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ccl5 receptor antagonist (R&D Systems)

Name: ccl5 receptor antagonist
Brand: R&D Systems
Rating: 92 (42 reviews)

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R&D Systems ccl5 receptor antagonist

<t>CCL5</t> induction in DILI patients and an AILI mouse model. a ELISA analysis of serum CCL5 levels in DILI patients (n = 15) and healthy controls (n = 15). b Representative IHC images of hepatic CCL5 expression in DILI patients and healthy controls (original magnification = ×200, scale bar = 100 μm). c Dynamic serum CCL5 levels in WT mice after APAP challenge at the indicated time points (n = 4–6). d Representative IHC images of hepatic CCL5 expression in WT mice 24 h after APAP treatment and in normal controls (original magnification = ×200, scale bar = 100 μm). e Relative Ccl5 mRNA expression was determined in liver tissues, primary hepatocytes (PMHs), and nonparenchymal cells (NPCs) 6 h after APAP treatment (n = 3–4). The data are shown as means ± SEM, *P < 0.05, ****P < 0.0001

Ccl5 Receptor Antagonist, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ccl5 receptor antagonist/product/R&D Systems
Average 92 stars, based on 42 article reviews

ccl5 receptor antagonist - by Bioz Stars, 2026-02

92/100 stars

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1) Product Images from "CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization"

Article Title: CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization

Journal: Cellular and Molecular Immunology

doi: 10.1038/s41423-019-0279-0

CCL5 induction in DILI patients and an AILI mouse model. a ELISA analysis of serum CCL5 levels in DILI patients (n = 15) and healthy controls (n = 15). b Representative IHC images of hepatic CCL5 expression in DILI patients and healthy controls (original magnification = ×200, scale bar = 100 μm). c Dynamic serum CCL5 levels in WT mice after APAP challenge at the indicated time points (n = 4–6). d Representative IHC images of hepatic CCL5 expression in WT mice 24 h after APAP treatment and in normal controls (original magnification = ×200, scale bar = 100 μm). e Relative Ccl5 mRNA expression was determined in liver tissues, primary hepatocytes (PMHs), and nonparenchymal cells (NPCs) 6 h after APAP treatment (n = 3–4). The data are shown as means ± SEM, *P < 0.05, ****P < 0.0001

Figure Legend Snippet: CCL5 induction in DILI patients and an AILI mouse model. a ELISA analysis of serum CCL5 levels in DILI patients (n = 15) and healthy controls (n = 15). b Representative IHC images of hepatic CCL5 expression in DILI patients and healthy controls (original magnification = ×200, scale bar = 100 μm). c Dynamic serum CCL5 levels in WT mice after APAP challenge at the indicated time points (n = 4–6). d Representative IHC images of hepatic CCL5 expression in WT mice 24 h after APAP treatment and in normal controls (original magnification = ×200, scale bar = 100 μm). e Relative Ccl5 mRNA expression was determined in liver tissues, primary hepatocytes (PMHs), and nonparenchymal cells (NPCs) 6 h after APAP treatment (n = 3–4). The data are shown as means ± SEM, *P < 0.05, ****P < 0.0001

Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing

Ccl5−/− mice display rapid liver recovery after APAP treatment. a–c APAP treatment in both Ccl5−/− and WT mice at the indicated time points (n = 4–6). a Serum levels of ALT/AST of both genotypes. b Representative images of H&E staining (original magnification = ×100, scale bar = 200 μm) and the statistical quantification of hepatic necrosis. c Representative images of TUNEL staining (original magnification = ×200, scale bar = 100 μm) and the statistical quantification of TUNEL-positive cells. d Survival curve of Ccl5−/− and WT mice in response to a lethal dose of APAP (n = 15). The data are shown as means ± SEM, *P < 0.05, **P < 0.01

Figure Legend Snippet: Ccl5−/− mice display rapid liver recovery after APAP treatment. a–c APAP treatment in both Ccl5−/− and WT mice at the indicated time points (n = 4–6). a Serum levels of ALT/AST of both genotypes. b Representative images of H&E staining (original magnification = ×100, scale bar = 200 μm) and the statistical quantification of hepatic necrosis. c Representative images of TUNEL staining (original magnification = ×200, scale bar = 100 μm) and the statistical quantification of TUNEL-positive cells. d Survival curve of Ccl5−/− and WT mice in response to a lethal dose of APAP (n = 15). The data are shown as means ± SEM, *P < 0.05, **P < 0.01

