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c5ar1 antagonist pmx205  (Tocris)


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    Tocris c5ar1 antagonist pmx205
    (A) Experimental design of permanent left anterior descending (LAD) coronary artery ligation in Pf4^cre+^ <t>C5ar1^fl/fl^</t> mice and Cre-negative littermate controls, followed by serial echocardiography and terminal analyses up to day 14. (B) Representative transverse left ventricular sections stained with TTC on day 14 after myocardial infarction, with infarcted myocardium appearing white and viable myocardium appearing red. Infarcted areas are indicated by a solid white outline (scale bar = 2 mm). (C) Quantification of infarct size expressed as percentage of left ventricle (LV). (D) Representative M-mode echocardiographic images. (E) Echocardiographic assessment of left ventricular ejection fraction (EF; left) and fractional shortening (FS; right) on day 1 and day 13 after myocardial infarction. (F) Representative immunofluorescence images of collagen I (red) and DNA (DAPI, blue) on day 14. (G) Quantification of collagen I–positive area (collagen I, % of LV section). (H) Representative CD31 (green) immunostaining with DNA staining (DAPI, blue) in the peri-infarct region on day 14. (I) Quantification of capillary density (CD31-positive area, %). Data are shown as mean ± SD; each dot represents one mouse. n = 4 mice per group for TTC and immunofluorescence analyses; n = 9–10 mice per group for echocardiography. Statistical analysis was performed using one-way ANOVA for EF and FS and two-tailed unpaired t-tests for all other comparisons. P < 0.05, P < 0.01, P < 0.001.
    C5ar1 Antagonist Pmx205, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 25 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pmx+205/PMX+205/bio_rxiv__64898__2026__01__12__699090-142-10-13
    Average 94 stars, based on 25 article reviews
    c5ar1 antagonist pmx205 - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Platelet C5aR1 Aggravates Myocardial Infarction through Platelet–Neutrophil Interactions and CXCL4-Dependent NET Release"

    Article Title: Platelet C5aR1 Aggravates Myocardial Infarction through Platelet–Neutrophil Interactions and CXCL4-Dependent NET Release

    Journal: bioRxiv

    doi: 10.64898/2026.01.12.699090

    (A) Experimental design of permanent left anterior descending (LAD) coronary artery ligation in Pf4^cre+^ C5ar1^fl/fl^ mice and Cre-negative littermate controls, followed by serial echocardiography and terminal analyses up to day 14. (B) Representative transverse left ventricular sections stained with TTC on day 14 after myocardial infarction, with infarcted myocardium appearing white and viable myocardium appearing red. Infarcted areas are indicated by a solid white outline (scale bar = 2 mm). (C) Quantification of infarct size expressed as percentage of left ventricle (LV). (D) Representative M-mode echocardiographic images. (E) Echocardiographic assessment of left ventricular ejection fraction (EF; left) and fractional shortening (FS; right) on day 1 and day 13 after myocardial infarction. (F) Representative immunofluorescence images of collagen I (red) and DNA (DAPI, blue) on day 14. (G) Quantification of collagen I–positive area (collagen I, % of LV section). (H) Representative CD31 (green) immunostaining with DNA staining (DAPI, blue) in the peri-infarct region on day 14. (I) Quantification of capillary density (CD31-positive area, %). Data are shown as mean ± SD; each dot represents one mouse. n = 4 mice per group for TTC and immunofluorescence analyses; n = 9–10 mice per group for echocardiography. Statistical analysis was performed using one-way ANOVA for EF and FS and two-tailed unpaired t-tests for all other comparisons. P < 0.05, P < 0.01, P < 0.001.
    Figure Legend Snippet: (A) Experimental design of permanent left anterior descending (LAD) coronary artery ligation in Pf4^cre+^ C5ar1^fl/fl^ mice and Cre-negative littermate controls, followed by serial echocardiography and terminal analyses up to day 14. (B) Representative transverse left ventricular sections stained with TTC on day 14 after myocardial infarction, with infarcted myocardium appearing white and viable myocardium appearing red. Infarcted areas are indicated by a solid white outline (scale bar = 2 mm). (C) Quantification of infarct size expressed as percentage of left ventricle (LV). (D) Representative M-mode echocardiographic images. (E) Echocardiographic assessment of left ventricular ejection fraction (EF; left) and fractional shortening (FS; right) on day 1 and day 13 after myocardial infarction. (F) Representative immunofluorescence images of collagen I (red) and DNA (DAPI, blue) on day 14. (G) Quantification of collagen I–positive area (collagen I, % of LV section). (H) Representative CD31 (green) immunostaining with DNA staining (DAPI, blue) in the peri-infarct region on day 14. (I) Quantification of capillary density (CD31-positive area, %). Data are shown as mean ± SD; each dot represents one mouse. n = 4 mice per group for TTC and immunofluorescence analyses; n = 9–10 mice per group for echocardiography. Statistical analysis was performed using one-way ANOVA for EF and FS and two-tailed unpaired t-tests for all other comparisons. P < 0.05, P < 0.01, P < 0.001.

    Techniques Used: Ligation, Staining, Immunofluorescence, Immunostaining, Two Tailed Test

