Heart tissue can experience a progressive accumulation of transthyretin (TTR), a small four subunit protein that transports holoretinol binding protein and thyroxine. This severe pathology is known as transthyretin amyloid cardiomyopathy. Numerous experimental studies indicated that the aggregation rate and toxicity of TTR fibrils could be altered by the presence of lipids; however, the role of plasmalogens in this process remains unknown. In this study, we investigate the effect of choline plasmalogens (CPs) with different lengths and saturations of fatty acids (FAs) on TTR aggregation. We found that CPs with saturated and unsaturated FAs strongly suppressed TTR aggregation. We also found that CPs with saturated FAs did not change the morphology of TTR fibrils; however, much thicker fibrillar species were formed in the presence of CPs with unsaturated FAs. Finally, we found that CPs with C16:0, C18:0, and C18:1 FAs substantially lowered the cytotoxicity of TTR fibrils that were formed in their presence.

中文翻译：

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缩醛磷脂改变甲状腺素运载蛋白的聚集率并降低甲状腺素运载蛋白原纤维的毒性

心脏组织会逐渐积累转甲状腺素蛋白 (TTR)，这是一种小的四亚基蛋白，可转运全视黄醇结合蛋白和甲状腺素。这种严重的病理学称为转甲状腺素蛋白淀粉样心肌病。大量实验研究表明，脂质的存在可以改变 TTR 原纤维的聚集速率和毒性；然而，缩醛磷脂在此过程中的作用仍不清楚。在本研究中，我们研究了不同长度和脂肪酸 (FA) 饱和度的胆碱缩醛磷脂 (CP) 对 TTR 聚集的影响。我们发现含有饱和和不饱和 FA 的 CP 强烈抑制 TTR 聚集。我们还发现含有饱和 FA 的 CP 不会改变 TTR 原纤维的形态；然而，在含有不饱和 FA 的 CP 存在下，形成了更粗的原纤维。最后，我们发现含有 C16:0、C18:0 和 C18:1 FA 的 CP 显着降低了在其存在下形成的 TTR 原纤维的细胞毒性。