplan‐Meier survival curves of CLP mice treated with PBS or JHU083 (n = 10 per group). (j) Representative H&E staining images of the ileum and lung tissues from each group. Scale bar, 100 µm. (k) Immunofluorescence staining of NeuN in lung sections. Scale bar, 50 µm. Error bars represent means ± SD. Differences between groups were tested using one‐way ANOVA followed by Tukey's multiple comparisons test, or unpaired Student's t‐test.

Article Snippet: The isolated cells were cultured in complete DMEM medium containing macrophage colony‐stimulating factor (M‐CSF) (20 ng/mL, Sangon Biotech) at 37 °C and 5% (v/v) CO 2 .

Techniques: RNA Sequencing, Control, Flow Cytometry, Derivative Assay, Staining, Immunofluorescence

(A) A schematic picture shows the experimental plan for osteoblast viability and mRNA expression study. (B–C) Cell viability of primary osteoblasts after exposure to 1, 10, 100 μM vildagliptin or omarigliptin. mRNA expression of osteoblast‐specific genes, that is, (D–E) Runx2, (F–G) alkaline phosphatase (ALP), (H–I) osteocalcin, and osteoclastogenic factors, that is, (J–K) macrophage‐colony stimulating factor (M‐CSF), (L–M) receptor activator of nuclear factor‐κB ligand (RANKL) in primary osteoblasts after treatment with 1, 10, 100 μM vildagliptin or omarigliptin for 5 days. n = 5–6; * p < 0.05, ** p < 0.01 vs. vehicle‐treated group (Veh) by one‐way analysis of variance (ANOVA) with Dunnett's multiple comparisons test.

Journal: Comprehensive Physiology

Article Title: Vildagliptin and Omarigliptin Differentially Bind to DPP‐4 Homodimers and Modulate Osteoclast‐Mediated Bone Resorption

doi: 10.1002/cph4.70103

Figure Lengend Snippet: (A) A schematic picture shows the experimental plan for osteoblast viability and mRNA expression study. (B–C) Cell viability of primary osteoblasts after exposure to 1, 10, 100 μM vildagliptin or omarigliptin. mRNA expression of osteoblast‐specific genes, that is, (D–E) Runx2, (F–G) alkaline phosphatase (ALP), (H–I) osteocalcin, and osteoclastogenic factors, that is, (J–K) macrophage‐colony stimulating factor (M‐CSF), (L–M) receptor activator of nuclear factor‐κB ligand (RANKL) in primary osteoblasts after treatment with 1, 10, 100 μM vildagliptin or omarigliptin for 5 days. n = 5–6; * p < 0.05, ** p < 0.01 vs. vehicle‐treated group (Veh) by one‐way analysis of variance (ANOVA) with Dunnett's multiple comparisons test.

Article Snippet: The osteoclast precursors were maintained in α‐MEM supplemented with 10% FBS and 10 ng/mL macrophage colony‐stimulating factor (M‐CSF) (catalog no. 216‐MC‐025; R&D Systems, Minneapolis, MN, USA) for 3 days.

Techniques: Expressing

Representative images of primary osteoclast captured by holotomographic microscope. Osteoclast morphology on (A) x‐y, (B) x‐z, (C) y‐z axis at day 7 after culture bone marrow cells with 10 ng/mL M‐CSF and RANKL. (D) Refractive index (RI) distribution in primary osteoclasts, (E) three‐dimentional (3D) rendered image of RI distribution. Blue is DAPI stained nuclei. Red is pseudocolor labeling for the remaining of intracellular compartments. (F) Correlation between number of nuclei and cell volume of multinucleated osteoclasts.

Journal: Comprehensive Physiology

Article Title: Vildagliptin and Omarigliptin Differentially Bind to DPP‐4 Homodimers and Modulate Osteoclast‐Mediated Bone Resorption

doi: 10.1002/cph4.70103

Figure Lengend Snippet: Representative images of primary osteoclast captured by holotomographic microscope. Osteoclast morphology on (A) x‐y, (B) x‐z, (C) y‐z axis at day 7 after culture bone marrow cells with 10 ng/mL M‐CSF and RANKL. (D) Refractive index (RI) distribution in primary osteoclasts, (E) three‐dimentional (3D) rendered image of RI distribution. Blue is DAPI stained nuclei. Red is pseudocolor labeling for the remaining of intracellular compartments. (F) Correlation between number of nuclei and cell volume of multinucleated osteoclasts.

Article Snippet: The osteoclast precursors were maintained in α‐MEM supplemented with 10% FBS and 10 ng/mL macrophage colony‐stimulating factor (M‐CSF) (catalog no. 216‐MC‐025; R&D Systems, Minneapolis, MN, USA) for 3 days.

Techniques: Microscopy, Refractive Index, Staining, Labeling