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<t>cEV</t> derived from ILK deficient mice propagate an inflammatory phenotype and induced cardiac dysfunction in wild‐ type mice. (A) Schematic representation of cEV transfer for the study of cardiovascular structure and function workflow. Recipient Wild‐type mice were treated every 48 h for 1 and 3 weeks with cEV isolated from CT mice (cEV CT ) and ecILK‐cKO mice (cEV ecILK‐cKO ) in a timely fashion. <t>PBS</t> was used as negative control. Cardiac function and structural studies were conducted in recipient WT mice at 1 and 3 weeks. (B) Representative immunofluorescence analysis of cardiac tissue illustrating endothelial inflammatory activation. Upper panels show staining for the acute inflammatory marker iNOS (magenta) while middle panels show staining for the endothelial activation marker ICAM‐1 (magenta), both colocalized with endothelial cells (CD31 + , yellow) and nuclei in blue in cEV CT and cEV ecILK‐cKO at 1 and 3 weeks. Lower panels show immunofluorescence of perivascular regions, depicting macrophage infiltration (CD68 + , yellow) and polarization toward a pro‐inflammatory M1 phenotype (CD86 + , magenta) under the same conditions as above. Phase‐contrast (PC) microscopy (grey) was used to visualize vascular structures. Scale bar = 20 µm. Quantification of CD31 + cells expressing (C) iNOS or (D) ICAM‐1. (E) CD68+ Perivascular macrophage infiltration (CD68 + cells within 10–20 µm of vessel wall). (F) CD68+/CD86+ ratio indicating M1 polarization. (G) Representative images of Sirius Red‐stained cardiac tissue sections +cEV CT , and +cEV ecILK‐cKO groups at 1 and 3 weeks. Scale bar = 1 mm. Quantification of Sirius Red–positive area (fibrosis) relative to total cardiac tissue area under the conditions shown in (A). (H) Quantification of vascular remodelling in cardiac tissue under the same conditions as in (A), expressed as arteriolar wall area‐to lumen area ratio. Vascular remodelling was significantly increased in WT mice treated for 3‐weeks with cEV ecILK‐cKO only in small vessels (10–60 mm) and remained unchanged in large vessels (>100 mm). For all analyses, data are presented as mean ± SD, with at least three randomly selected cardiac regions analysed per mouse across ventricular sections. Values represent the mean ± SD per animal. Statistical significance was determined using Student's t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001.
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<t>cEV</t> derived from ILK deficient mice propagate an inflammatory phenotype and induced cardiac dysfunction in wild‐ type mice. (A) Schematic representation of cEV transfer for the study of cardiovascular structure and function workflow. Recipient Wild‐type mice were treated every 48 h for 1 and 3 weeks with cEV isolated from CT mice (cEV CT ) and ecILK‐cKO mice (cEV ecILK‐cKO ) in a timely fashion. <t>PBS</t> was used as negative control. Cardiac function and structural studies were conducted in recipient WT mice at 1 and 3 weeks. (B) Representative immunofluorescence analysis of cardiac tissue illustrating endothelial inflammatory activation. Upper panels show staining for the acute inflammatory marker iNOS (magenta) while middle panels show staining for the endothelial activation marker ICAM‐1 (magenta), both colocalized with endothelial cells (CD31 + , yellow) and nuclei in blue in cEV CT and cEV ecILK‐cKO at 1 and 3 weeks. Lower panels show immunofluorescence of perivascular regions, depicting macrophage infiltration (CD68 + , yellow) and polarization toward a pro‐inflammatory M1 phenotype (CD86 + , magenta) under the same conditions as above. Phase‐contrast (PC) microscopy (grey) was used to visualize vascular structures. Scale bar = 20 µm. Quantification of CD31 + cells expressing (C) iNOS or (D) ICAM‐1. (E) CD68+ Perivascular macrophage infiltration (CD68 + cells within 10–20 µm of vessel wall). (F) CD68+/CD86+ ratio indicating M1 polarization. (G) Representative images of Sirius Red‐stained cardiac tissue sections +cEV CT , and +cEV ecILK‐cKO groups at 1 and 3 weeks. Scale bar = 1 mm. Quantification of Sirius Red–positive area (fibrosis) relative to total cardiac tissue area under the conditions shown in (A). (H) Quantification of vascular remodelling in cardiac tissue under the same conditions as in (A), expressed as arteriolar wall area‐to lumen area ratio. Vascular remodelling was significantly increased in WT mice treated for 3‐weeks with cEV ecILK‐cKO only in small vessels (10–60 mm) and remained unchanged in large vessels (>100 mm). For all analyses, data are presented as mean ± SD, with at least three randomly selected cardiac regions analysed per mouse across ventricular sections. Values represent the mean ± SD per animal. Statistical significance was determined using Student's t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001.