Techniques Used: Staining, TUNEL Assay

Enhanced inflammation resolution and liver regeneration in Ccl5−/− mice at the late phase of APAP treatment. a–e APAP treatment in both Ccl5−/− and WT mice at the indicated time points (n = 4–6). a ELISA analyses of the serum levels of IL-6 and TNFα. b Representative FACS plots and the statistical quantification of hepatic neutrophils (Ly6G+CD11b+). c Representative IHC images and the statistical quantification of hepatic Ly6G+ cells in liver sections (original magnification = ×400, scale bar = 50 μm). d Representative immunohistochemical staining of hepatic Ki67 in liver sections of Ccl5−/− and control mice at the indicated time points after APAP treatment and the quantification of Ki67-positive cells in liver sections (n = 4–6). e Western blot analysis showing the expression of hepatic PCNA in Ccl5−/− and control mice at the indicated time points after APAP treatment and the quantification of hepatic PCNA levels normalized to β-actin (n = 3–4). The data are shown as means ± SEM, *P < 0.05, **P < 0.01

Figure Legend Snippet: Enhanced inflammation resolution and liver regeneration in Ccl5−/− mice at the late phase of APAP treatment. a–e APAP treatment in both Ccl5−/− and WT mice at the indicated time points (n = 4–6). a ELISA analyses of the serum levels of IL-6 and TNFα. b Representative FACS plots and the statistical quantification of hepatic neutrophils (Ly6G+CD11b+). c Representative IHC images and the statistical quantification of hepatic Ly6G+ cells in liver sections (original magnification = ×400, scale bar = 50 μm). d Representative immunohistochemical staining of hepatic Ki67 in liver sections of Ccl5−/− and control mice at the indicated time points after APAP treatment and the quantification of Ki67-positive cells in liver sections (n = 4–6). e Western blot analysis showing the expression of hepatic PCNA in Ccl5−/− and control mice at the indicated time points after APAP treatment and the quantification of hepatic PCNA levels normalized to β-actin (n = 3–4). The data are shown as means ± SEM, *P < 0.05, **P < 0.01

Techniques Used: Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Staining, Western Blot, Expressing

Increased M2 macrophages in Ccl5−/− mice at the late phase of APAP treatment. a–d APAP treatment in both Ccl5−/− and WT mice at 36 h. a Representative MoMF (CD11bhighF4/80int) and KC (CD11bint F4/80high) profiles of CD45+ liver nongranulocytes from Ccl5−/− and WT mice 36 h after APAP treatment and the quantification of the proportion of MoMFs and KCs relative to total CD45+ liver nongranulocytes (n = 4–6). b Representative FACS plots and the statistical quantification of CD206+ hepatic macrophages (hMφ) (n = 4–6). c The relative expression of M1 markers (iNOS, IL-1β, and TNFα) and M2 markers (Arg1, Ym1, and CD206) was determined in FACS-sorted hepatic macrophages (CD45+CD11b+F4/80+) (n = 4). d Representative images and the statistical quantification of hepatic cells positive for CD68 (a panmacrophage marker) and Ym1 (an M2 macrophage marker) in liver sections (original magnification = ×400, scale bar = 50 μm). The data are shown as the means ± SEM, *P < 0.05, **P < 0.01. hMφ hepatic macrophages

Figure Legend Snippet: Increased M2 macrophages in Ccl5−/− mice at the late phase of APAP treatment. a–d APAP treatment in both Ccl5−/− and WT mice at 36 h. a Representative MoMF (CD11bhighF4/80int) and KC (CD11bint F4/80high) profiles of CD45+ liver nongranulocytes from Ccl5−/− and WT mice 36 h after APAP treatment and the quantification of the proportion of MoMFs and KCs relative to total CD45+ liver nongranulocytes (n = 4–6). b Representative FACS plots and the statistical quantification of CD206+ hepatic macrophages (hMφ) (n = 4–6). c The relative expression of M1 markers (iNOS, IL-1β, and TNFα) and M2 markers (Arg1, Ym1, and CD206) was determined in FACS-sorted hepatic macrophages (CD45+CD11b+F4/80+) (n = 4). d Representative images and the statistical quantification of hepatic cells positive for CD68 (a panmacrophage marker) and Ym1 (an M2 macrophage marker) in liver sections (original magnification = ×400, scale bar = 50 μm). The data are shown as the means ± SEM, *P < 0.05, **P < 0.01. hMφ hepatic macrophages

