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(A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. <t>CD11b</t> was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.
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(A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. <t>CD11b</t> was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.
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(A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. <t>CD11b</t> was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.
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(A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. <t>CD11b</t> was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.
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(A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. <t>CD11b</t> was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.
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(A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. <t>CD11b</t> was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.
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(A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. <t>CD11b</t> was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.
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(A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. CD11b was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.

Journal: bioRxiv

Article Title: Integrin Activation Enhances Lesion-Specific Targeting of Monocyte-Mimetic Nanoparticles in Atherosclerosis

doi: 10.64898/2026.03.04.707824

Figure Lengend Snippet: (A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. CD11b was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.

Article Snippet: Membrane proteins were assessed by Western blot using antibodies against CD11b (Cell Signaling #17800, 1:1000), Na + /K + ATPase (Cell Signaling #3010, 1:1000), α4-integrin (Invitrogen #PA5-20599, 1:1000), and β1-integrin (Cell Signaling #4706S, 1:1000).

Techniques: Cell Adhesion Assay, Labeling, Western Blot, Binding Assay, Recombinant, Control

(A) Schematic illustration of the experimental design. (B–C) Nanoparticle characterization after serum incubation, showing (B) DLS analysis of hydrodynamic size and (C) protein corona composition by Western blot; CD11b was used as a loading control for all MoNP formulations. (D–E) IVIS images and quantification of residual nanoparticles, including (D) ex vivo measurement of nanoparticles remaining in plasma after incubation with whole blood and (E) in vivo measurement of circulating nanoparticles at 3- and 24-hour post-injection. (B, D): *p < 0.05 vs. bare NP. Data are presented as mean ± SD from n = 3 independent experiments.

Journal: bioRxiv

Article Title: Integrin Activation Enhances Lesion-Specific Targeting of Monocyte-Mimetic Nanoparticles in Atherosclerosis

doi: 10.64898/2026.03.04.707824

Figure Lengend Snippet: (A) Schematic illustration of the experimental design. (B–C) Nanoparticle characterization after serum incubation, showing (B) DLS analysis of hydrodynamic size and (C) protein corona composition by Western blot; CD11b was used as a loading control for all MoNP formulations. (D–E) IVIS images and quantification of residual nanoparticles, including (D) ex vivo measurement of nanoparticles remaining in plasma after incubation with whole blood and (E) in vivo measurement of circulating nanoparticles at 3- and 24-hour post-injection. (B, D): *p < 0.05 vs. bare NP. Data are presented as mean ± SD from n = 3 independent experiments.

Article Snippet: Membrane proteins were assessed by Western blot using antibodies against CD11b (Cell Signaling #17800, 1:1000), Na + /K + ATPase (Cell Signaling #3010, 1:1000), α4-integrin (Invitrogen #PA5-20599, 1:1000), and β1-integrin (Cell Signaling #4706S, 1:1000).

Techniques: Incubation, Western Blot, Control, Ex Vivo, Clinical Proteomics, In Vivo, Injection

(A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. CD11b was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.

Journal: bioRxiv

Article Title: Integrin Activation Enhances Lesion-Specific Targeting of Monocyte-Mimetic Nanoparticles in Atherosclerosis

doi: 10.64898/2026.03.04.707824

Figure Lengend Snippet: (A) Representative images and quantitative of adhesion of CCL2-, Mn 2+ -, or PBS-treated monocytes to TNFα-treated ECs. (B) Schematic of the monocyte adhesion assay under SS and quantification of fluorescently labeled monocyte attachment to TNFα-treated ECs. (C) Schematic illustration of C-IA@MoNPs and M-IA@MoNPs formulations. (D) DLS characterization showing hydrodynamic diameter and ζ-potential of IA@MoNPs. (E) Western blot and (F) SPR analyses demonstrating enhanced IA@MoNP binding affinity to recombinant VCAM1. CD11b was used as a loading control for all MoNP formulations. Data in (A) and (B) were normalized to PBS-treated monocytes and static conditions, respectively. (A–B) *p < 0.05 vs. PBS-treated monocytes. For all experiments, n = 3 independent replicates.

Article Snippet: The adsorbed protein corona was analyzed by Western blot using antibodies against complement 3 (C3) (Abcam #ab200999, 1:1000), immunoglobulin G (IgG) (Jackson ImmunoResearch #anti-rabbit IgG secondary antibody, 1:1000), ApoE (Cell Signaling #49285, 1:1000), and CD11b (Cell Signaling #17800, 1:1000).

Techniques: Cell Adhesion Assay, Labeling, Western Blot, Binding Assay, Recombinant, Control

(A) Schematic illustration of the experimental design. (B–C) Nanoparticle characterization after serum incubation, showing (B) DLS analysis of hydrodynamic size and (C) protein corona composition by Western blot; CD11b was used as a loading control for all MoNP formulations. (D–E) IVIS images and quantification of residual nanoparticles, including (D) ex vivo measurement of nanoparticles remaining in plasma after incubation with whole blood and (E) in vivo measurement of circulating nanoparticles at 3- and 24-hour post-injection. (B, D): *p < 0.05 vs. bare NP. Data are presented as mean ± SD from n = 3 independent experiments.

Journal: bioRxiv

Article Title: Integrin Activation Enhances Lesion-Specific Targeting of Monocyte-Mimetic Nanoparticles in Atherosclerosis

doi: 10.64898/2026.03.04.707824

Figure Lengend Snippet: (A) Schematic illustration of the experimental design. (B–C) Nanoparticle characterization after serum incubation, showing (B) DLS analysis of hydrodynamic size and (C) protein corona composition by Western blot; CD11b was used as a loading control for all MoNP formulations. (D–E) IVIS images and quantification of residual nanoparticles, including (D) ex vivo measurement of nanoparticles remaining in plasma after incubation with whole blood and (E) in vivo measurement of circulating nanoparticles at 3- and 24-hour post-injection. (B, D): *p < 0.05 vs. bare NP. Data are presented as mean ± SD from n = 3 independent experiments.

Article Snippet: The adsorbed protein corona was analyzed by Western blot using antibodies against complement 3 (C3) (Abcam #ab200999, 1:1000), immunoglobulin G (IgG) (Jackson ImmunoResearch #anti-rabbit IgG secondary antibody, 1:1000), ApoE (Cell Signaling #49285, 1:1000), and CD11b (Cell Signaling #17800, 1:1000).

Techniques: Incubation, Western Blot, Control, Ex Vivo, Clinical Proteomics, In Vivo, Injection