    (A) Representative immunofluorescence images of peri-infarct myocardium stained for Ly6G (red) and CD42b (green) with DNA staining (DAPI, blue), showing myocardial platelet–neutrophil complexes (PNCs). (B) Quantification of myocardial PNC density (mm⁻²) in the peri-infarct region (see also Supplementary Figure 10 for platelet and neutrophil infiltration). (C) Representative immunofluorescence images of peri-infarct myocardium stained for myeloperoxidase (MPO, red) and citrullinated histone H3 (H3Cit, green) with DNA (DAPI, blue), showing neutrophil extracellular traps (NETs). (D) Quantification of NET burden expressed as percentage of H3Cit⁺ area of the left ventricle (LV). (E) Flow cytometric gating strategy for platelet–neutrophil complexes (PNCs) in whole blood. Neutrophils were identified by Ly6G, and PNCs were defined as Ly6G⁺CD42b⁺ events. (F) Circulating PNCs expressed as percentage of CD42b⁺ events among Ly6G⁺ neutrophils on day 1 and day 14 after myocardial infarction in Pf4^cre+ C5ar1^fl/fl mice and Cre-negative littermate controls. (G) Spearman correlation analysis demonstrating an inverse relationship between circulating PNCs on day 1 after myocardial infarction and myocardial PNC density on day 14 across individual mice (r = −0.83, P = 0.02). Data are shown as mean ± SD; each dot represents one mouse. n = 4 mice per group for immunofluorescence analyses (A–D) and n = 9 mice per group for flow cytometric analyses (E–F). Statistical analysis was performed using two-tailed unpaired t-tests for immunofluorescence data, one-way ANOVA for flow cytometric analyses, and Spearman’s rank correlation for association analysis (G). P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 20 µm (A) and 10 µm (C).
    Figure Legend Snippet: (A) Representative immunofluorescence images of peri-infarct myocardium stained for Ly6G (red) and CD42b (green) with DNA staining (DAPI, blue), showing myocardial platelet–neutrophil complexes (PNCs). (B) Quantification of myocardial PNC density (mm⁻²) in the peri-infarct region (see also Supplementary Figure 10 for platelet and neutrophil infiltration). (C) Representative immunofluorescence images of peri-infarct myocardium stained for myeloperoxidase (MPO, red) and citrullinated histone H3 (H3Cit, green) with DNA (DAPI, blue), showing neutrophil extracellular traps (NETs). (D) Quantification of NET burden expressed as percentage of H3Cit⁺ area of the left ventricle (LV). (E) Flow cytometric gating strategy for platelet–neutrophil complexes (PNCs) in whole blood. Neutrophils were identified by Ly6G, and PNCs were defined as Ly6G⁺CD42b⁺ events. (F) Circulating PNCs expressed as percentage of CD42b⁺ events among Ly6G⁺ neutrophils on day 1 and day 14 after myocardial infarction in Pf4^cre+ C5ar1^fl/fl mice and Cre-negative littermate controls. (G) Spearman correlation analysis demonstrating an inverse relationship between circulating PNCs on day 1 after myocardial infarction and myocardial PNC density on day 14 across individual mice (r = −0.83, P = 0.02). Data are shown as mean ± SD; each dot represents one mouse. n = 4 mice per group for immunofluorescence analyses (A–D) and n = 9 mice per group for flow cytometric analyses (E–F). Statistical analysis was performed using two-tailed unpaired t-tests for immunofluorescence data, one-way ANOVA for flow cytometric analyses, and Spearman’s rank correlation for association analysis (G). P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 20 µm (A) and 10 µm (C).

    Techniques Used: Immunofluorescence, Staining, Two Tailed Test

    (A) Representative single-plane confocal immunofluorescence images of fixed and permeabilized resting wild-type (WT) and C5aR1-deficient platelets stained for P-selectin (CD62P, green) and CXCL4 (red), illustrating altered α-granule organization. (B) Quantification of intracellular α-granule content per platelet, expressed as total area of P-selectin–positive granules and colocalized P-selectin/CXCL4 granules, measured by confocal microscopy. Data are shown as individual platelet values pooled from n = 3 independent experiments. Outliers were identified and removed using the ROUT method (Q = 1%) prior to analysis. (C) Flow cytometric analysis of platelet surface P-selectin expression 24 h after myocardial infarction following ex vivo stimulation of whole blood with 100 nM phorbol 12-myristate 13-acetate (PMA), expressed as geometric mean fluorescence intensity (GMFI) of CD42b⁺ platelets. (D) Flow cytometric analysis of platelet integrin GPIIb/IIIa activation under the same conditions, expressed as percentage of activated GPIIb/IIIa among CD42b⁺ platelets. (E) Plasma CXCL4 concentrations after MI in Pf4^cre+^ C5aR1^fl/fl^ mice and Cre-negative littermate controls. (F) Schematic of the in vitro platelet–neutrophil co-incubation assay. WT or C5aR1-deficient platelets were stimulated with C5a and co-incubated with neutrophils, followed by confocal immunofluorescence staining for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI) to assess NET formation, in the presence or absence of low-dose heparin or recombinant CXCL4 (rCXCL4). (G) Representative immunofluorescence images of neutrophils after co-incubation, stained for MPO (red), H3Cit (green), and DNA (DAPI, blue), illustrating NET formation under the indicated conditions (see Supplementary Figure 13 for neutrophil-intrinsic and platelet-mediated control conditions). (H) Quantification of NET formation expressed as percentage of H3Cit⁺ neutrophils. Data are shown as mean ± SD unless otherwise indicated; each dot represents one biological replicate or mouse, as indicated. For α-granule analyses (A–B), data are shown as individual platelet values pooled from n = 3 independent experiments and analyzed using two-tailed unpaired t-tests following ROUT-based outlier exclusion (Q = 1%). Flow cytometry data (C–D) were analyzed using one-way ANOVA across time points and genotypes (see also Supplementary Figures for day 14 analyses). Plasma CXCL4 measurements (E) were analyzed using two-tailed unpaired t-tests. NET formation assays (H) were analyzed using one-way ANOVA with appropriate post hoc correction. P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 2 µm (A) and 20 µm (G).
    Figure Legend Snippet: (A) Representative single-plane confocal immunofluorescence images of fixed and permeabilized resting wild-type (WT) and C5aR1-deficient platelets stained for P-selectin (CD62P, green) and CXCL4 (red), illustrating altered α-granule organization. (B) Quantification of intracellular α-granule content per platelet, expressed as total area of P-selectin–positive granules and colocalized P-selectin/CXCL4 granules, measured by confocal microscopy. Data are shown as individual platelet values pooled from n = 3 independent experiments. Outliers were identified and removed using the ROUT method (Q = 1%) prior to analysis. (C) Flow cytometric analysis of platelet surface P-selectin expression 24 h after myocardial infarction following ex vivo stimulation of whole blood with 100 nM phorbol 12-myristate 13-acetate (PMA), expressed as geometric mean fluorescence intensity (GMFI) of CD42b⁺ platelets. (D) Flow cytometric analysis of platelet integrin GPIIb/IIIa activation under the same conditions, expressed as percentage of activated GPIIb/IIIa among CD42b⁺ platelets. (E) Plasma CXCL4 concentrations after MI in Pf4^cre+^ C5aR1^fl/fl^ mice and Cre-negative littermate controls. (F) Schematic of the in vitro platelet–neutrophil co-incubation assay. WT or C5aR1-deficient platelets were stimulated with C5a and co-incubated with neutrophils, followed by confocal immunofluorescence staining for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI) to assess NET formation, in the presence or absence of low-dose heparin or recombinant CXCL4 (rCXCL4). (G) Representative immunofluorescence images of neutrophils after co-incubation, stained for MPO (red), H3Cit (green), and DNA (DAPI, blue), illustrating NET formation under the indicated conditions (see Supplementary Figure 13 for neutrophil-intrinsic and platelet-mediated control conditions). (H) Quantification of NET formation expressed as percentage of H3Cit⁺ neutrophils. Data are shown as mean ± SD unless otherwise indicated; each dot represents one biological replicate or mouse, as indicated. For α-granule analyses (A–B), data are shown as individual platelet values pooled from n = 3 independent experiments and analyzed using two-tailed unpaired t-tests following ROUT-based outlier exclusion (Q = 1%). Flow cytometry data (C–D) were analyzed using one-way ANOVA across time points and genotypes (see also Supplementary Figures for day 14 analyses). Plasma CXCL4 measurements (E) were analyzed using two-tailed unpaired t-tests. NET formation assays (H) were analyzed using one-way ANOVA with appropriate post hoc correction. P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 2 µm (A) and 20 µm (G).