Techniques Used: Expressing, Marker

CCL5 directly regulates macrophage polarization. Mouse peritoneal macrophages (PMφ) and bone marrow-derived macrophages (BMMφ) were stimulated with 100 ng/ml rmCCL5 for 6 h, and the expression of M1 macrophage markers (iNOS, IL-1β, and TNFα) was detected by qPCR in PMφ (a) and BMMφ (b). PMφ and BMMφ were stimulated with 20 ng/ml IL4 and with or without 100 ng/ml rmCCL5 for 6 h, and the expression of M2 macrophage markers (Arg1, Ym1, and CD206) was detected by qPCR in PMφ (c) and BMMφ (d). PMφ and BMMφ were stimulated with 20 ng/ml IL4 and with or without 100 ng/ml rmCCL5 for 24 h, and the expression of M2 macrophage markers (Arg1, Ym1, and CD206) was detected by western blot analysis in PMφ (e) and BMMφ (f). The data are represented as the mean ± SEM of at least three independent experiments. **P < 0.01, ***P < 0.001

Figure Legend Snippet: CCL5 directly regulates macrophage polarization. Mouse peritoneal macrophages (PMφ) and bone marrow-derived macrophages (BMMφ) were stimulated with 100 ng/ml rmCCL5 for 6 h, and the expression of M1 macrophage markers (iNOS, IL-1β, and TNFα) was detected by qPCR in PMφ (a) and BMMφ (b). PMφ and BMMφ were stimulated with 20 ng/ml IL4 and with or without 100 ng/ml rmCCL5 for 6 h, and the expression of M2 macrophage markers (Arg1, Ym1, and CD206) was detected by qPCR in PMφ (c) and BMMφ (d). PMφ and BMMφ were stimulated with 20 ng/ml IL4 and with or without 100 ng/ml rmCCL5 for 24 h, and the expression of M2 macrophage markers (Arg1, Ym1, and CD206) was detected by western blot analysis in PMφ (e) and BMMφ (f). The data are represented as the mean ± SEM of at least three independent experiments. **P < 0.01, ***P < 0.001

Techniques Used: Derivative Assay, Expressing, Western Blot

CCL5 regulates macrophage polarization mainly through CCR1- and CCR5-related MAPK/NF-κB pathways. a Mouse peritoneal macrophages (PMφ) were stimulated with 100 ng/ml rmCCL5 for 0–60 min, and the signaling activation of the MAPK and NF-κB pathways was detected by western blot analysis. b PMφ were pretreated with a CCR1/3/5 antagonist separately for 1 h and then stimulated with 100 ng/ml rmCCL5 for 30 min. The signaling activation of the MAPK and NF-κB pathways was detected by western blot analysis. c PMφ were pretreated with a CCR1/3/5 antagonist separately for 1 h and then stimulated with 100 ng/ml rmCCL5 for 6 h. qPCR analysis of M1 marker and M2 marker expression was performed (n = 4). d, e Raw 264.7 cells were pretreated with control, CCR1, or CCR5 siRNA separately for 48 h. d Western blot analysis detected the knockdown of CCR1 and CCR5. siRNA-treated cells were stimulated with 100 ng/ml rmCCL5 for 30 min, and the signaling activation of the MAPK and NF-κB pathways was detected by western blot analysis. e siRNA-treated cells were stimulated with 100 ng/ml rmCCL5 for 6 h, and qPCR analysis of M1 marker and M2 marker expression was performed (n = 4). The data are shown as means ± SEM, *P < 0.05. **P < 0.01, ***P < 0.001

Figure Legend Snippet: CCL5 regulates macrophage polarization mainly through CCR1- and CCR5-related MAPK/NF-κB pathways. a Mouse peritoneal macrophages (PMφ) were stimulated with 100 ng/ml rmCCL5 for 0–60 min, and the signaling activation of the MAPK and NF-κB pathways was detected by western blot analysis. b PMφ were pretreated with a CCR1/3/5 antagonist separately for 1 h and then stimulated with 100 ng/ml rmCCL5 for 30 min. The signaling activation of the MAPK and NF-κB pathways was detected by western blot analysis. c PMφ were pretreated with a CCR1/3/5 antagonist separately for 1 h and then stimulated with 100 ng/ml rmCCL5 for 6 h. qPCR analysis of M1 marker and M2 marker expression was performed (n = 4). d, e Raw 264.7 cells were pretreated with control, CCR1, or CCR5 siRNA separately for 48 h. d Western blot analysis detected the knockdown of CCR1 and CCR5. siRNA-treated cells were stimulated with 100 ng/ml rmCCL5 for 30 min, and the signaling activation of the MAPK and NF-κB pathways was detected by western blot analysis. e siRNA-treated cells were stimulated with 100 ng/ml rmCCL5 for 6 h, and qPCR analysis of M1 marker and M2 marker expression was performed (n = 4). The data are shown as means ± SEM, *P < 0.05. **P < 0.01, ***P < 0.001

