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ccr2 antagonist rs  (MedChemExpress)


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    MedChemExpress ccr2 antagonist rs
    Ccr2 Antagonist Rs, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 32 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ccr2 antagonist rs/product/MedChemExpress
    Average 93 stars, based on 32 article reviews
    ccr2 antagonist rs - by Bioz Stars, 2026-02
    93/100 stars

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    (A) Conditioned medium (CM) was collected from primary WT and Slc4a4 KO astrocytes and subjected to LC-MS/MS-based unbiased proteomics and cytokine/chemokine array. (B) Angiogenic factors detected from LC-MS/MS-based unbiased proteomics. (C) Cytokine/chemokines changed in the CM from WT and Slc4a4 KO astrocytes. Pooled CM from three independent cultures per genotype were used (D) CCL2 level was measured by ELISA in CM collected under either normal or oxygen-glucose-deprivation (OGD) condition cortices from uninjured and stroked (1 dpi) brains from WT and Slc4a4-icKO mice. Each dot represents CM or cortices collected from an individual animal. n = 3–5 per genotype. * p < 0.05, ** p < 0.01 by Student’s t test. In vivo astrocytic CCL2 expression after stroke at 4 dpi was quantified from double immunostaining. n = 17–21 cells collected from 3–5 mice per genotype. * p < 0.05 by Student’s t test. (E) Representative images of astrocytic CCL2 expression at 4 dpi by double immunostaining of CCL2/GFAP. (F and G) Endothelial <t>CCR2</t> mRNA expression was visualized by RNA scope and CD31 staining and quantified by counts of CCR2+ puncta. Each dot represents an individual blood vessel. n = 49 vessels collected from 4 mice per genotype. **** p < 0.0001 by Student’s t test. (H and I) Representative images and quantification of endothelial CCR2 expression from double immunostaining. Each dot represents an individual animal. n = 4–5 per genotype. * p < 0.05 by Student’s t test. (J) Proposed model for the Slc4a4-CCL2-CCR2 axis regulating astrocyte-endothelial interaction. All data are presented as mean ± SEM.
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    (A) Conditioned medium (CM) was collected from primary WT and Slc4a4 KO astrocytes and subjected to LC-MS/MS-based unbiased proteomics and cytokine/chemokine array. (B) Angiogenic factors detected from LC-MS/MS-based unbiased proteomics. (C) Cytokine/chemokines changed in the CM from WT and Slc4a4 KO astrocytes. Pooled CM from three independent cultures per genotype were used (D) CCL2 level was measured by ELISA in CM collected under either normal or oxygen-glucose-deprivation (OGD) condition cortices from uninjured and stroked (1 dpi) brains from WT and Slc4a4-icKO mice. Each dot represents CM or cortices collected from an individual animal. n = 3–5 per genotype. * p < 0.05, ** p < 0.01 by Student’s t test. In vivo astrocytic CCL2 expression after stroke at 4 dpi was quantified from double immunostaining. n = 17–21 cells collected from 3–5 mice per genotype. * p < 0.05 by Student’s t test. (E) Representative images of astrocytic CCL2 expression at 4 dpi by double immunostaining of CCL2/GFAP. (F and G) Endothelial <t>CCR2</t> mRNA expression was visualized by RNA scope and CD31 staining and quantified by counts of CCR2+ puncta. Each dot represents an individual blood vessel. n = 49 vessels collected from 4 mice per genotype. **** p < 0.0001 by Student’s t test. (H and I) Representative images and quantification of endothelial CCR2 expression from double immunostaining. Each dot represents an individual animal. n = 4–5 per genotype. * p < 0.05 by Student’s t test. (J) Proposed model for the Slc4a4-CCL2-CCR2 axis regulating astrocyte-endothelial interaction. All data are presented as mean ± SEM.
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    (A) Conditioned medium (CM) was collected from primary WT and Slc4a4 KO astrocytes and subjected to LC-MS/MS-based unbiased proteomics and cytokine/chemokine array. (B) Angiogenic factors detected from LC-MS/MS-based unbiased proteomics. (C) Cytokine/chemokines changed in the CM from WT and Slc4a4 KO astrocytes. Pooled CM from three independent cultures per genotype were used (D) CCL2 level was measured by ELISA in CM collected under either normal or oxygen-glucose-deprivation (OGD) condition cortices from uninjured and stroked (1 dpi) brains from WT and Slc4a4-icKO mice. Each dot represents CM or cortices collected from an individual animal. n = 3–5 per genotype. * p < 0.05, ** p < 0.01 by Student’s t test. In vivo astrocytic CCL2 expression after stroke at 4 dpi was quantified from double immunostaining. n = 17–21 cells collected from 3–5 mice per genotype. * p < 0.05 by Student’s t test. (E) Representative images of astrocytic CCL2 expression at 4 dpi by double immunostaining of CCL2/GFAP. (F and G) Endothelial <t>CCR2</t> mRNA expression was visualized by RNA scope and CD31 staining and quantified by counts of CCR2+ puncta. Each dot represents an individual blood vessel. n = 49 vessels collected from 4 mice per genotype. **** p < 0.0001 by Student’s t test. (H and I) Representative images and quantification of endothelial CCR2 expression from double immunostaining. Each dot represents an individual animal. n = 4–5 per genotype. * p < 0.05 by Student’s t test. (J) Proposed model for the Slc4a4-CCL2-CCR2 axis regulating astrocyte-endothelial interaction. All data are presented as mean ± SEM.
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    (A) Conditioned medium (CM) was collected from primary WT and Slc4a4 KO astrocytes and subjected to LC-MS/MS-based unbiased proteomics and cytokine/chemokine array. (B) Angiogenic factors detected from LC-MS/MS-based unbiased proteomics. (C) Cytokine/chemokines changed in the CM from WT and Slc4a4 KO astrocytes. Pooled CM from three independent cultures per genotype were used (D) CCL2 level was measured by ELISA in CM collected under either normal or oxygen-glucose-deprivation (OGD) condition cortices from uninjured and stroked (1 dpi) brains from WT and Slc4a4-icKO mice. Each dot represents CM or cortices collected from an individual animal. n = 3–5 per genotype. * p < 0.05, ** p < 0.01 by Student’s t test. In vivo astrocytic CCL2 expression after stroke at 4 dpi was quantified from double immunostaining. n = 17–21 cells collected from 3–5 mice per genotype. * p < 0.05 by Student’s t test. (E) Representative images of astrocytic CCL2 expression at 4 dpi by double immunostaining of CCL2/GFAP. (F and G) Endothelial <t>CCR2</t> mRNA expression was visualized by RNA scope and CD31 staining and quantified by counts of CCR2+ puncta. Each dot represents an individual blood vessel. n = 49 vessels collected from 4 mice per genotype. **** p < 0.0001 by Student’s t test. (H and I) Representative images and quantification of endothelial CCR2 expression from double immunostaining. Each dot represents an individual animal. n = 4–5 per genotype. * p < 0.05 by Student’s t test. (J) Proposed model for the Slc4a4-CCL2-CCR2 axis regulating astrocyte-endothelial interaction. All data are presented as mean ± SEM.
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    Image Search Results


