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GC-induced MΦ are highly efficient in C1q-mediated phagocytosis. ( A ) Gene set enrichment analysis (GSEA) of DEGs in MΦ exposed to CM of steroidogenic NCI-H295R cells in comparison to controls. ( B ) Visualization of the enrichment results on phagocytosis ( p < 2.2e-16; FDR: 0.011718). ( C ) Representative flow cytometry plots and ( D ) quantification of phagocytosis by MΦ exposed to CM of steroidogenic NCI-H295R cells or control. CD64 + CFSE+ double-positive cells were considered phagocytic macrophages. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. N = 4 biological replicates from independent healthy blood donors ( E ) Percentages of phagocytic MΦ exposed to dexamethasone (100 nM) or control. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Differences were compared using unpaired t-test. ( F ) Phagocytosis of M1-polarized MΦ after exposure to 10 µg/ml or 20 µg/ml purified human C1q. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( G ) Phagocytosis of dexamethasone (100 nM) -polarized MΦ after exposure to 1 µg/ml, 10 µg/ml or 50 µg/ml anti-C1QA antibody. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( H ) Phagocytosis of dexamethasone (100 nM)-polarized MΦ after exposure to the MerTK inhibitor <t>UNC1062</t> (100 nM), anti-Gas6 antibody (20 µg/ml) or goat control IgG (20 µg/ml). N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( I ) Kaplan-Meier plots of PFS and OS according to tumoral CSF1 and C1QA expression. Higher gene expression was significantly associated with favorable PFS and OS. RNA expression and survival data was extracted from the TCGA dataset ( n = 76). NCI-R = NCI-H295R; mety=metyrapone.
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GC-induced MΦ are highly efficient in C1q-mediated phagocytosis. ( A ) Gene set enrichment analysis (GSEA) of DEGs in MΦ exposed to CM of steroidogenic NCI-H295R cells in comparison to controls. ( B ) Visualization of the enrichment results on phagocytosis ( p < 2.2e-16; FDR: 0.011718). ( C ) Representative flow cytometry plots and ( D ) quantification of phagocytosis by MΦ exposed to CM of steroidogenic NCI-H295R cells or control. CD64 + CFSE+ double-positive cells were considered phagocytic macrophages. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. N = 4 biological replicates from independent healthy blood donors ( E ) Percentages of phagocytic MΦ exposed to dexamethasone (100 nM) or control. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Differences were compared using unpaired t-test. ( F ) Phagocytosis of M1-polarized MΦ after exposure to 10 µg/ml or 20 µg/ml purified human C1q. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( G ) Phagocytosis of dexamethasone (100 nM) -polarized MΦ after exposure to 1 µg/ml, 10 µg/ml or 50 µg/ml anti-C1QA antibody. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( H ) Phagocytosis of dexamethasone (100 nM)-polarized MΦ after exposure to the MerTK inhibitor <t>UNC1062</t> (100 nM), anti-Gas6 antibody (20 µg/ml) or goat control IgG (20 µg/ml). N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( I ) Kaplan-Meier plots of PFS and OS according to tumoral CSF1 and C1QA expression. Higher gene expression was significantly associated with favorable PFS and OS. RNA expression and survival data was extracted from the TCGA dataset ( n = 76). NCI-R = NCI-H295R; mety=metyrapone.
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Pharmacological modulation of MERTK and VCAM1 implicates a VCAM1-linked efferocytosis and anti-inflammatory mechanism for YQHXP. (A) Flow cytometry analysis of PKH67 + /F4/80 + double-positive cells in BV2–HT22 co-culture across seven groups. (B) Quantification of efferocytosis rate(n=3). (C) Flow cytometry plots of apoptotic BV2 cells (Annexin V/PI staining). (D) Quantification of apoptosis rate(n=3). (E) Western blot and quantification of C1QB protein expression(n=3). (F) Western blot and quantification of MERTK protein expression(n=3). (G) Western blot and quantification of VCAM1 protein expression(n=3). (H) TNF-α levels in BV2 supernatant measured by ELISA(n=3). IL-6 levels in BV2 supernatant measured by ELISA(n=3). *P < 0.05 relative to the model group; **P < 0.01, ***P < 0.001 relative to the model group. # P < 0.05 relative to the <t>UNC2250</t> group; ## P < 0.01 relative to the UNC2250 group; ### P < 0.001 relative to the UNC2250 group.
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Pharmacological modulation of MERTK and VCAM1 implicates a VCAM1-linked efferocytosis and anti-inflammatory mechanism for YQHXP. (A) Flow cytometry analysis of PKH67 + /F4/80 + double-positive cells in BV2–HT22 co-culture across seven groups. (B) Quantification of efferocytosis rate(n=3). (C) Flow cytometry plots of apoptotic BV2 cells (Annexin V/PI staining). (D) Quantification of apoptosis rate(n=3). (E) Western blot and quantification of C1QB protein expression(n=3). (F) Western blot and quantification of MERTK protein expression(n=3). (G) Western blot and quantification of VCAM1 protein expression(n=3). (H) TNF-α levels in BV2 supernatant measured by ELISA(n=3). IL-6 levels in BV2 supernatant measured by ELISA(n=3). *P < 0.05 relative to the model group; **P < 0.01, ***P < 0.001 relative to the model group. # P < 0.05 relative to the <t>UNC2250</t> group; ## P < 0.01 relative to the UNC2250 group; ### P < 0.001 relative to the UNC2250 group.
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The antibody-drug conjugate RGX-019-MMAE induced cytotoxic activity in <t>MERTK-expressing</t> AML cell lines. A MERTK expression in the indicated AML cell lines; leukemic cells (1 × 10 6 ) were stained with anti-MERTK-APC antibody, and the expression was measured by flow cytometry. Data are plotted as mean values with error bars representing standard error. B - F Bar graph showing the percentage of relative luminescence in Kasumi 1 ( B ), OCI-AML3 ( C ), MOLM-13 ( D ), MOLM-14 ( E ), and MV4-11 ( F ) cells treated with the indicated concentrations of RGX-019-MMAE <t>and</t> <t>monoclonal</t> antibody RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test). * p ≤0.05, ** p ≤0.01, *** p ≤0.001, **** p ≤0.0001. UT = untreated
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The antibody-drug conjugate RGX-019-MMAE induced cytotoxic activity in <t>MERTK-expressing</t> AML cell lines. A MERTK expression in the indicated AML cell lines; leukemic cells (1 × 10 6 ) were stained with anti-MERTK-APC antibody, and the expression was measured by flow cytometry. Data are plotted as mean values with error bars representing standard error. B - F Bar graph showing the percentage of relative luminescence in Kasumi 1 ( B ), OCI-AML3 ( C ), MOLM-13 ( D ), MOLM-14 ( E ), and MV4-11 ( F ) cells treated with the indicated concentrations of RGX-019-MMAE <t>and</t> <t>monoclonal</t> antibody RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test). * p ≤0.05, ** p ≤0.01, *** p ≤0.001, **** p ≤0.0001. UT = untreated
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The antibody-drug conjugate RGX-019-MMAE induced cytotoxic activity in <t>MERTK-expressing</t> AML cell lines. A MERTK expression in the indicated AML cell lines; leukemic cells (1 × 10 6 ) were stained with anti-MERTK-APC antibody, and the expression was measured by flow cytometry. Data are plotted as mean values with error bars representing standard error. B - F Bar graph showing the percentage of relative luminescence in Kasumi 1 ( B ), OCI-AML3 ( C ), MOLM-13 ( D ), MOLM-14 ( E ), and MV4-11 ( F ) cells treated with the indicated concentrations of RGX-019-MMAE <t>and</t> <t>monoclonal</t> antibody RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test). * p ≤0.05, ** p ≤0.01, *** p ≤0.001, **** p ≤0.0001. UT = untreated
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Image Search Results