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<t>cEV</t> derived from ILK deficient mice propagate an inflammatory phenotype and induced cardiac dysfunction in wild‐ type mice. (A) Schematic representation of cEV transfer for the study of cardiovascular structure and function workflow. Recipient Wild‐type mice were treated every 48 h for 1 and 3 weeks with cEV isolated from CT mice (cEV CT ) and ecILK‐cKO mice (cEV ecILK‐cKO ) in a timely fashion. <t>PBS</t> was used as negative control. Cardiac function and structural studies were conducted in recipient WT mice at 1 and 3 weeks. (B) Representative immunofluorescence analysis of cardiac tissue illustrating endothelial inflammatory activation. Upper panels show staining for the acute inflammatory marker iNOS (magenta) while middle panels show staining for the endothelial activation marker ICAM‐1 (magenta), both colocalized with endothelial cells (CD31 + , yellow) and nuclei in blue in cEV CT and cEV ecILK‐cKO at 1 and 3 weeks. Lower panels show immunofluorescence of perivascular regions, depicting macrophage infiltration (CD68 + , yellow) and polarization toward a pro‐inflammatory M1 phenotype (CD86 + , magenta) under the same conditions as above. Phase‐contrast (PC) microscopy (grey) was used to visualize vascular structures. Scale bar = 20 µm. Quantification of CD31 + cells expressing (C) iNOS or (D) ICAM‐1. (E) CD68+ Perivascular macrophage infiltration (CD68 + cells within 10–20 µm of vessel wall). (F) CD68+/CD86+ ratio indicating M1 polarization. (G) Representative images of Sirius Red‐stained cardiac tissue sections +cEV CT , and +cEV ecILK‐cKO groups at 1 and 3 weeks. Scale bar = 1 mm. Quantification of Sirius Red–positive area (fibrosis) relative to total cardiac tissue area under the conditions shown in (A). (H) Quantification of vascular remodelling in cardiac tissue under the same conditions as in (A), expressed as arteriolar wall area‐to lumen area ratio. Vascular remodelling was significantly increased in WT mice treated for 3‐weeks with cEV ecILK‐cKO only in small vessels (10–60 mm) and remained unchanged in large vessels (>100 mm). For all analyses, data are presented as mean ± SD, with at least three randomly selected cardiac regions analysed per mouse across ventricular sections. Values represent the mean ± SD per animal. Statistical significance was determined using Student's t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001.
