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human monocyte chemoattractant protein 1  (R&D Systems)


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    Structured Review

    R&D Systems human monocyte chemoattractant protein 1
    Human retinal Müller glial cells were left untreated or treated with ultra-low molecular weight hyaluronan (ULMW-HA) (50 µg/mL) for 24 (h) (A) Protein expression of phospho-ERK1/2 and phospho-NFκB in cell lysates was determined by Western blot analysis. Levels of high mobility group box-1 (HMGB1) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate (*p < 0.05; independent t-test). (B) Human retinal Müller glial cells were left untreated or treated with ULMW-HA, ULMW-HA plus BAY11-7085 (5 µM) or (C) ULMW-HA plus U-0126 (5 µM). Levels of vascular endothelial growth factor (VEGF), angiopoietin and monocyte <t>chemotactic</t> <t>protein-1</t> <t>(MCP-1/CCL2)</t> were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells; #p < 0.05 compared with ULMW-HA plus BAY11–7085 or U-0126 treated cells. (D, E) Human retinal Müller glial cells were left untreated or treated with high glucose (HG) (25 mM), cobalt chloride (CoCl 2 ) (300 µM) or tumor necrosis factor-α (TNF-α) (5 ng/mL) with or without apigenin (10 µg/mL) for 24 (h) For HG treatment, cultures containing 25 mM mannitol were used as a control. Levels of monocyte chemotactic protein-1 (MCP-1/CCL2) (D) and vascular endothelial growth factor (VEGF) (E) were quantified in the culture media by ELISA. The results are expressed as mean ± standard deviation from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells. #p < 0.05 compared with values obtained from stimulated cells.
    Human Monocyte Chemoattractant Protein 1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 180 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/monocyte+chemoattractant+protein/Human+CCL2%2FMCP-1+DuoSet+ELISA/pmc12956526-85-31-55
    Average 96 stars, based on 180 article reviews
    human monocyte chemoattractant protein 1 - by Bioz Stars, 2026-09
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    Images

    1) Product Images from "Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy"

    Article Title: Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2026.1724199

    Human retinal Müller glial cells were left untreated or treated with ultra-low molecular weight hyaluronan (ULMW-HA) (50 µg/mL) for 24 (h) (A) Protein expression of phospho-ERK1/2 and phospho-NFκB in cell lysates was determined by Western blot analysis. Levels of high mobility group box-1 (HMGB1) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate (*p < 0.05; independent t-test). (B) Human retinal Müller glial cells were left untreated or treated with ULMW-HA, ULMW-HA plus BAY11-7085 (5 µM) or (C) ULMW-HA plus U-0126 (5 µM). Levels of vascular endothelial growth factor (VEGF), angiopoietin and monocyte chemotactic protein-1 (MCP-1/CCL2) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells; #p < 0.05 compared with ULMW-HA plus BAY11–7085 or U-0126 treated cells. (D, E) Human retinal Müller glial cells were left untreated or treated with high glucose (HG) (25 mM), cobalt chloride (CoCl 2 ) (300 µM) or tumor necrosis factor-α (TNF-α) (5 ng/mL) with or without apigenin (10 µg/mL) for 24 (h) For HG treatment, cultures containing 25 mM mannitol were used as a control. Levels of monocyte chemotactic protein-1 (MCP-1/CCL2) (D) and vascular endothelial growth factor (VEGF) (E) were quantified in the culture media by ELISA. The results are expressed as mean ± standard deviation from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells. #p < 0.05 compared with values obtained from stimulated cells.
    Figure Legend Snippet: Human retinal Müller glial cells were left untreated or treated with ultra-low molecular weight hyaluronan (ULMW-HA) (50 µg/mL) for 24 (h) (A) Protein expression of phospho-ERK1/2 and phospho-NFκB in cell lysates was determined by Western blot analysis. Levels of high mobility group box-1 (HMGB1) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate (*p < 0.05; independent t-test). (B) Human retinal Müller glial cells were left untreated or treated with ULMW-HA, ULMW-HA plus BAY11-7085 (5 µM) or (C) ULMW-HA plus U-0126 (5 µM). Levels of vascular endothelial growth factor (VEGF), angiopoietin and monocyte chemotactic protein-1 (MCP-1/CCL2) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells; #p < 0.05 compared with ULMW-HA plus BAY11–7085 or U-0126 treated cells. (D, E) Human retinal Müller glial cells were left untreated or treated with high glucose (HG) (25 mM), cobalt chloride (CoCl 2 ) (300 µM) or tumor necrosis factor-α (TNF-α) (5 ng/mL) with or without apigenin (10 µg/mL) for 24 (h) For HG treatment, cultures containing 25 mM mannitol were used as a control. Levels of monocyte chemotactic protein-1 (MCP-1/CCL2) (D) and vascular endothelial growth factor (VEGF) (E) were quantified in the culture media by ELISA. The results are expressed as mean ± standard deviation from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells. #p < 0.05 compared with values obtained from stimulated cells.