GC-induced MΦ are highly efficient in C1q-mediated phagocytosis. ( A ) Gene set enrichment analysis (GSEA) of DEGs in MΦ exposed to CM of steroidogenic NCI-H295R cells in comparison to controls. ( B ) Visualization of the enrichment results on phagocytosis ( p < 2.2e-16; FDR: 0.011718). ( C ) Representative flow cytometry plots and ( D ) quantification of phagocytosis by MΦ exposed to CM of steroidogenic NCI-H295R cells or control. CD64 + CFSE+ double-positive cells were considered phagocytic macrophages. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. N = 4 biological replicates from independent healthy blood donors ( E ) Percentages of phagocytic MΦ exposed to dexamethasone (100 nM) or control. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Differences were compared using unpaired t-test. ( F ) Phagocytosis of M1-polarized MΦ after exposure to 10 µg/ml or 20 µg/ml purified human C1q. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( G ) Phagocytosis of dexamethasone (100 nM) -polarized MΦ after exposure to 1 µg/ml, 10 µg/ml or 50 µg/ml anti-C1QA antibody. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( H ) Phagocytosis of dexamethasone (100 nM)-polarized MΦ after exposure to the MerTK inhibitor UNC1062 (100 nM), anti-Gas6 antibody (20 µg/ml) or goat control IgG (20 µg/ml). N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( I ) Kaplan-Meier plots of PFS and OS according to tumoral CSF1 and C1QA expression. Higher gene expression was significantly associated with favorable PFS and OS. RNA expression and survival data was extracted from the TCGA dataset ( n = 76). NCI-R = NCI-H295R; mety=metyrapone.