    Techniques Used: Immunofluorescence, Staining, Confocal Microscopy, Expressing, Ex Vivo, Fluorescence, Activation Assay, Clinical Proteomics, In Vitro, Incubation, Recombinant, Control, Two Tailed Test, Flow Cytometry

    (A) Experimental design for daily subcutaneous administration of the C5aR1 inhibitor PMX205 or PBS for 14 days following permanent left anterior descending (LAD) coronary artery ligation. (B) Representative TTC-stained transverse left ventricular sections on day 14 after myocardial infarction, with infarcted myocardium appearing white and viable myocardium appearing red. Infarcted areas are indicated by a solid white outline (left). Corresponding quantification of infarct size, expressed as percentage of left ventricular (LV) area (right). (C) Quantification of collagen I–positive area in immunofluorescence staining, expressed as percentage of LV area. (D) Representative M-mode echocardiographic images on day 13 after myocardial infarction. (E) Echocardiographic assessment of left ventricular ejection fraction (EF; left) and fractional shortening (FS; right) on day 1 and day 13 after myocardial infarction. (F) Representative immunofluorescence images of peri-infarct myocardium stained for Ly6G (red) and CD42b (green) with DNA (DAPI, blue), illustrating myocardial platelet–neutrophil complexes (PNCs). (G) Quantification of myocardial PNC density (mm⁻²). (H) Quantification of myocardial NET burden expressed as percentage of H3Cit⁺ neutrophils. (I) Representative immunofluorescence images of peri-infarct myocardium stained for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI), illustrating NET deposition. (J) Representative flow cytometry plots of platelet surface P-selectin expression and activated GPIIb/IIIa (αIIbβ3) in PMA-stimulated whole blood 24 h after myocardial infarction. (K) Quantification of platelet surface P-selectin expression in PMA-stimulated whole blood 24 h after myocardial infarction. (L) Quantification of platelet GPIIb/IIIa activation in PMA-stimulated whole blood 24 h after myocardial infarction. Data are shown as mean ± SD; each dot represents one mouse. Statistical analysis was performed using two-tailed unpaired t-tests for infarct size and collagen I quantification (B, C) and for myocardial PNC and NET quantification (G, H). Echocardiographic parameters (E) and flow cytometric platelet activation analyses (K, L) were analyzed using one-way ANOVA across time points and treatment groups (see also Supplementary Information for day 14 analyses). P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Gating strategies are provided in the Supplementary Information. Scale bars, 2 mm (B) and 20 µm (F, I).
    Figure Legend Snippet: (A) Experimental design for daily subcutaneous administration of the C5aR1 inhibitor PMX205 or PBS for 14 days following permanent left anterior descending (LAD) coronary artery ligation. (B) Representative TTC-stained transverse left ventricular sections on day 14 after myocardial infarction, with infarcted myocardium appearing white and viable myocardium appearing red. Infarcted areas are indicated by a solid white outline (left). Corresponding quantification of infarct size, expressed as percentage of left ventricular (LV) area (right). (C) Quantification of collagen I–positive area in immunofluorescence staining, expressed as percentage of LV area. (D) Representative M-mode echocardiographic images on day 13 after myocardial infarction. (E) Echocardiographic assessment of left ventricular ejection fraction (EF; left) and fractional shortening (FS; right) on day 1 and day 13 after myocardial infarction. (F) Representative immunofluorescence images of peri-infarct myocardium stained for Ly6G (red) and CD42b (green) with DNA (DAPI, blue), illustrating myocardial platelet–neutrophil complexes (PNCs). (G) Quantification of myocardial PNC density (mm⁻²). (H) Quantification of myocardial NET burden expressed as percentage of H3Cit⁺ neutrophils. (I) Representative immunofluorescence images of peri-infarct myocardium stained for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI), illustrating NET deposition. (J) Representative flow cytometry plots of platelet surface P-selectin expression and activated GPIIb/IIIa (αIIbβ3) in PMA-stimulated whole blood 24 h after myocardial infarction. (K) Quantification of platelet surface P-selectin expression in PMA-stimulated whole blood 24 h after myocardial infarction. (L) Quantification of platelet GPIIb/IIIa activation in PMA-stimulated whole blood 24 h after myocardial infarction. Data are shown as mean ± SD; each dot represents one mouse. Statistical analysis was performed using two-tailed unpaired t-tests for infarct size and collagen I quantification (B, C) and for myocardial PNC and NET quantification (G, H). Echocardiographic parameters (E) and flow cytometric platelet activation analyses (K, L) were analyzed using one-way ANOVA across time points and treatment groups (see also Supplementary Information for day 14 analyses). P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Gating strategies are provided in the Supplementary Information. Scale bars, 2 mm (B) and 20 µm (F, I).

    Techniques Used: Ligation, Staining, Immunofluorescence, Flow Cytometry, Expressing, Activation Assay, Two Tailed Test



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    Image Search Results


    (A) Experimental design of permanent left anterior descending (LAD) coronary artery ligation in Pf4^cre+^ C5ar1^fl/fl^ mice and Cre-negative littermate controls, followed by serial echocardiography and terminal analyses up to day 14. (B) Representative transverse left ventricular sections stained with TTC on day 14 after myocardial infarction, with infarcted myocardium appearing white and viable myocardium appearing red. Infarcted areas are indicated by a solid white outline (scale bar = 2 mm). (C) Quantification of infarct size expressed as percentage of left ventricle (LV). (D) Representative M-mode echocardiographic images. (E) Echocardiographic assessment of left ventricular ejection fraction (EF; left) and fractional shortening (FS; right) on day 1 and day 13 after myocardial infarction. (F) Representative immunofluorescence images of collagen I (red) and DNA (DAPI, blue) on day 14. (G) Quantification of collagen I–positive area (collagen I, % of LV section). (H) Representative CD31 (green) immunostaining with DNA staining (DAPI, blue) in the peri-infarct region on day 14. (I) Quantification of capillary density (CD31-positive area, %). Data are shown as mean ± SD; each dot represents one mouse. n = 4 mice per group for TTC and immunofluorescence analyses; n = 9–10 mice per group for echocardiography. Statistical analysis was performed using one-way ANOVA for EF and FS and two-tailed unpaired t-tests for all other comparisons. P < 0.05, P < 0.01, P < 0.001.

