pai 1  (Innovative Research Inc)

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Drug Targeting of Plasminogen Activator Inhibitor-1 Inhibits Metabolic Dysfunction and Atherosclerosis in a Murine Model of Metabolic Syndrome

doi: 10.1161/ATVBAHA.119.313775

Figure Lengend Snippet: Ldlr−/− mice were fed WD containing or lacking PAI-1 inhibitor for 12 weeks, after which aortic root atherosclerotic plaque composition was assessed. (A) PAI-039 decreases fibrous cap macrophage content. Quantified data (n=5/group; *P<0.05) and representative images demonstrating macrophage invasion (brown color) are shown. (B) MDI-2268 decreases fibrous cap macrophage content. Quantified data (n=6–7/group; *P<0.05) and representative images are shown. (C) MDI-2268 does not significantly affect intimal SMC content, assessed by SMC-α actin immunostaining (brown color). Quantified data (n=4–6/group, difference between groups did not achieve statistical significance; P>0.6) and representative images are shown. (D) MDI-2268 does not significantly affect plaque collagen content, assessed by picrosirius red (PSR) staining. Quantified data (n=6–7/group, difference between groups did not achieve statistical significance; P>0.08) and representative images are shown. L, lumen.

Article Snippet: Plasma PAI-1 antigen was measured either by a Luminex multiplex assay 39 or a standard ELISA utilizing anti-murine PAI-1 capture antibody (Molecular Innovations clone H34G6; coating concentration 1 μg/mL) and biotinylated anti-murine PAI-1 detection antibody (Molecular Innovations, ASMPAI-GF-BIO, 1 μg/mL).

Techniques: Immunostaining, Staining

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Drug Targeting of Plasminogen Activator Inhibitor-1 Inhibits Metabolic Dysfunction and Atherosclerosis in a Murine Model of Metabolic Syndrome

doi: 10.1161/ATVBAHA.119.313775

Figure Lengend Snippet: (A) SMCs were incubated for 24 hours with recombinant PAI-1 (10 μg/mL), recombinant PAI-1 and PAI-039 (25 μM), or vehicle control, after which SA-βGal expression (% positive cells) was measured; n= 5–7/group; *P<0.05 vs. other groups. (B) SMCs (passage number 6–8) were incubated 12 hours with or without anti-LRP1 antibody (at indicated concentrations [μg/mL]), after which PAI-1 (1 μg/mL, “+”) or vehicle control (“-”) was added. Cells were incubated an additional 24 hours, after which SA-βGal expression was measured; n=5/group, *P<0.05 vs. control (untreated SMCs). (C) SMCs (passage number 7) were incubated 24 hours with PAI-1-I91L (recombinant PAI-1 mutant with increased stability, normal anti-protease activity, and normal LRP1-binding affinity, concentration 1 μg/mL), PAI-1-I91L,K80/207A (recombinant PAI-1 mutant with increased stability, normal anti-protease activity, and a greater than 20-fold reduction in LRP1-binding affinity; concentration 1 μg/mL), or vehicle control, after which SA-βGal expression was measured; n=4/group; *P<0.001 vs. other groups.

Article Snippet: Plasma PAI-1 antigen was measured either by a Luminex multiplex assay 39 or a standard ELISA utilizing anti-murine PAI-1 capture antibody (Molecular Innovations clone H34G6; coating concentration 1 μg/mL) and biotinylated anti-murine PAI-1 detection antibody (Molecular Innovations, ASMPAI-GF-BIO, 1 μg/mL).

Techniques: Incubation, Recombinant, Expressing, Mutagenesis, Activity Assay, Binding Assay, Concentration Assay