Journal: Scientific Reports

Article Title: Glucocorticoids induce a phagocytic C1Q+ macrophage phenotype primed for IFNγ-dependent CXCL9 secretion

doi: 10.1038/s41598-026-52733-y

Figure Lengend Snippet: GC-induced MΦ are highly efficient in C1q-mediated phagocytosis. ( A ) Gene set enrichment analysis (GSEA) of DEGs in MΦ exposed to CM of steroidogenic NCI-H295R cells in comparison to controls. ( B ) Visualization of the enrichment results on phagocytosis ( p < 2.2e-16; FDR: 0.011718). ( C ) Representative flow cytometry plots and ( D ) quantification of phagocytosis by MΦ exposed to CM of steroidogenic NCI-H295R cells or control. CD64 + CFSE+ double-positive cells were considered phagocytic macrophages. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. N = 4 biological replicates from independent healthy blood donors ( E ) Percentages of phagocytic MΦ exposed to dexamethasone (100 nM) or control. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Differences were compared using unpaired t-test. ( F ) Phagocytosis of M1-polarized MΦ after exposure to 10 µg/ml or 20 µg/ml purified human C1q. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( G ) Phagocytosis of dexamethasone (100 nM) -polarized MΦ after exposure to 1 µg/ml, 10 µg/ml or 50 µg/ml anti-C1QA antibody. N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( H ) Phagocytosis of dexamethasone (100 nM)-polarized MΦ after exposure to the MerTK inhibitor UNC1062 (100 nM), anti-Gas6 antibody (20 µg/ml) or goat control IgG (20 µg/ml). N = 3 biological replicates from independent healthy blood donors are shown in mean +/- SD. Groups were compared using one-way ANOVA with Tukey’s multiple comparisons test. ( I ) Kaplan-Meier plots of PFS and OS according to tumoral CSF1 and C1QA expression. Higher gene expression was significantly associated with favorable PFS and OS. RNA expression and survival data was extracted from the TCGA dataset ( n = 76). NCI-R = NCI-H295R; mety=metyrapone.

Article Snippet: For inhibition studies, MФ were pre-incubated with the selective MerTK inhibitor UNC1062 (100 nM; MCE: Cat# HY-117548), anti-Gas6 antibody (20 μg/ml; R&D Systems, Cat# AB885, RRID: AB_354376), a goat isotype IgG control (20 μg/ml; Thermo Fisher Scientific, Cat# 02–6202, RRID: AB_2532946), purified C1q (Merck; Cat# C1740) or anti-C1QA antibody (LS-Bio; Cat# LS‐C100911; RRID: AB_2067267) for 30 min before they were added to early ferroptotic tumor cells.

Techniques: Comparison, Flow Cytometry, Control, Purification, Expressing, Gene Expression, RNA Expression

Pharmacological modulation of MERTK and VCAM1 implicates a VCAM1-linked efferocytosis and anti-inflammatory mechanism for YQHXP. (A) Flow cytometry analysis of PKH67 + /F4/80 + double-positive cells in BV2–HT22 co-culture across seven groups. (B) Quantification of efferocytosis rate(n=3). (C) Flow cytometry plots of apoptotic BV2 cells (Annexin V/PI staining). (D) Quantification of apoptosis rate(n=3). (E) Western blot and quantification of C1QB protein expression(n=3). (F) Western blot and quantification of MERTK protein expression(n=3). (G) Western blot and quantification of VCAM1 protein expression(n=3). (H) TNF-α levels in BV2 supernatant measured by ELISA(n=3). IL-6 levels in BV2 supernatant measured by ELISA(n=3). *P < 0.05 relative to the model group; **P < 0.01, ***P < 0.001 relative to the model group. # P < 0.05 relative to the UNC2250 group; ## P < 0.01 relative to the UNC2250 group; ### P < 0.001 relative to the UNC2250 group.

Journal: Frontiers in Immunology

Article Title: YiQi-HuoXue prescription ameliorates LPS-induced sepsis-associated encephalopathy via VCAM-1–mediated microglial efferocytosis

doi: 10.3389/fimmu.2026.1792688

Figure Lengend Snippet: Pharmacological modulation of MERTK and VCAM1 implicates a VCAM1-linked efferocytosis and anti-inflammatory mechanism for YQHXP. (A) Flow cytometry analysis of PKH67 + /F4/80 + double-positive cells in BV2–HT22 co-culture across seven groups. (B) Quantification of efferocytosis rate(n=3). (C) Flow cytometry plots of apoptotic BV2 cells (Annexin V/PI staining). (D) Quantification of apoptosis rate(n=3). (E) Western blot and quantification of C1QB protein expression(n=3). (F) Western blot and quantification of MERTK protein expression(n=3). (G) Western blot and quantification of VCAM1 protein expression(n=3). (H) TNF-α levels in BV2 supernatant measured by ELISA(n=3). IL-6 levels in BV2 supernatant measured by ELISA(n=3). *P < 0.05 relative to the model group; **P < 0.01, ***P < 0.001 relative to the model group. # P < 0.05 relative to the UNC2250 group; ## P < 0.01 relative to the UNC2250 group; ### P < 0.001 relative to the UNC2250 group.

