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. 2022 Mar 23;9:839917. doi: 10.3389/fmolb.2022.839917

FIGURE 5.

FIGURE 5

TTR in Serum-derived EVs is reduced in patients with ATTRv amyloidosis. (A) Western blotting analysis of S-EVs derived from patients and controls. TTR ladder bands were more obvious in the controls than in the patients. (B) EV ELISA using serum of controls and patients. Absorbance of TTR aggregates was significantly higher in the healthy controls than in the patients with ATTRv amyloidosis, whereas absorbance of CD63 was significantly higher in the patients than in the healthy controls. N = 6, mean ± S.E.; *, p < 0.05; **, p < 0.005, Mann–Whitney U test. (C) A model of EV-mediated V30M-TTR cell deposition. TTR is mainly produced by the liver and secreted into the bloodstream, but the majority of patients with ATTRv amyloidosis produce TTR with the V30M mutation, which promotes aggregation of V30M-TTR on the membranes of Serum-derived EVs and facilitates deposition on cells and other surfaces, resulting in reduced TTR in Serum-derived EVs for patients with ATTRv amyloidosis. Increasing the amount of EVs in patients with ATTRv amyloidosis could further promote this deposition.