Techniques Used: Activation Assay, Western Blot, Marker, Expressing

CCL5 neutralization or inhibition facilitates liver recovery after acute liver injury. a A schematic of CCL5 inhibition by anti-CCL5 or Met-CCL5 in the APAP overdose model. The dose of anti-CCL5 and Met-CCL5 was 10 μg. b Serum levels of ALT/AST were detected after anti-CCL5- or Met-CCL5-mediated CCL5 blockage (n = 4–6). c Representative images of H&E staining (original magnification = ×100, scale bar = 200 μm) and the statistical quantification of hepatic necrosis upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition (n = 4–6). d Representative images and the statistical quantification of hepatic Ly6G+ cells in liver sections (original magnification = ×400, scale bar = 50 μm) upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition (n = 4–6). e Representative FACS plots and the statistical quantification of CD206+ hepatic macrophages (hMφ) upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition (n = 4–6). f Survival curves of mice (n = 10–12) in response to a lethal dose of APAP treatment upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition. The data are shown as means ± SEM, *P < 0.05

Figure Legend Snippet: CCL5 neutralization or inhibition facilitates liver recovery after acute liver injury. a A schematic of CCL5 inhibition by anti-CCL5 or Met-CCL5 in the APAP overdose model. The dose of anti-CCL5 and Met-CCL5 was 10 μg. b Serum levels of ALT/AST were detected after anti-CCL5- or Met-CCL5-mediated CCL5 blockage (n = 4–6). c Representative images of H&E staining (original magnification = ×100, scale bar = 200 μm) and the statistical quantification of hepatic necrosis upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition (n = 4–6). d Representative images and the statistical quantification of hepatic Ly6G+ cells in liver sections (original magnification = ×400, scale bar = 50 μm) upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition (n = 4–6). e Representative FACS plots and the statistical quantification of CD206+ hepatic macrophages (hMφ) upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition (n = 4–6). f Survival curves of mice (n = 10–12) in response to a lethal dose of APAP treatment upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition. The data are shown as means ± SEM, *P < 0.05

Techniques Used: Neutralization, Inhibition, Staining

Image Search Results

Journal: Cellular and Molecular Immunology

Article Title: CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization

doi: 10.1038/s41423-019-0279-0

Figure Lengend Snippet: CCL5 induction in DILI patients and an AILI mouse model. a ELISA analysis of serum CCL5 levels in DILI patients (n = 15) and healthy controls (n = 15). b Representative IHC images of hepatic CCL5 expression in DILI patients and healthy controls (original magnification = ×200, scale bar = 100 μm). c Dynamic serum CCL5 levels in WT mice after APAP challenge at the indicated time points (n = 4–6). d Representative IHC images of hepatic CCL5 expression in WT mice 24 h after APAP treatment and in normal controls (original magnification = ×200, scale bar = 100 μm). e Relative Ccl5 mRNA expression was determined in liver tissues, primary hepatocytes (PMHs), and nonparenchymal cells (NPCs) 6 h after APAP treatment (n = 3–4). The data are shown as means ± SEM, *P < 0.05, ****P < 0.0001

Article Snippet: To evaluate the therapeutic potential of CCL5 inhibition, a CCL5-neutralizing antibody (anti-CCL5, AF478, R&D, USA); control IgG (AB-108-C, R&D, USA); or a CCL5 receptor antagonist (Met-CCL5, 335-RM/CF, R&D, USA) were reconstituted in sterile PBS and administered to WT mice (10 μg/injection, i.p) 6 and 24 h after APAP overdose.

Techniques: Enzyme-linked Immunosorbent Assay, Expressing

Journal: Cellular and Molecular Immunology

Article Title: CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization

doi: 10.1038/s41423-019-0279-0

Figure Lengend Snippet: Ccl5−/− mice display rapid liver recovery after APAP treatment. a–c APAP treatment in both Ccl5−/− and WT mice at the indicated time points (n = 4–6). a Serum levels of ALT/AST of both genotypes. b Representative images of H&E staining (original magnification = ×100, scale bar = 200 μm) and the statistical quantification of hepatic necrosis. c Representative images of TUNEL staining (original magnification = ×200, scale bar = 100 μm) and the statistical quantification of TUNEL-positive cells. d Survival curve of Ccl5−/− and WT mice in response to a lethal dose of APAP (n = 15). The data are shown as means ± SEM, *P < 0.05, **P < 0.01