    Journal: bioRxiv

    Article Title: Platelet C5aR1 Aggravates Myocardial Infarction through Platelet–Neutrophil Interactions and CXCL4-Dependent NET Release

    doi: 10.64898/2026.01.12.699090

    Figure Lengend Snippet: (A) Experimental design of permanent left anterior descending (LAD) coronary artery ligation in Pf4^cre+^ C5ar1^fl/fl^ mice and Cre-negative littermate controls, followed by serial echocardiography and terminal analyses up to day 14. (B) Representative transverse left ventricular sections stained with TTC on day 14 after myocardial infarction, with infarcted myocardium appearing white and viable myocardium appearing red. Infarcted areas are indicated by a solid white outline (scale bar = 2 mm). (C) Quantification of infarct size expressed as percentage of left ventricle (LV). (D) Representative M-mode echocardiographic images. (E) Echocardiographic assessment of left ventricular ejection fraction (EF; left) and fractional shortening (FS; right) on day 1 and day 13 after myocardial infarction. (F) Representative immunofluorescence images of collagen I (red) and DNA (DAPI, blue) on day 14. (G) Quantification of collagen I–positive area (collagen I, % of LV section). (H) Representative CD31 (green) immunostaining with DNA staining (DAPI, blue) in the peri-infarct region on day 14. (I) Quantification of capillary density (CD31-positive area, %). Data are shown as mean ± SD; each dot represents one mouse. n = 4 mice per group for TTC and immunofluorescence analyses; n = 9–10 mice per group for echocardiography. Statistical analysis was performed using one-way ANOVA for EF and FS and two-tailed unpaired t-tests for all other comparisons. P < 0.05, P < 0.01, P < 0.001.

    Article Snippet: For pharmacological inhibition experiments, wild-type mice only received the selective C5aR1 antagonist PMX205 (Tocris) or PBS vehicle.

    Techniques: Ligation, Staining, Immunofluorescence, Immunostaining, Two Tailed Test

    (A) Representative immunofluorescence images of peri-infarct myocardium stained for Ly6G (red) and CD42b (green) with DNA staining (DAPI, blue), showing myocardial platelet–neutrophil complexes (PNCs). (B) Quantification of myocardial PNC density (mm⁻²) in the peri-infarct region (see also Supplementary Figure 10 for platelet and neutrophil infiltration). (C) Representative immunofluorescence images of peri-infarct myocardium stained for myeloperoxidase (MPO, red) and citrullinated histone H3 (H3Cit, green) with DNA (DAPI, blue), showing neutrophil extracellular traps (NETs). (D) Quantification of NET burden expressed as percentage of H3Cit⁺ area of the left ventricle (LV). (E) Flow cytometric gating strategy for platelet–neutrophil complexes (PNCs) in whole blood. Neutrophils were identified by Ly6G, and PNCs were defined as Ly6G⁺CD42b⁺ events. (F) Circulating PNCs expressed as percentage of CD42b⁺ events among Ly6G⁺ neutrophils on day 1 and day 14 after myocardial infarction in Pf4^cre+ C5ar1^fl/fl mice and Cre-negative littermate controls. (G) Spearman correlation analysis demonstrating an inverse relationship between circulating PNCs on day 1 after myocardial infarction and myocardial PNC density on day 14 across individual mice (r = −0.83, P = 0.02). Data are shown as mean ± SD; each dot represents one mouse. n = 4 mice per group for immunofluorescence analyses (A–D) and n = 9 mice per group for flow cytometric analyses (E–F). Statistical analysis was performed using two-tailed unpaired t-tests for immunofluorescence data, one-way ANOVA for flow cytometric analyses, and Spearman’s rank correlation for association analysis (G). P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 20 µm (A) and 10 µm (C).

    Journal: bioRxiv

    Article Title: Platelet C5aR1 Aggravates Myocardial Infarction through Platelet–Neutrophil Interactions and CXCL4-Dependent NET Release

    doi: 10.64898/2026.01.12.699090

    Figure Lengend Snippet: (A) Representative immunofluorescence images of peri-infarct myocardium stained for Ly6G (red) and CD42b (green) with DNA staining (DAPI, blue), showing myocardial platelet–neutrophil complexes (PNCs). (B) Quantification of myocardial PNC density (mm⁻²) in the peri-infarct region (see also Supplementary Figure 10 for platelet and neutrophil infiltration). (C) Representative immunofluorescence images of peri-infarct myocardium stained for myeloperoxidase (MPO, red) and citrullinated histone H3 (H3Cit, green) with DNA (DAPI, blue), showing neutrophil extracellular traps (NETs). (D) Quantification of NET burden expressed as percentage of H3Cit⁺ area of the left ventricle (LV). (E) Flow cytometric gating strategy for platelet–neutrophil complexes (PNCs) in whole blood. Neutrophils were identified by Ly6G, and PNCs were defined as Ly6G⁺CD42b⁺ events. (F) Circulating PNCs expressed as percentage of CD42b⁺ events among Ly6G⁺ neutrophils on day 1 and day 14 after myocardial infarction in Pf4^cre+ C5ar1^fl/fl mice and Cre-negative littermate controls. (G) Spearman correlation analysis demonstrating an inverse relationship between circulating PNCs on day 1 after myocardial infarction and myocardial PNC density on day 14 across individual mice (r = −0.83, P = 0.02). Data are shown as mean ± SD; each dot represents one mouse. n = 4 mice per group for immunofluorescence analyses (A–D) and n = 9 mice per group for flow cytometric analyses (E–F). Statistical analysis was performed using two-tailed unpaired t-tests for immunofluorescence data, one-way ANOVA for flow cytometric analyses, and Spearman’s rank correlation for association analysis (G). P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 20 µm (A) and 10 µm (C).

    Article Snippet: For pharmacological inhibition experiments, wild-type mice only received the selective C5aR1 antagonist PMX205 (Tocris) or PBS vehicle.