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<t>cEV</t> derived from ILK deficient mice propagate an inflammatory phenotype and induced cardiac dysfunction in wild‐ type mice. (A) Schematic representation of cEV transfer for the study of cardiovascular structure and function workflow. Recipient Wild‐type mice were treated every 48 h for 1 and 3 weeks with cEV isolated from CT mice (cEV CT ) and ecILK‐cKO mice (cEV ecILK‐cKO ) in a timely fashion. <t>PBS</t> was used as negative control. Cardiac function and structural studies were conducted in recipient WT mice at 1 and 3 weeks. (B) Representative immunofluorescence analysis of cardiac tissue illustrating endothelial inflammatory activation. Upper panels show staining for the acute inflammatory marker iNOS (magenta) while middle panels show staining for the endothelial activation marker ICAM‐1 (magenta), both colocalized with endothelial cells (CD31 + , yellow) and nuclei in blue in cEV CT and cEV ecILK‐cKO at 1 and 3 weeks. Lower panels show immunofluorescence of perivascular regions, depicting macrophage infiltration (CD68 + , yellow) and polarization toward a pro‐inflammatory M1 phenotype (CD86 + , magenta) under the same conditions as above. Phase‐contrast (PC) microscopy (grey) was used to visualize vascular structures. Scale bar = 20 µm. Quantification of CD31 + cells expressing (C) iNOS or (D) ICAM‐1. (E) CD68+ Perivascular macrophage infiltration (CD68 + cells within 10–20 µm of vessel wall). (F) CD68+/CD86+ ratio indicating M1 polarization. (G) Representative images of Sirius Red‐stained cardiac tissue sections +cEV CT , and +cEV ecILK‐cKO groups at 1 and 3 weeks. Scale bar = 1 mm. Quantification of Sirius Red–positive area (fibrosis) relative to total cardiac tissue area under the conditions shown in (A). (H) Quantification of vascular remodelling in cardiac tissue under the same conditions as in (A), expressed as arteriolar wall area‐to lumen area ratio. Vascular remodelling was significantly increased in WT mice treated for 3‐weeks with cEV ecILK‐cKO only in small vessels (10–60 mm) and remained unchanged in large vessels (>100 mm). For all analyses, data are presented as mean ± SD, with at least three randomly selected cardiac regions analysed per mouse across ventricular sections. Values represent the mean ± SD per animal. Statistical significance was determined using Student's t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001.
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<t>cEV</t> derived from ILK deficient mice propagate an inflammatory phenotype and induced cardiac dysfunction in wild‐ type mice. (A) Schematic representation of cEV transfer for the study of cardiovascular structure and function workflow. Recipient Wild‐type mice were treated every 48 h for 1 and 3 weeks with cEV isolated from CT mice (cEV CT ) and ecILK‐cKO mice (cEV ecILK‐cKO ) in a timely fashion. <t>PBS</t> was used as negative control. Cardiac function and structural studies were conducted in recipient WT mice at 1 and 3 weeks. (B) Representative immunofluorescence analysis of cardiac tissue illustrating endothelial inflammatory activation. Upper panels show staining for the acute inflammatory marker iNOS (magenta) while middle panels show staining for the endothelial activation marker ICAM‐1 (magenta), both colocalized with endothelial cells (CD31 + , yellow) and nuclei in blue in cEV CT and cEV ecILK‐cKO at 1 and 3 weeks. Lower panels show immunofluorescence of perivascular regions, depicting macrophage infiltration (CD68 + , yellow) and polarization toward a pro‐inflammatory M1 phenotype (CD86 + , magenta) under the same conditions as above. Phase‐contrast (PC) microscopy (grey) was used to visualize vascular structures. Scale bar = 20 µm. Quantification of CD31 + cells expressing (C) iNOS or (D) ICAM‐1. (E) CD68+ Perivascular macrophage infiltration (CD68 + cells within 10–20 µm of vessel wall). (F) CD68+/CD86+ ratio indicating M1 polarization. (G) Representative images of Sirius Red‐stained cardiac tissue sections +cEV CT , and +cEV ecILK‐cKO groups at 1 and 3 weeks. Scale bar = 1 mm. Quantification of Sirius Red–positive area (fibrosis) relative to total cardiac tissue area under the conditions shown in (A). (H) Quantification of vascular remodelling in cardiac tissue under the same conditions as in (A), expressed as arteriolar wall area‐to lumen area ratio. Vascular remodelling was significantly increased in WT mice treated for 3‐weeks with cEV ecILK‐cKO only in small vessels (10–60 mm) and remained unchanged in large vessels (>100 mm). For all analyses, data are presented as mean ± SD, with at least three randomly selected cardiac regions analysed per mouse across ventricular sections. Values represent the mean ± SD per animal. Statistical significance was determined using Student's t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001.