Techniques: Staining, TUNEL Assay

Journal: Cellular and Molecular Immunology

Article Title: CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization

doi: 10.1038/s41423-019-0279-0

Figure Lengend Snippet: Enhanced inflammation resolution and liver regeneration in Ccl5−/− mice at the late phase of APAP treatment. a–e APAP treatment in both Ccl5−/− and WT mice at the indicated time points (n = 4–6). a ELISA analyses of the serum levels of IL-6 and TNFα. b Representative FACS plots and the statistical quantification of hepatic neutrophils (Ly6G+CD11b+). c Representative IHC images and the statistical quantification of hepatic Ly6G+ cells in liver sections (original magnification = ×400, scale bar = 50 μm). d Representative immunohistochemical staining of hepatic Ki67 in liver sections of Ccl5−/− and control mice at the indicated time points after APAP treatment and the quantification of Ki67-positive cells in liver sections (n = 4–6). e Western blot analysis showing the expression of hepatic PCNA in Ccl5−/− and control mice at the indicated time points after APAP treatment and the quantification of hepatic PCNA levels normalized to β-actin (n = 3–4). The data are shown as means ± SEM, *P < 0.05, **P < 0.01

Techniques: Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Staining, Western Blot, Expressing

Journal: Cellular and Molecular Immunology

Article Title: CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization

doi: 10.1038/s41423-019-0279-0

Figure Lengend Snippet: Increased M2 macrophages in Ccl5−/− mice at the late phase of APAP treatment. a–d APAP treatment in both Ccl5−/− and WT mice at 36 h. a Representative MoMF (CD11bhighF4/80int) and KC (CD11bint F4/80high) profiles of CD45+ liver nongranulocytes from Ccl5−/− and WT mice 36 h after APAP treatment and the quantification of the proportion of MoMFs and KCs relative to total CD45+ liver nongranulocytes (n = 4–6). b Representative FACS plots and the statistical quantification of CD206+ hepatic macrophages (hMφ) (n = 4–6). c The relative expression of M1 markers (iNOS, IL-1β, and TNFα) and M2 markers (Arg1, Ym1, and CD206) was determined in FACS-sorted hepatic macrophages (CD45+CD11b+F4/80+) (n = 4). d Representative images and the statistical quantification of hepatic cells positive for CD68 (a panmacrophage marker) and Ym1 (an M2 macrophage marker) in liver sections (original magnification = ×400, scale bar = 50 μm). The data are shown as the means ± SEM, *P < 0.05, **P < 0.01. hMφ hepatic macrophages

Techniques: Expressing, Marker

Journal: Cellular and Molecular Immunology

Article Title: CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization

doi: 10.1038/s41423-019-0279-0

Figure Lengend Snippet: CCL5 directly regulates macrophage polarization. Mouse peritoneal macrophages (PMφ) and bone marrow-derived macrophages (BMMφ) were stimulated with 100 ng/ml rmCCL5 for 6 h, and the expression of M1 macrophage markers (iNOS, IL-1β, and TNFα) was detected by qPCR in PMφ (a) and BMMφ (b). PMφ and BMMφ were stimulated with 20 ng/ml IL4 and with or without 100 ng/ml rmCCL5 for 6 h, and the expression of M2 macrophage markers (Arg1, Ym1, and CD206) was detected by qPCR in PMφ (c) and BMMφ (d). PMφ and BMMφ were stimulated with 20 ng/ml IL4 and with or without 100 ng/ml rmCCL5 for 24 h, and the expression of M2 macrophage markers (Arg1, Ym1, and CD206) was detected by western blot analysis in PMφ (e) and BMMφ (f). The data are represented as the mean ± SEM of at least three independent experiments. **P < 0.01, ***P < 0.001