    (A) Conditioned medium (CM) was collected from primary WT and Slc4a4 KO astrocytes and subjected to LC-MS/MS-based unbiased proteomics and cytokine/chemokine array. (B) Angiogenic factors detected from LC-MS/MS-based unbiased proteomics. (C) Cytokine/chemokines changed in the CM from WT and Slc4a4 KO astrocytes. Pooled CM from three independent cultures per genotype were used (D) CCL2 level was measured by ELISA in CM collected under either normal or oxygen-glucose-deprivation (OGD) condition cortices from uninjured and stroked (1 dpi) brains from WT and Slc4a4-icKO mice. Each dot represents CM or cortices collected from an individual animal. n = 3–5 per genotype. * p < 0.05, ** p < 0.01 by Student’s t test. In vivo astrocytic CCL2 expression after stroke at 4 dpi was quantified from double immunostaining. n = 17–21 cells collected from 3–5 mice per genotype. * p < 0.05 by Student’s t test. (E) Representative images of astrocytic CCL2 expression at 4 dpi by double immunostaining of CCL2/GFAP. (F and G) Endothelial CCR2 mRNA expression was visualized by RNA scope and CD31 staining and quantified by counts of CCR2+ puncta. Each dot represents an individual blood vessel. n = 49 vessels collected from 4 mice per genotype. **** p < 0.0001 by Student’s t test. (H and I) Representative images and quantification of endothelial CCR2 expression from double immunostaining. Each dot represents an individual animal. n = 4–5 per genotype. * p < 0.05 by Student’s t test. (J) Proposed model for the Slc4a4-CCL2-CCR2 axis regulating astrocyte-endothelial interaction. All data are presented as mean ± SEM.