    Techniques: Immunofluorescence, Staining, Two Tailed Test

    (A) Representative single-plane confocal immunofluorescence images of fixed and permeabilized resting wild-type (WT) and C5aR1-deficient platelets stained for P-selectin (CD62P, green) and CXCL4 (red), illustrating altered α-granule organization. (B) Quantification of intracellular α-granule content per platelet, expressed as total area of P-selectin–positive granules and colocalized P-selectin/CXCL4 granules, measured by confocal microscopy. Data are shown as individual platelet values pooled from n = 3 independent experiments. Outliers were identified and removed using the ROUT method (Q = 1%) prior to analysis. (C) Flow cytometric analysis of platelet surface P-selectin expression 24 h after myocardial infarction following ex vivo stimulation of whole blood with 100 nM phorbol 12-myristate 13-acetate (PMA), expressed as geometric mean fluorescence intensity (GMFI) of CD42b⁺ platelets. (D) Flow cytometric analysis of platelet integrin GPIIb/IIIa activation under the same conditions, expressed as percentage of activated GPIIb/IIIa among CD42b⁺ platelets. (E) Plasma CXCL4 concentrations after MI in Pf4^cre+^ C5aR1^fl/fl^ mice and Cre-negative littermate controls. (F) Schematic of the in vitro platelet–neutrophil co-incubation assay. WT or C5aR1-deficient platelets were stimulated with C5a and co-incubated with neutrophils, followed by confocal immunofluorescence staining for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI) to assess NET formation, in the presence or absence of low-dose heparin or recombinant CXCL4 (rCXCL4). (G) Representative immunofluorescence images of neutrophils after co-incubation, stained for MPO (red), H3Cit (green), and DNA (DAPI, blue), illustrating NET formation under the indicated conditions (see Supplementary Figure 13 for neutrophil-intrinsic and platelet-mediated control conditions). (H) Quantification of NET formation expressed as percentage of H3Cit⁺ neutrophils. Data are shown as mean ± SD unless otherwise indicated; each dot represents one biological replicate or mouse, as indicated. For α-granule analyses (A–B), data are shown as individual platelet values pooled from n = 3 independent experiments and analyzed using two-tailed unpaired t-tests following ROUT-based outlier exclusion (Q = 1%). Flow cytometry data (C–D) were analyzed using one-way ANOVA across time points and genotypes (see also Supplementary Figures for day 14 analyses). Plasma CXCL4 measurements (E) were analyzed using two-tailed unpaired t-tests. NET formation assays (H) were analyzed using one-way ANOVA with appropriate post hoc correction. P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 2 µm (A) and 20 µm (G).

    Journal: bioRxiv

    Article Title: Platelet C5aR1 Aggravates Myocardial Infarction through Platelet–Neutrophil Interactions and CXCL4-Dependent NET Release

    doi: 10.64898/2026.01.12.699090

    Figure Lengend Snippet: (A) Representative single-plane confocal immunofluorescence images of fixed and permeabilized resting wild-type (WT) and C5aR1-deficient platelets stained for P-selectin (CD62P, green) and CXCL4 (red), illustrating altered α-granule organization. (B) Quantification of intracellular α-granule content per platelet, expressed as total area of P-selectin–positive granules and colocalized P-selectin/CXCL4 granules, measured by confocal microscopy. Data are shown as individual platelet values pooled from n = 3 independent experiments. Outliers were identified and removed using the ROUT method (Q = 1%) prior to analysis. (C) Flow cytometric analysis of platelet surface P-selectin expression 24 h after myocardial infarction following ex vivo stimulation of whole blood with 100 nM phorbol 12-myristate 13-acetate (PMA), expressed as geometric mean fluorescence intensity (GMFI) of CD42b⁺ platelets. (D) Flow cytometric analysis of platelet integrin GPIIb/IIIa activation under the same conditions, expressed as percentage of activated GPIIb/IIIa among CD42b⁺ platelets. (E) Plasma CXCL4 concentrations after MI in Pf4^cre+^ C5aR1^fl/fl^ mice and Cre-negative littermate controls. (F) Schematic of the in vitro platelet–neutrophil co-incubation assay. WT or C5aR1-deficient platelets were stimulated with C5a and co-incubated with neutrophils, followed by confocal immunofluorescence staining for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI) to assess NET formation, in the presence or absence of low-dose heparin or recombinant CXCL4 (rCXCL4). (G) Representative immunofluorescence images of neutrophils after co-incubation, stained for MPO (red), H3Cit (green), and DNA (DAPI, blue), illustrating NET formation under the indicated conditions (see Supplementary Figure 13 for neutrophil-intrinsic and platelet-mediated control conditions). (H) Quantification of NET formation expressed as percentage of H3Cit⁺ neutrophils. Data are shown as mean ± SD unless otherwise indicated; each dot represents one biological replicate or mouse, as indicated. For α-granule analyses (A–B), data are shown as individual platelet values pooled from n = 3 independent experiments and analyzed using two-tailed unpaired t-tests following ROUT-based outlier exclusion (Q = 1%). Flow cytometry data (C–D) were analyzed using one-way ANOVA across time points and genotypes (see also Supplementary Figures for day 14 analyses). Plasma CXCL4 measurements (E) were analyzed using two-tailed unpaired t-tests. NET formation assays (H) were analyzed using one-way ANOVA with appropriate post hoc correction. P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Scale bars, 2 µm (A) and 20 µm (G).

    Article Snippet: For pharmacological inhibition experiments, wild-type mice only received the selective C5aR1 antagonist PMX205 (Tocris) or PBS vehicle.

    Techniques: Immunofluorescence, Staining, Confocal Microscopy, Expressing, Ex Vivo, Fluorescence, Activation Assay, Clinical Proteomics, In Vitro, Incubation, Recombinant, Control, Two Tailed Test, Flow Cytometry

    (A) Experimental design for daily subcutaneous administration of the C5aR1 inhibitor PMX205 or PBS for 14 days following permanent left anterior descending (LAD) coronary artery ligation. (B) Representative TTC-stained transverse left ventricular sections on day 14 after myocardial infarction, with infarcted myocardium appearing white and viable myocardium appearing red. Infarcted areas are indicated by a solid white outline (left). Corresponding quantification of infarct size, expressed as percentage of left ventricular (LV) area (right). (C) Quantification of collagen I–positive area in immunofluorescence staining, expressed as percentage of LV area. (D) Representative M-mode echocardiographic images on day 13 after myocardial infarction. (E) Echocardiographic assessment of left ventricular ejection fraction (EF; left) and fractional shortening (FS; right) on day 1 and day 13 after myocardial infarction. (F) Representative immunofluorescence images of peri-infarct myocardium stained for Ly6G (red) and CD42b (green) with DNA (DAPI, blue), illustrating myocardial platelet–neutrophil complexes (PNCs). (G) Quantification of myocardial PNC density (mm⁻²). (H) Quantification of myocardial NET burden expressed as percentage of H3Cit⁺ neutrophils. (I) Representative immunofluorescence images of peri-infarct myocardium stained for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI), illustrating NET deposition. (J) Representative flow cytometry plots of platelet surface P-selectin expression and activated GPIIb/IIIa (αIIbβ3) in PMA-stimulated whole blood 24 h after myocardial infarction. (K) Quantification of platelet surface P-selectin expression in PMA-stimulated whole blood 24 h after myocardial infarction. (L) Quantification of platelet GPIIb/IIIa activation in PMA-stimulated whole blood 24 h after myocardial infarction. Data are shown as mean ± SD; each dot represents one mouse. Statistical analysis was performed using two-tailed unpaired t-tests for infarct size and collagen I quantification (B, C) and for myocardial PNC and NET quantification (G, H). Echocardiographic parameters (E) and flow cytometric platelet activation analyses (K, L) were analyzed using one-way ANOVA across time points and treatment groups (see also Supplementary Information for day 14 analyses). P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Gating strategies are provided in the Supplementary Information. Scale bars, 2 mm (B) and 20 µm (F, I).