Techniques: Derivative Assay, Expressing, Western Blot

Journal: Cellular and Molecular Immunology

Article Title: CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization

doi: 10.1038/s41423-019-0279-0

Figure Lengend Snippet: CCL5 regulates macrophage polarization mainly through CCR1- and CCR5-related MAPK/NF-κB pathways. a Mouse peritoneal macrophages (PMφ) were stimulated with 100 ng/ml rmCCL5 for 0–60 min, and the signaling activation of the MAPK and NF-κB pathways was detected by western blot analysis. b PMφ were pretreated with a CCR1/3/5 antagonist separately for 1 h and then stimulated with 100 ng/ml rmCCL5 for 30 min. The signaling activation of the MAPK and NF-κB pathways was detected by western blot analysis. c PMφ were pretreated with a CCR1/3/5 antagonist separately for 1 h and then stimulated with 100 ng/ml rmCCL5 for 6 h. qPCR analysis of M1 marker and M2 marker expression was performed (n = 4). d, e Raw 264.7 cells were pretreated with control, CCR1, or CCR5 siRNA separately for 48 h. d Western blot analysis detected the knockdown of CCR1 and CCR5. siRNA-treated cells were stimulated with 100 ng/ml rmCCL5 for 30 min, and the signaling activation of the MAPK and NF-κB pathways was detected by western blot analysis. e siRNA-treated cells were stimulated with 100 ng/ml rmCCL5 for 6 h, and qPCR analysis of M1 marker and M2 marker expression was performed (n = 4). The data are shown as means ± SEM, *P < 0.05. **P < 0.01, ***P < 0.001

Techniques: Activation Assay, Western Blot, Marker, Expressing

Journal: Cellular and Molecular Immunology

Article Title: CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization

doi: 10.1038/s41423-019-0279-0

Figure Lengend Snippet: CCL5 neutralization or inhibition facilitates liver recovery after acute liver injury. a A schematic of CCL5 inhibition by anti-CCL5 or Met-CCL5 in the APAP overdose model. The dose of anti-CCL5 and Met-CCL5 was 10 μg. b Serum levels of ALT/AST were detected after anti-CCL5- or Met-CCL5-mediated CCL5 blockage (n = 4–6). c Representative images of H&E staining (original magnification = ×100, scale bar = 200 μm) and the statistical quantification of hepatic necrosis upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition (n = 4–6). d Representative images and the statistical quantification of hepatic Ly6G+ cells in liver sections (original magnification = ×400, scale bar = 50 μm) upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition (n = 4–6). e Representative FACS plots and the statistical quantification of CD206+ hepatic macrophages (hMφ) upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition (n = 4–6). f Survival curves of mice (n = 10–12) in response to a lethal dose of APAP treatment upon anti-CCL5- or Met-CCL5-mediated CCL5 inhibition. The data are shown as means ± SEM, *P < 0.05

Techniques: Neutralization, Inhibition, Staining

CCL5/CCR1 axis mediates hMSC-enhanced metastatic phenotype. ( a ) The concentration of CCL5 in CM or TCM was determined by ELISA assay from three independent experiments. *** P <0.001 versus control group; ( b ) after 24 h of scrambled or ccl5 siRNA treatment, hMSCs were treated with 10 ng/ml TNF- α for 24 h and collected for TCM. SW1116 cells were plated in the upper chamber and evaluated their migratory ability toward TCM by transwell assay. Quantification was presented as mean±S.D. from three independent experiments. * P <0.05; ** P <0.01, NS, no significance; ( c ) real-time PCR analysis of ccr expression in SW1116 cells treated with CM or TCM for 24 h. Data are presented as the means±S.D. n =3. * P <0.05; ** P <0.01; ( d ) The effect of CCR1 antagonist BX471 on TCM- or CCL5-induced migration was determined by transwell assay. 2 μ M BX471 was added into SW1116 cells and seeded in the upper chamber, TCM or 20 ng/ml CCL5 were added in the lower chamber. Quantification was presented as mean±S.D. from three independent experiments.* P <0.05,** P <0.01; ( e ) 2 μ M BX471 was added simultaneously with 20 ng/ml CCL5 into SW1116, the expression of EMT markers was determined by real-time PCR. Data are presented as the means±S.D., n =3. * P <0.05, ** P <0.01, *** P <0.001

Journal: Cell Death & Disease

Article Title: Human MSCs promotes colorectal cancer epithelial–mesenchymal transition and progression via CCL5/ β -catenin/Slug pathway

