Fig 1: Amyloid plaque infiltration by macrophages and neutrophils: serial sections stomach sections from mice representing the four groups of mice were stained with Thioflavin-S, α-TTR, the pan-macrophage marker α-CD68 and the neutrophil marker α-Neutrophil elastase (ELANE). Immunofluorescence on the stomach tissue from the untreated mouse indicates the complete absence of neutrophils from the plaque, while there is some co-expression with CD68 (A). A similar pattern was observed with the mouse treated with the PMX53 antagonist molecule (B), while complete co-localization with both CD68 and ELANE was observed in the mouse treated with the full agonist molecule (C). Immunofluorescence on the mouse treated with the modified agonist EP67 however revealed complete plaque co-localization with CD68 and the complete absence of ELANE from the region (D). Scale bar = 75 μm.
Fig 2: Amyloid deposition: amyloid plaques were quantified through Thioflavin-S staining (A). All groups exhibited significant difference from one another, with the PMX53 treated mice having the greatest amount of deposition and the full agonist treated group having the lowest recorded amount. n = 6/group, data presented as mean ± 1 SD. *p < 0.05, **p < 0.01, ***p < 0.001. (B) Amyloid plaque in the stomach that stains with Congo red and exhibits apple green birefringence (Bi,ii). The same plaque stains Thioflavin-S positive (Biii) and is composed of human transthyretin (TTR; Biv). The area of co-localization of Thioflavin-S and TTR labeling appears yellow (Bv) and morphometric measurements are carried out with the ImageJ software (Bvi). Scale bar = 150 μm.
Fig 3: The plasma (A) RBP4 and (B) TTR concentrations at 25–28 weeks gestation (SD1), 28–32 weeks gestation (SD2), and 3–4 months PP (SD3) were measured from 23 healthy pregnant women. The ratio of (C) retinol to RBP4 and (D) retinol to TTR were lower on both SD1 and SD2 in comparison to SD3. In panels C,D, one subject had insufficient sample to measure SD3 retinol concentrations (red symbols) and was excluded from the statistical comparison (n = 22 pregnant women).
Fig 4: Amount of hTTR found in the serum and stomach: (A) TTR in the serum was quantified using enzyme-linked immunosorbent assay (ELISA). Results show that no statistical difference in the amount of circulating TTR was recorded between the four groups of mice. n = 4/group, data presented as mean ± 1 SD. (B) hTTR levels in the stomach were measured via immunoblotting. Significant decrease was observed in the mice treated with the two agonist molecules when compared to the untreated control mice. n = 6/group. Data presented as mean ± 1 SD. Indicative images from each group shown in (Bi–iv). *p < 0.05, **p < 0.01, ***p < 0.001.
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