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<t>cEV</t> derived from ILK deficient mice propagate an inflammatory phenotype and induced cardiac dysfunction in wild‐ type mice. (A) Schematic representation of cEV transfer for the study of cardiovascular structure and function workflow. Recipient Wild‐type mice were treated every 48 h for 1 and 3 weeks with cEV isolated from CT mice (cEV CT ) and ecILK‐cKO mice (cEV ecILK‐cKO ) in a timely fashion. <t>PBS</t> was used as negative control. Cardiac function and structural studies were conducted in recipient WT mice at 1 and 3 weeks. (B) Representative immunofluorescence analysis of cardiac tissue illustrating endothelial inflammatory activation. Upper panels show staining for the acute inflammatory marker iNOS (magenta) while middle panels show staining for the endothelial activation marker ICAM‐1 (magenta), both colocalized with endothelial cells (CD31 + , yellow) and nuclei in blue in cEV CT and cEV ecILK‐cKO at 1 and 3 weeks. Lower panels show immunofluorescence of perivascular regions, depicting macrophage infiltration (CD68 + , yellow) and polarization toward a pro‐inflammatory M1 phenotype (CD86 + , magenta) under the same conditions as above. Phase‐contrast (PC) microscopy (grey) was used to visualize vascular structures. Scale bar = 20 µm. Quantification of CD31 + cells expressing (C) iNOS or (D) ICAM‐1. (E) CD68+ Perivascular macrophage infiltration (CD68 + cells within 10–20 µm of vessel wall). (F) CD68+/CD86+ ratio indicating M1 polarization. (G) Representative images of Sirius Red‐stained cardiac tissue sections +cEV CT , and +cEV ecILK‐cKO groups at 1 and 3 weeks. Scale bar = 1 mm. Quantification of Sirius Red–positive area (fibrosis) relative to total cardiac tissue area under the conditions shown in (A). (H) Quantification of vascular remodelling in cardiac tissue under the same conditions as in (A), expressed as arteriolar wall area‐to lumen area ratio. Vascular remodelling was significantly increased in WT mice treated for 3‐weeks with cEV ecILK‐cKO only in small vessels (10–60 mm) and remained unchanged in large vessels (>100 mm). For all analyses, data are presented as mean ± SD, with at least three randomly selected cardiac regions analysed per mouse across ventricular sections. Values represent the mean ± SD per animal. Statistical significance was determined using Student's t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001.
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cEV derived from ILK deficient mice propagate an inflammatory phenotype and induced cardiac dysfunction in wild‐ type mice. (A) Schematic representation of cEV transfer for the study of cardiovascular structure and function workflow. Recipient Wild‐type mice were treated every 48 h for 1 and 3 weeks with cEV isolated from CT mice (cEV CT ) and ecILK‐cKO mice (cEV ecILK‐cKO ) in a timely fashion. PBS was used as negative control. Cardiac function and structural studies were conducted in recipient WT mice at 1 and 3 weeks. (B) Representative immunofluorescence analysis of cardiac tissue illustrating endothelial inflammatory activation. Upper panels show staining for the acute inflammatory marker iNOS (magenta) while middle panels show staining for the endothelial activation marker ICAM‐1 (magenta), both colocalized with endothelial cells (CD31 + , yellow) and nuclei in blue in cEV CT and cEV ecILK‐cKO at 1 and 3 weeks. Lower panels show immunofluorescence of perivascular regions, depicting macrophage infiltration (CD68 + , yellow) and polarization toward a pro‐inflammatory M1 phenotype (CD86 + , magenta) under the same conditions as above. Phase‐contrast (PC) microscopy (grey) was used to visualize vascular structures. Scale bar = 20 µm. Quantification of CD31 + cells expressing (C) iNOS or (D) ICAM‐1. (E) CD68+ Perivascular macrophage infiltration (CD68 + cells within 10–20 µm of vessel wall). (F) CD68+/CD86+ ratio