doi: 10.1038/cddis.2017.138

Figure Lengend Snippet: CCL5/CCR1 axis mediates hMSC-enhanced metastatic phenotype. ( a ) The concentration of CCL5 in CM or TCM was determined by ELISA assay from three independent experiments. *** P <0.001 versus control group; ( b ) after 24 h of scrambled or ccl5 siRNA treatment, hMSCs were treated with 10 ng/ml TNF- α for 24 h and collected for TCM. SW1116 cells were plated in the upper chamber and evaluated their migratory ability toward TCM by transwell assay. Quantification was presented as mean±S.D. from three independent experiments. * P <0.05; ** P <0.01, NS, no significance; ( c ) real-time PCR analysis of ccr expression in SW1116 cells treated with CM or TCM for 24 h. Data are presented as the means±S.D. n =3. * P <0.05; ** P <0.01; ( d ) The effect of CCR1 antagonist BX471 on TCM- or CCL5-induced migration was determined by transwell assay. 2 μ M BX471 was added into SW1116 cells and seeded in the upper chamber, TCM or 20 ng/ml CCL5 were added in the lower chamber. Quantification was presented as mean±S.D. from three independent experiments.* P <0.05,** P <0.01; ( e ) 2 μ M BX471 was added simultaneously with 20 ng/ml CCL5 into SW1116, the expression of EMT markers was determined by real-time PCR. Data are presented as the means±S.D., n =3. * P <0.05, ** P <0.01, *** P <0.001

Article Snippet: To determine the role of CCL5/CCR1/ β -catenin signaling in CRC progression, SW1116 were seeded into the upper chambers of transwell together with CCL5 receptor antagonists BX471 (Sigma, sml0020) or Wnt inhibitor DKK1 (R&D, 5439-DK) and evaluated for migratory ability.

Techniques: Concentration Assay, Enzyme-linked Immunosorbent Assay, Transwell Assay, Real-time Polymerase Chain Reaction, Expressing, Migration

CCL5 activates Slug in colon cancer cells. ( a ) After Scrambled or Slug siRNA treatment, the SW1116 cells were exposed to TCM or 20 ng/ml for 24 h. The expression of Slug was determined by real-time PCR analysis in SW1116. Data are presented as the means±S.D. n =3. * P <0.05, *** P <0.001; ( b ) The expression of Slug was determined by western blot analysis in SW1116 treated with TCM or 20 ng/ml CCL5 for 24 h. Data are presented as the means±S.D. n =3. ** P <0.01, *** P <0.001. Representative blot was shown below; ( c ) After 24 hours of Scrambled or Slug siRNA treatment, SW1116 cells were seeded in the upper chamber and examined their migratory capability to TCM or CCL5. Quantification was presented as mean±S.D. from three independent experiments. * P <0.05; ** P <0.01; ( d ) After 24 h of Scrambled or ccl5 siRNA treatment, hMSCs were treated with 10 ng/ml TNF- α for 24 h and collected for TCM. SW1116 cells were treated with TCM for 24 h and examined for Slug expression by real-time PCR. Data are presented as the means±S.D. n =3. * P <0.05, *** P <0.001

Journal: Cell Death & Disease

Article Title: Human MSCs promotes colorectal cancer epithelial–mesenchymal transition and progression via CCL5/ β -catenin/Slug pathway

doi: 10.1038/cddis.2017.138

Figure Lengend Snippet: CCL5 activates Slug in colon cancer cells. ( a ) After Scrambled or Slug siRNA treatment, the SW1116 cells were exposed to TCM or 20 ng/ml for 24 h. The expression of Slug was determined by real-time PCR analysis in SW1116. Data are presented as the means±S.D. n =3. * P <0.05, *** P <0.001; ( b ) The expression of Slug was determined by western blot analysis in SW1116 treated with TCM or 20 ng/ml CCL5 for 24 h. Data are presented as the means±S.D. n =3. ** P <0.01, *** P <0.001. Representative blot was shown below; ( c ) After 24 hours of Scrambled or Slug siRNA treatment, SW1116 cells were seeded in the upper chamber and examined their migratory capability to TCM or CCL5. Quantification was presented as mean±S.D. from three independent experiments. * P <0.05; ** P <0.01; ( d ) After 24 h of Scrambled or ccl5 siRNA treatment, hMSCs were treated with 10 ng/ml TNF- α for 24 h and collected for TCM. SW1116 cells were treated with TCM for 24 h and examined for Slug expression by real-time PCR. Data are presented as the means±S.D. n =3. * P <0.05, *** P <0.001

Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot

CCL5 activates β -catenin pathway. ( a ) The expression of β -catenin was determined by real-time PCR in SW1116 cells treated with CM/TCM or 20 ng/ml CCL5 for 24 hours. * P <0.05, *** P <0.001 versus control group; ( b , c ) The nuclear expression of β -catenin was determined by western blot in SW1116 cells treated with CM/TCM ( b ) or 20 ng/ml CCL5 ( c ) for 24 hours. ** P <0.01, *** P <0.001 versus control group. Representative blots were shown in above; ( d ) The effect of Wnt/ β -catenin inhibitor DKK1 on TCM- or CCL5-induced migration was determined by transwell assay. 2 μ M DKK1 was added into SW1116 cells and seeded in the upper chamber, TCM or 20 ng/ml CCL5 were added in the lower chamber. Quantification was presented as mean±S.D. from three independent experiments. * P <0.05, *** P <0.001; ( e , f ) 2 μ M DKK1 was added simultaneously with 20 ng/ml CCL5 or TCM into SW1116, the expression of Slug was determined by real-time PCR ( e ) or western blot ( f ). Data are presented as the means±S.D., n =3. * P <0.05, ** P <0.01, *** P <0.001. Representative blot was shown in below f