    Journal: bioRxiv

    Article Title: Platelet C5aR1 Aggravates Myocardial Infarction through Platelet–Neutrophil Interactions and CXCL4-Dependent NET Release

    doi: 10.64898/2026.01.12.699090

    Figure Lengend Snippet: (A) Experimental design for daily subcutaneous administration of the C5aR1 inhibitor PMX205 or PBS for 14 days following permanent left anterior descending (LAD) coronary artery ligation. (B) Representative TTC-stained transverse left ventricular sections on day 14 after myocardial infarction, with infarcted myocardium appearing white and viable myocardium appearing red. Infarcted areas are indicated by a solid white outline (left). Corresponding quantification of infarct size, expressed as percentage of left ventricular (LV) area (right). (C) Quantification of collagen I–positive area in immunofluorescence staining, expressed as percentage of LV area. (D) Representative M-mode echocardiographic images on day 13 after myocardial infarction. (E) Echocardiographic assessment of left ventricular ejection fraction (EF; left) and fractional shortening (FS; right) on day 1 and day 13 after myocardial infarction. (F) Representative immunofluorescence images of peri-infarct myocardium stained for Ly6G (red) and CD42b (green) with DNA (DAPI, blue), illustrating myocardial platelet–neutrophil complexes (PNCs). (G) Quantification of myocardial PNC density (mm⁻²). (H) Quantification of myocardial NET burden expressed as percentage of H3Cit⁺ neutrophils. (I) Representative immunofluorescence images of peri-infarct myocardium stained for myeloperoxidase (MPO), citrullinated histone H3 (H3Cit), and DNA (DAPI), illustrating NET deposition. (J) Representative flow cytometry plots of platelet surface P-selectin expression and activated GPIIb/IIIa (αIIbβ3) in PMA-stimulated whole blood 24 h after myocardial infarction. (K) Quantification of platelet surface P-selectin expression in PMA-stimulated whole blood 24 h after myocardial infarction. (L) Quantification of platelet GPIIb/IIIa activation in PMA-stimulated whole blood 24 h after myocardial infarction. Data are shown as mean ± SD; each dot represents one mouse. Statistical analysis was performed using two-tailed unpaired t-tests for infarct size and collagen I quantification (B, C) and for myocardial PNC and NET quantification (G, H). Echocardiographic parameters (E) and flow cytometric platelet activation analyses (K, L) were analyzed using one-way ANOVA across time points and treatment groups (see also Supplementary Information for day 14 analyses). P < 0.05, P < 0.01, P < 0.001, P < 0.0001. Gating strategies are provided in the Supplementary Information. Scale bars, 2 mm (B) and 20 µm (F, I).

    Article Snippet: For pharmacological inhibition experiments, wild-type mice only received the selective C5aR1 antagonist PMX205 (Tocris) or PBS vehicle.

    Techniques: Ligation, Staining, Immunofluorescence, Flow Cytometry, Expressing, Activation Assay, Two Tailed Test

    (A) UMAP of 17, 693 cells distributed by annotated unsupervised clustering. (B) Dot plot showing expression of specific macrophage-associated genes in different macrophage subtypes in unirradiated mouse small intestines. Mean expression reflects expression relative to other cell types and genes in the graph. Expression levels are log-normalised and scaled. The percent expressing reflects the proportion of cells of each type expressing the gene. (C) Dot plot showing expression of specific macrophage-associated genes in different macrophage subtypes in irradiated mouse small intestines 3 days after RT. Mean expression reflects expression relative to other cell types and genes in the graph. Expression levels are log-normalised and scaled. The percent expressing reflects the proportion of cells of each type expressing the gene. (D) Graph shows the % of CD45 + and IL-10 + cells found in small intestines of WT or C5ar1 -/- mice. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group. (E) Graph shows the % IL-10 positivity in F4/80 + and CX3CR1 + cells found in small intestines of WT or C5aR1 -/- mice. ** = p<0.01, 2-tailed t-test. Individual points represent individual mice per group. (F) Schematic representation of experimental design. (G)-(I). Expression of macrophage maturation signature (from spatial transcriptomics data including from ) in WT and C5ar1 -/- mice receiving anti-IL-10 antibody or IgG2b treatment and 9 Gy total abdominal irradiation. Intestines were harvested 3 days post-RT. (J) Graph shows the number of TUNEL+ cells in WT or C5ar1 -/- mice irradiated with 9 Gy total abdominal irradiation and treated with 3 doses of either IgG or IL-10 blocking antibody (flanking the irradiation). Intestines were harvested 3 days post-RT. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group. (K) Graph shows the number of TUNEL + cells in mice irradiated with 9 Gy total abdominal irradiation and treated with 3 doses of either IgG or IL-10 blocking antibody (flanking the irradiation) +/- PMX205. Intestines were harvested 3 days post-RT. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group.

    Journal: bioRxiv

    Article Title: Targeting C5aR1 Reveals Protective Macrophage Maturation States in Intestinal Injury

    doi: 10.1101/2025.11.11.687632

    Figure Lengend Snippet: (A) UMAP of 17, 693 cells distributed by annotated unsupervised clustering. (B) Dot plot showing expression of specific macrophage-associated genes in different macrophage subtypes in unirradiated mouse small intestines. Mean expression reflects expression relative to other cell types and genes in the graph. Expression levels are log-normalised and scaled. The percent expressing reflects the proportion of cells of each type expressing the gene. (C) Dot plot showing expression of specific macrophage-associated genes in different macrophage subtypes in irradiated mouse small intestines 3 days after RT. Mean expression reflects expression relative to other cell types and genes in the graph. Expression levels are log-normalised and scaled. The percent expressing reflects the proportion of cells of each type expressing the gene. (D) Graph shows the % of CD45 + and IL-10 + cells found in small intestines of WT or C5ar1 -/- mice. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group. (E) Graph shows the % IL-10 positivity in F4/80 + and CX3CR1 + cells found in small intestines of WT or C5aR1 -/- mice. ** = p<0.01, 2-tailed t-test. Individual points represent individual mice per group. (F) Schematic representation of experimental design. (G)-(I). Expression of macrophage maturation signature (from spatial transcriptomics data including from ) in WT and C5ar1 -/- mice receiving anti-IL-10 antibody or IgG2b treatment and 9 Gy total abdominal irradiation. Intestines were harvested 3 days post-RT. (J) Graph shows the number of TUNEL+ cells in WT or C5ar1 -/- mice irradiated with 9 Gy total abdominal irradiation and treated with 3 doses of either IgG or IL-10 blocking antibody (flanking the irradiation). Intestines were harvested 3 days post-RT. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group. (K) Graph shows the number of TUNEL + cells in mice irradiated with 9 Gy total abdominal irradiation and treated with 3 doses of either IgG or IL-10 blocking antibody (flanking the irradiation) +/- PMX205. Intestines were harvested 3 days post-RT. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group.