Article Snippet: The MERTK inhibitor UNC2250 (Cat. HY-15797), rutin (Cat. HY-N0148), and Ginsenoside Rg1 (Cat. HY-N0045) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Flow Cytometry, Co-Culture Assay, Staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

The antibody-drug conjugate RGX-019-MMAE induced cytotoxic activity in MERTK-expressing AML cell lines. A MERTK expression in the indicated AML cell lines; leukemic cells (1 × 10 6 ) were stained with anti-MERTK-APC antibody, and the expression was measured by flow cytometry. Data are plotted as mean values with error bars representing standard error. B - F Bar graph showing the percentage of relative luminescence in Kasumi 1 ( B ), OCI-AML3 ( C ), MOLM-13 ( D ), MOLM-14 ( E ), and MV4-11 ( F ) cells treated with the indicated concentrations of RGX-019-MMAE and monoclonal antibody RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test). * p ≤0.05, ** p ≤0.01, *** p ≤0.001, **** p ≤0.0001. UT = untreated

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: RGX-019-MMAE inhibits leukemia progression by targeting MER proto-oncogene tyrosine kinase (MERTK) in acute myeloid leukemia

doi: 10.1186/s13046-026-03657-y

Figure Lengend Snippet: The antibody-drug conjugate RGX-019-MMAE induced cytotoxic activity in MERTK-expressing AML cell lines. A MERTK expression in the indicated AML cell lines; leukemic cells (1 × 10 6 ) were stained with anti-MERTK-APC antibody, and the expression was measured by flow cytometry. Data are plotted as mean values with error bars representing standard error. B - F Bar graph showing the percentage of relative luminescence in Kasumi 1 ( B ), OCI-AML3 ( C ), MOLM-13 ( D ), MOLM-14 ( E ), and MV4-11 ( F ) cells treated with the indicated concentrations of RGX-019-MMAE and monoclonal antibody RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test). * p ≤0.05, ** p ≤0.01, *** p ≤0.001, **** p ≤0.0001. UT = untreated

Article Snippet: Mouse IgG1/kappa light chain MERTK-specific monoclonal antibodies were generated in mice by immunization with Fc-tagged human MERTK peptide (R&D Systems, Minneapolis, MN) USA).

Techniques: Activity Assay, Expressing, Staining, Flow Cytometry

The antibody-drug conjugate RGX-019-MMAE induced cytotoxic activity in MERTK-expressing AML primary cells. A - D Bar graphs show the percentage of relative luminescence in primary AML cells, RGX946 ( A ), RGX694 ( B ), RGX702 ( C ), and RGX470 ( D ) treated with the indicated concentrations of RGX-019-MMAE or the monoclonal antibody RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test). E Representative figures of colony-forming units for normal peripheral blood mononuclear cells in response to DMSO and indicated concentrations of RGX-019-MMAE and RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test) * p ≤0.05, ** p ≤0.01, *** p ≤0.001, **** p ≤0.0001

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: RGX-019-MMAE inhibits leukemia progression by targeting MER proto-oncogene tyrosine kinase (MERTK) in acute myeloid leukemia

doi: 10.1186/s13046-026-03657-y

Figure Lengend Snippet: The antibody-drug conjugate RGX-019-MMAE induced cytotoxic activity in MERTK-expressing AML primary cells. A - D Bar graphs show the percentage of relative luminescence in primary AML cells, RGX946 ( A ), RGX694 ( B ), RGX702 ( C ), and RGX470 ( D ) treated with the indicated concentrations of RGX-019-MMAE or the monoclonal antibody RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test). E Representative figures of colony-forming units for normal peripheral blood mononuclear cells in response to DMSO and indicated concentrations of RGX-019-MMAE and RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test) * p ≤0.05, ** p ≤0.01, *** p ≤0.001, **** p ≤0.0001

Article Snippet: Mouse IgG1/kappa light chain MERTK-specific monoclonal antibodies were generated in mice by immunization with Fc-tagged human MERTK peptide (R&D Systems, Minneapolis, MN) USA).

Techniques: Activity Assay, Expressing