    Journal: Cell reports

    Article Title: Astrocytic Slc4a4 regulates blood-brain barrier integrity in healthy and stroke brains via a CCL2-CCR2 pathway and NO dysregulation

    doi: 10.1016/j.celrep.2024.114193

    Figure Lengend Snippet: (A) Conditioned medium (CM) was collected from primary WT and Slc4a4 KO astrocytes and subjected to LC-MS/MS-based unbiased proteomics and cytokine/chemokine array. (B) Angiogenic factors detected from LC-MS/MS-based unbiased proteomics. (C) Cytokine/chemokines changed in the CM from WT and Slc4a4 KO astrocytes. Pooled CM from three independent cultures per genotype were used (D) CCL2 level was measured by ELISA in CM collected under either normal or oxygen-glucose-deprivation (OGD) condition cortices from uninjured and stroked (1 dpi) brains from WT and Slc4a4-icKO mice. Each dot represents CM or cortices collected from an individual animal. n = 3–5 per genotype. * p < 0.05, ** p < 0.01 by Student’s t test. In vivo astrocytic CCL2 expression after stroke at 4 dpi was quantified from double immunostaining. n = 17–21 cells collected from 3–5 mice per genotype. * p < 0.05 by Student’s t test. (E) Representative images of astrocytic CCL2 expression at 4 dpi by double immunostaining of CCL2/GFAP. (F and G) Endothelial CCR2 mRNA expression was visualized by RNA scope and CD31 staining and quantified by counts of CCR2+ puncta. Each dot represents an individual blood vessel. n = 49 vessels collected from 4 mice per genotype. **** p < 0.0001 by Student’s t test. (H and I) Representative images and quantification of endothelial CCR2 expression from double immunostaining. Each dot represents an individual animal. n = 4–5 per genotype. * p < 0.05 by Student’s t test. (J) Proposed model for the Slc4a4-CCL2-CCR2 axis regulating astrocyte-endothelial interaction. All data are presented as mean ± SEM.

    Article Snippet: CCR2 antagonist , Tocris , 2517/10.

    Techniques: Liquid Chromatography with Mass Spectroscopy, Enzyme-linked Immunosorbent Assay, In Vivo, Expressing, Double Immunostaining, RNAscope, Staining

    Journal: Cell reports

    Article Title: Astrocytic Slc4a4 regulates blood-brain barrier integrity in healthy and stroke brains via a CCL2-CCR2 pathway and NO dysregulation

    doi: 10.1016/j.celrep.2024.114193

    Figure Lengend Snippet:

    Article Snippet: CCR2 antagonist , Tocris , 2517/10.

    Techniques: Purification, Virus, Recombinant, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Colorimetric Assay, Mutagenesis, Software, Microscopy