    Article Snippet: For in vivo experiments involving PMX205 treatment, 10 mg/kg PMX205 (Tocris #5196, or synthesized and purified as previously described ) was administered to mice (orally) flanking the irradiation doses.

    Techniques: Expressing, Irradiation, TUNEL Assay, Blocking Assay

    (A) The graph represents the number of apoptotic/non-apoptotic cells expressed as a % of the whole population for HCT116 cells treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody from 1 hour before irradiation with either 0 or 9 Gy. Cells were harvested 48 hours post-RT. n=3. **** = p<0.0001 by 2-way ANOVA with Dunnett’s comparison test. (B) The graph represents the number of apoptotic/non-apoptotic cells expressed as a % of the whole population for HT29 cells treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody from 1 hour before irradiation with either 0 or 9 Gy. Cells were harvested 48 hours post-RT. Independent fields of view are show, n=3. **** = p<0.0001 by 2-way ANOVA with Tukey-Kramer comparison test. (C) Schematic representation of experimental design. (D) The graph represents the number of TUNEL+ cells found in MC38 subcutaneous tumours treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody 1 day before irradiation (10 Gy), on the day of and 1 day post-irradiation. Individual points represent independent fields of view from up to 3 different tumours per group. **** = p<0.0001, n.s = not significant, 2-way ANOVA with Dunnett’s comparison test. (E) Relative tumour growth curves are shown for MC38 colorectal cancer cells treated with 10 Gy single dose irradiation, PMX205 treatment and either IgG or IL-10 blocking antibody for 3 doses flanking the irradiation dose (on day 0, 1 and 2). * = p<0.05, ** = p<0.01 **** = p<0.0001 by 2-way ANOVA. Individual points represent individual mice per group. (F) Relative tumour growth curves are shown for MC38 colorectal cancer cells treated with 10 Gy single dose irradiation, vehicle treatment and either IgG or IL-10 blocking antibody for 3 doses flanking the irradiation dose (on day 0, 1 and 2). Individual points represent individual mice per group.

    Journal: bioRxiv

    Article Title: Targeting C5aR1 Reveals Protective Macrophage Maturation States in Intestinal Injury

    doi: 10.1101/2025.11.11.687632

    Figure Lengend Snippet: (A) The graph represents the number of apoptotic/non-apoptotic cells expressed as a % of the whole population for HCT116 cells treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody from 1 hour before irradiation with either 0 or 9 Gy. Cells were harvested 48 hours post-RT. n=3. **** = p<0.0001 by 2-way ANOVA with Dunnett’s comparison test. (B) The graph represents the number of apoptotic/non-apoptotic cells expressed as a % of the whole population for HT29 cells treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody from 1 hour before irradiation with either 0 or 9 Gy. Cells were harvested 48 hours post-RT. Independent fields of view are show, n=3. **** = p<0.0001 by 2-way ANOVA with Tukey-Kramer comparison test. (C) Schematic representation of experimental design. (D) The graph represents the number of TUNEL+ cells found in MC38 subcutaneous tumours treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody 1 day before irradiation (10 Gy), on the day of and 1 day post-irradiation. Individual points represent independent fields of view from up to 3 different tumours per group. **** = p<0.0001, n.s = not significant, 2-way ANOVA with Dunnett’s comparison test. (E) Relative tumour growth curves are shown for MC38 colorectal cancer cells treated with 10 Gy single dose irradiation, PMX205 treatment and either IgG or IL-10 blocking antibody for 3 doses flanking the irradiation dose (on day 0, 1 and 2). * = p<0.05, ** = p<0.01 **** = p<0.0001 by 2-way ANOVA. Individual points represent individual mice per group. (F) Relative tumour growth curves are shown for MC38 colorectal cancer cells treated with 10 Gy single dose irradiation, vehicle treatment and either IgG or IL-10 blocking antibody for 3 doses flanking the irradiation dose (on day 0, 1 and 2). Individual points represent individual mice per group.

    Article Snippet: For in vivo experiments involving PMX205 treatment, 10 mg/kg PMX205 (Tocris #5196, or synthesized and purified as previously described ) was administered to mice (orally) flanking the irradiation doses.

    Techniques: Blocking Assay, Irradiation, Comparison, TUNEL Assay

    (A) UMAP of 17, 693 cells distributed by annotated unsupervised clustering. (B) Dot plot showing expression of specific macrophage-associated genes in different macrophage subtypes in unirradiated mouse small intestines. Mean expression reflects expression relative to other cell types and genes in the graph. Expression levels are log-normalised and scaled. The percent expressing reflects the proportion of cells of each type expressing the gene. (C) Dot plot showing expression of specific macrophage-associated genes in different macrophage subtypes in irradiated mouse small intestines 3 days after RT. Mean expression reflects expression relative to other cell types and genes in the graph. Expression levels are log-normalised and scaled. The percent expressing reflects the proportion of cells of each type expressing the gene. (D) Graph shows the % of CD45 + and IL-10 + cells found in small intestines of WT or C5ar1 -/- mice. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group. (E) Graph shows the % IL-10 positivity in F4/80 + and CX3CR1 + cells found in small intestines of WT or C5aR1 -/- mice. ** = p<0.01, 2-tailed t-test. Individual points represent individual mice per group. (F) Schematic representation of experimental design. (G)-(I). Expression of macrophage maturation signature (from spatial transcriptomics data including from ) in WT and C5ar1 -/- mice receiving anti-IL-10 antibody or IgG2b treatment and 9 Gy total abdominal irradiation. Intestines were harvested 3 days post-RT. (J) Graph shows the number of TUNEL+ cells in WT or C5ar1 -/- mice irradiated with 9 Gy total abdominal irradiation and treated with 3 doses of either IgG or IL-10 blocking antibody (flanking the irradiation). Intestines were harvested 3 days post-RT. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group. (K) Graph shows the number of TUNEL + cells in mice irradiated with 9 Gy total abdominal irradiation and treated with 3 doses of either IgG or IL-10 blocking antibody (flanking the irradiation) +/- PMX205. Intestines were harvested 3 days post-RT. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group.