    Techniques Used: Molecular Weight, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Standard Deviation, Control



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    Human retinal Müller glial cells were left untreated or treated with ultra-low molecular weight hyaluronan (ULMW-HA) (50 µg/mL) for 24 (h) (A) Protein expression of phospho-ERK1/2 and phospho-NFκB in cell lysates was determined by Western blot analysis. Levels of high mobility group box-1 (HMGB1) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate (*p < 0.05; independent t-test). (B) Human retinal Müller glial cells were left untreated or treated with ULMW-HA, ULMW-HA plus BAY11-7085 (5 µM) or (C) ULMW-HA plus U-0126 (5 µM). Levels of vascular endothelial growth factor (VEGF), angiopoietin and monocyte <t>chemotactic</t> <t>protein-1</t> <t>(MCP-1/CCL2)</t> were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells; #p < 0.05 compared with ULMW-HA plus BAY11–7085 or U-0126 treated cells. (D, E) Human retinal Müller glial cells were left untreated or treated with high glucose (HG) (25 mM), cobalt chloride (CoCl 2 ) (300 µM) or tumor necrosis factor-α (TNF-α) (5 ng/mL) with or without apigenin (10 µg/mL) for 24 (h) For HG treatment, cultures containing 25 mM mannitol were used as a control. Levels of monocyte chemotactic protein-1 (MCP-1/CCL2) (D) and vascular endothelial growth factor (VEGF) (E) were quantified in the culture media by ELISA. The results are expressed as mean ± standard deviation from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells. #p < 0.05 compared with values obtained from stimulated cells.
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    Human retinal Müller glial cells were left untreated or treated with ultra-low molecular weight hyaluronan (ULMW-HA) (50 µg/mL) for 24 (h) (A) Protein expression of phospho-ERK1/2 and phospho-NFκB in cell lysates was determined by Western blot analysis. Levels of high mobility group box-1 (HMGB1) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate (*p < 0.05; independent t-test). (B) Human retinal Müller glial cells were left untreated or treated with ULMW-HA, ULMW-HA plus BAY11-7085 (5 µM) or (C) ULMW-HA plus U-0126 (5 µM). Levels of vascular endothelial growth factor (VEGF), angiopoietin and monocyte <t>chemotactic</t> <t>protein-1</t> <t>(MCP-1/CCL2)</t> were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells; #p < 0.05 compared with ULMW-HA plus BAY11–7085 or U-0126 treated cells. (D, E) Human retinal Müller glial cells were left untreated or treated with high glucose (HG) (25 mM), cobalt chloride (CoCl 2 ) (300 µM) or tumor necrosis factor-α (TNF-α) (5 ng/mL) with or without apigenin (10 µg/mL) for 24 (h) For HG treatment, cultures containing 25 mM mannitol were used as a control. Levels of monocyte chemotactic protein-1 (MCP-1/CCL2) (D) and vascular endothelial growth factor (VEGF) (E) were quantified in the culture media by ELISA. The results are expressed as mean ± standard deviation from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells. #p < 0.05 compared with values obtained from stimulated cells.
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    Image Search Results