indicating M1 polarization. (G) Representative images of Sirius Red‐stained cardiac tissue sections +cEV CT , and +cEV ecILK‐cKO groups at 1 and 3 weeks. Scale bar = 1 mm. Quantification of Sirius Red–positive area (fibrosis) relative to total cardiac tissue area under the conditions shown in (A). (H) Quantification of vascular remodelling in cardiac tissue under the same conditions as in (A), expressed as arteriolar wall area‐to lumen area ratio. Vascular remodelling was significantly increased in WT mice treated for 3‐weeks with cEV ecILK‐cKO only in small vessels (10–60 mm) and remained unchanged in large vessels (>100 mm). For all analyses, data are presented as mean ± SD, with at least three randomly selected cardiac regions analysed per mouse across ventricular sections. Values represent the mean ± SD per animal. Statistical significance was determined using Student's t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Journal of Extracellular Vesicles

Article Title: Endothelial Integrin‐Linked Kinase (ILK) Deficiency Promotes Endothelial Activation and Cardiovascular Dysfunction via Receptor Interacting Protein Kinase‐1 (RIPK1) Enriched‐Extracellular Vesicle Signalling

doi: 10.1002/jev2.70335

Figure Lengend Snippet: cEV derived from ILK deficient mice propagate an inflammatory phenotype and induced cardiac dysfunction in wild‐ type mice. (A) Schematic representation of cEV transfer for the study of cardiovascular structure and function workflow. Recipient Wild‐type mice were treated every 48 h for 1 and 3 weeks with cEV isolated from CT mice (cEV CT ) and ecILK‐cKO mice (cEV ecILK‐cKO ) in a timely fashion. PBS was used as negative control. Cardiac function and structural studies were conducted in recipient WT mice at 1 and 3 weeks. (B) Representative immunofluorescence analysis of cardiac tissue illustrating endothelial inflammatory activation. Upper panels show staining for the acute inflammatory marker iNOS (magenta) while middle panels show staining for the endothelial activation marker ICAM‐1 (magenta), both colocalized with endothelial cells (CD31 + , yellow) and nuclei in blue in cEV CT and cEV ecILK‐cKO at 1 and 3 weeks. Lower panels show immunofluorescence of perivascular regions, depicting macrophage infiltration (CD68 + , yellow) and polarization toward a pro‐inflammatory M1 phenotype (CD86 + , magenta) under the same conditions as above. Phase‐contrast (PC) microscopy (grey) was used to visualize vascular structures. Scale bar = 20 µm. Quantification of CD31 + cells expressing (C) iNOS or (D) ICAM‐1. (E) CD68+ Perivascular macrophage infiltration (CD68 + cells within 10–20 µm of vessel wall). (F) CD68+/CD86+ ratio indicating M1 polarization. (G) Representative images of Sirius Red‐stained cardiac tissue sections +cEV CT , and +cEV ecILK‐cKO groups at 1 and 3 weeks. Scale bar = 1 mm. Quantification of Sirius Red–positive area (fibrosis) relative to total cardiac tissue area under the conditions shown in (A). (H) Quantification of vascular remodelling in cardiac tissue under the same conditions as in (A), expressed as arteriolar wall area‐to lumen area ratio. Vascular remodelling was significantly increased in WT mice treated for 3‐weeks with cEV ecILK‐cKO only in small vessels (10–60 mm) and remained unchanged in large vessels (>100 mm). For all analyses, data are presented as mean ± SD, with at least three randomly selected cardiac regions analysed per mouse across ventricular sections. Values represent the mean ± SD per animal. Statistical significance was determined using Student's t ‐test; * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: After a final washing step, cEV were resuspended in PBS and analysed using a MACSQuant Analyzer 10 Flow Cytometer (Miltenyi Biotec, Bergisch Gladbach, Germany).

Techniques: Derivative Assay, Isolation, Negative Control, Immunofluorescence, Activation Assay, Staining, Marker, Microscopy, Expressing