Journal: Cell Death & Disease

Article Title: Human MSCs promotes colorectal cancer epithelial–mesenchymal transition and progression via CCL5/ β -catenin/Slug pathway

doi: 10.1038/cddis.2017.138

Figure Lengend Snippet: CCL5 activates β -catenin pathway. ( a ) The expression of β -catenin was determined by real-time PCR in SW1116 cells treated with CM/TCM or 20 ng/ml CCL5 for 24 hours. * P <0.05, *** P <0.001 versus control group; ( b , c ) The nuclear expression of β -catenin was determined by western blot in SW1116 cells treated with CM/TCM ( b ) or 20 ng/ml CCL5 ( c ) for 24 hours. ** P <0.01, *** P <0.001 versus control group. Representative blots were shown in above; ( d ) The effect of Wnt/ β -catenin inhibitor DKK1 on TCM- or CCL5-induced migration was determined by transwell assay. 2 μ M DKK1 was added into SW1116 cells and seeded in the upper chamber, TCM or 20 ng/ml CCL5 were added in the lower chamber. Quantification was presented as mean±S.D. from three independent experiments. * P <0.05, *** P <0.001; ( e , f ) 2 μ M DKK1 was added simultaneously with 20 ng/ml CCL5 or TCM into SW1116, the expression of Slug was determined by real-time PCR ( e ) or western blot ( f ). Data are presented as the means±S.D., n =3. * P <0.05, ** P <0.01, *** P <0.001. Representative blot was shown in below f

Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Migration, Transwell Assay

hMSCs promote CRC development and EMT in vivo BALB/C mice were subcutaneously injected with 1 × 10 7 HT29 cells mixed with 1x10 7 hMSCs ( n =4) or alone ( n =5). ( a ) The tumors were excised after 2 weeks, and tumor average size and tumor volume in xenograft model were measured. ** P <0.01, versus PBS group; ( b ) H&E staining and immunohistochemical staining for PCNA (proliferating cell nuclear antigen) of xenograft tumors from either HT29 alone or co-injection group; quantification data are from at least five high fields. * P <0.05. Scale bar, 50 μ m and 100 μ m; ( c ) immunohistochemical staining for EMT markers (E-cadherin and Vimentin), β -catenin and Slug. Scale bar, 100 μ m; ( d ). The expression of CCL5 is increased in nude mice injected with HT29 and hMSCs. Tumor tissues were collected from mice injected with HT29 alone or HT29 with hMSCs. RNA was extracted and determined for expression of CCL5 by real-time PCR. Data are presented as the means±S.D. n =3 * P <0.05 versus control

Journal: Cell Death & Disease

Article Title: Human MSCs promotes colorectal cancer epithelial–mesenchymal transition and progression via CCL5/ β -catenin/Slug pathway

doi: 10.1038/cddis.2017.138

Figure Lengend Snippet: hMSCs promote CRC development and EMT in vivo BALB/C mice were subcutaneously injected with 1 × 10 7 HT29 cells mixed with 1x10 7 hMSCs ( n =4) or alone ( n =5). ( a ) The tumors were excised after 2 weeks, and tumor average size and tumor volume in xenograft model were measured. ** P <0.01, versus PBS group; ( b ) H&E staining and immunohistochemical staining for PCNA (proliferating cell nuclear antigen) of xenograft tumors from either HT29 alone or co-injection group; quantification data are from at least five high fields. * P <0.05. Scale bar, 50 μ m and 100 μ m; ( c ) immunohistochemical staining for EMT markers (E-cadherin and Vimentin), β -catenin and Slug. Scale bar, 100 μ m; ( d ). The expression of CCL5 is increased in nude mice injected with HT29 and hMSCs. Tumor tissues were collected from mice injected with HT29 alone or HT29 with hMSCs. RNA was extracted and determined for expression of CCL5 by real-time PCR. Data are presented as the means±S.D. n =3 * P <0.05 versus control

Techniques: In Vivo, Injection, Staining, Immunohistochemical staining, Expressing, Real-time Polymerase Chain Reaction

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