    Human retinal Müller glial cells were left untreated or treated with ultra-low molecular weight hyaluronan (ULMW-HA) (50 µg/mL) for 24 (h) (A) Protein expression of phospho-ERK1/2 and phospho-NFκB in cell lysates was determined by Western blot analysis. Levels of high mobility group box-1 (HMGB1) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate (*p < 0.05; independent t-test). (B) Human retinal Müller glial cells were left untreated or treated with ULMW-HA, ULMW-HA plus BAY11-7085 (5 µM) or (C) ULMW-HA plus U-0126 (5 µM). Levels of vascular endothelial growth factor (VEGF), angiopoietin and monocyte chemotactic protein-1 (MCP-1/CCL2) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells; #p < 0.05 compared with ULMW-HA plus BAY11–7085 or U-0126 treated cells. (D, E) Human retinal Müller glial cells were left untreated or treated with high glucose (HG) (25 mM), cobalt chloride (CoCl 2 ) (300 µM) or tumor necrosis factor-α (TNF-α) (5 ng/mL) with or without apigenin (10 µg/mL) for 24 (h) For HG treatment, cultures containing 25 mM mannitol were used as a control. Levels of monocyte chemotactic protein-1 (MCP-1/CCL2) (D) and vascular endothelial growth factor (VEGF) (E) were quantified in the culture media by ELISA. The results are expressed as mean ± standard deviation from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells. #p < 0.05 compared with values obtained from stimulated cells.

    Journal: Frontiers in Immunology

    Article Title: Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy

    doi: 10.3389/fimmu.2026.1724199

    Figure Lengend Snippet: Human retinal Müller glial cells were left untreated or treated with ultra-low molecular weight hyaluronan (ULMW-HA) (50 µg/mL) for 24 (h) (A) Protein expression of phospho-ERK1/2 and phospho-NFκB in cell lysates was determined by Western blot analysis. Levels of high mobility group box-1 (HMGB1) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate (*p < 0.05; independent t-test). (B) Human retinal Müller glial cells were left untreated or treated with ULMW-HA, ULMW-HA plus BAY11-7085 (5 µM) or (C) ULMW-HA plus U-0126 (5 µM). Levels of vascular endothelial growth factor (VEGF), angiopoietin and monocyte chemotactic protein-1 (MCP-1/CCL2) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells; #p < 0.05 compared with ULMW-HA plus BAY11–7085 or U-0126 treated cells. (D, E) Human retinal Müller glial cells were left untreated or treated with high glucose (HG) (25 mM), cobalt chloride (CoCl 2 ) (300 µM) or tumor necrosis factor-α (TNF-α) (5 ng/mL) with or without apigenin (10 µg/mL) for 24 (h) For HG treatment, cultures containing 25 mM mannitol were used as a control. Levels of monocyte chemotactic protein-1 (MCP-1/CCL2) (D) and vascular endothelial growth factor (VEGF) (E) were quantified in the culture media by ELISA. The results are expressed as mean ± standard deviation from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells. #p < 0.05 compared with values obtained from stimulated cells.

    Article Snippet: Enzyme-linked immunosorbent assay (ELISA) kits for human Hyal-1 (Cat No DY7358), human Hyaluronan (Cat No DY3614-05), and human syndecan-1 (Cat No DY2780), human vascular endothelial growth factor (VEGF) (Cat No DY293B), human monocyte chemoattractant protein-1 (MCP-1/CCL2) (Cat No DY279), human matrix metalloproteinase-9 (MMP-9) (Cat No DY911) and human angiopoietin-2 (Cat No DY623) were purchased from R&D Systems.

    Techniques: Molecular Weight, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Standard Deviation, Control