    Journal: bioRxiv

    Article Title: Targeting C5aR1 Reveals Protective Macrophage Maturation States in Intestinal Injury

    doi: 10.1101/2025.11.11.687632

    Figure Lengend Snippet: (A) UMAP of 17, 693 cells distributed by annotated unsupervised clustering. (B) Dot plot showing expression of specific macrophage-associated genes in different macrophage subtypes in unirradiated mouse small intestines. Mean expression reflects expression relative to other cell types and genes in the graph. Expression levels are log-normalised and scaled. The percent expressing reflects the proportion of cells of each type expressing the gene. (C) Dot plot showing expression of specific macrophage-associated genes in different macrophage subtypes in irradiated mouse small intestines 3 days after RT. Mean expression reflects expression relative to other cell types and genes in the graph. Expression levels are log-normalised and scaled. The percent expressing reflects the proportion of cells of each type expressing the gene. (D) Graph shows the % of CD45 + and IL-10 + cells found in small intestines of WT or C5ar1 -/- mice. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group. (E) Graph shows the % IL-10 positivity in F4/80 + and CX3CR1 + cells found in small intestines of WT or C5aR1 -/- mice. ** = p<0.01, 2-tailed t-test. Individual points represent individual mice per group. (F) Schematic representation of experimental design. (G)-(I). Expression of macrophage maturation signature (from spatial transcriptomics data including from ) in WT and C5ar1 -/- mice receiving anti-IL-10 antibody or IgG2b treatment and 9 Gy total abdominal irradiation. Intestines were harvested 3 days post-RT. (J) Graph shows the number of TUNEL+ cells in WT or C5ar1 -/- mice irradiated with 9 Gy total abdominal irradiation and treated with 3 doses of either IgG or IL-10 blocking antibody (flanking the irradiation). Intestines were harvested 3 days post-RT. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group. (K) Graph shows the number of TUNEL + cells in mice irradiated with 9 Gy total abdominal irradiation and treated with 3 doses of either IgG or IL-10 blocking antibody (flanking the irradiation) +/- PMX205. Intestines were harvested 3 days post-RT. * = p<0.05, 2-tailed t-test. Individual points represent individual mice per group.

    Article Snippet: For in vivo experiments involving PMX205 treatment, 10 mg/kg PMX205 (Tocris #5196, or synthesized and purified as previously described ) was administered to mice (orally) flanking the irradiation doses.

    Techniques: Expressing, Irradiation, TUNEL Assay, Blocking Assay

    (A) The graph represents the number of apoptotic/non-apoptotic cells expressed as a % of the whole population for HCT116 cells treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody from 1 hour before irradiation with either 0 or 9 Gy. Cells were harvested 48 hours post-RT. n=3. **** = p<0.0001 by 2-way ANOVA with Dunnett’s comparison test. (B) The graph represents the number of apoptotic/non-apoptotic cells expressed as a % of the whole population for HT29 cells treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody from 1 hour before irradiation with either 0 or 9 Gy. Cells were harvested 48 hours post-RT. Independent fields of view are show, n=3. **** = p<0.0001 by 2-way ANOVA with Tukey-Kramer comparison test. (C) Schematic representation of experimental design. (D) The graph represents the number of TUNEL+ cells found in MC38 subcutaneous tumours treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody 1 day before irradiation (10 Gy), on the day of and 1 day post-irradiation. Individual points represent independent fields of view from up to 3 different tumours per group. **** = p<0.0001, n.s = not significant, 2-way ANOVA with Dunnett’s comparison test. (E) Relative tumour growth curves are shown for MC38 colorectal cancer cells treated with 10 Gy single dose irradiation, PMX205 treatment and either IgG or IL-10 blocking antibody for 3 doses flanking the irradiation dose (on day 0, 1 and 2). * = p<0.05, ** = p<0.01 **** = p<0.0001 by 2-way ANOVA. Individual points represent individual mice per group. (F) Relative tumour growth curves are shown for MC38 colorectal cancer cells treated with 10 Gy single dose irradiation, vehicle treatment and either IgG or IL-10 blocking antibody for 3 doses flanking the irradiation dose (on day 0, 1 and 2). Individual points represent individual mice per group.

    Journal: bioRxiv

    Article Title: Targeting C5aR1 Reveals Protective Macrophage Maturation States in Intestinal Injury

    doi: 10.1101/2025.11.11.687632

    Figure Lengend Snippet: (A) The graph represents the number of apoptotic/non-apoptotic cells expressed as a % of the whole population for HCT116 cells treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody from 1 hour before irradiation with either 0 or 9 Gy. Cells were harvested 48 hours post-RT. n=3. **** = p<0.0001 by 2-way ANOVA with Dunnett’s comparison test. (B) The graph represents the number of apoptotic/non-apoptotic cells expressed as a % of the whole population for HT29 cells treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody from 1 hour before irradiation with either 0 or 9 Gy. Cells were harvested 48 hours post-RT. Independent fields of view are show, n=3. **** = p<0.0001 by 2-way ANOVA with Tukey-Kramer comparison test. (C) Schematic representation of experimental design. (D) The graph represents the number of TUNEL+ cells found in MC38 subcutaneous tumours treated with either vehicle or PMX205 and either IgG or IL-10 blocking antibody 1 day before irradiation (10 Gy), on the day of and 1 day post-irradiation. Individual points represent independent fields of view from up to 3 different tumours per group. **** = p<0.0001, n.s = not significant, 2-way ANOVA with Dunnett’s comparison test. (E) Relative tumour growth curves are shown for MC38 colorectal cancer cells treated with 10 Gy single dose irradiation, PMX205 treatment and either IgG or IL-10 blocking antibody for 3 doses flanking the irradiation dose (on day 0, 1 and 2). * = p<0.05, ** = p<0.01 **** = p<0.0001 by 2-way ANOVA. Individual points represent individual mice per group. (F) Relative tumour growth curves are shown for MC38 colorectal cancer cells treated with 10 Gy single dose irradiation, vehicle treatment and either IgG or IL-10 blocking antibody for 3 doses flanking the irradiation dose (on day 0, 1 and 2). Individual points represent individual mice per group.

    Article Snippet: For in vivo experiments involving PMX205 treatment, 10 mg/kg PMX205 (Tocris #5196, or synthesized and purified as previously described ) was administered to mice (orally) flanking the irradiation doses.

    Techniques: Blocking Assay, Irradiation, Comparison, TUNEL Assay