Lipid Metabolism, Center for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Department of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan, Republic of Korea.
PLoS One. 2021 May 13;16(5):e0251599. doi: 10.1371/journal.pone.0251599. eCollection 2021.
Chronic HIV infection may exacerbate atherosclerotic vascular disease, which at advanced stages presents as necrotic plaques rich in crystalline cholesterol. Such lesions can catastrophically rupture precipitating myocardial infarct and stroke, now important causes of mortality in those living with HIV. However, in this population little is known about plaque structure relative to crystalline content and its chemical composition. Here, we first interrogated plaque crystal structure and composition in atherosclerotic SIV-infected macaques using non-linear optical microscopy. By stimulated Raman scattering and second harmonic generation approaches both amorphous and crystalline plaque lipid was detected and the crystal spectral profile indicated a cholesterol ester (CE) dominated composition. Versus controls, SIV+ samples had a greater number of cholesterol crystals (CCs), with the difference, in part, accounted for by crystals of a smaller length. Given the ester finding, we profiled HIV+ plaques and also observed a CE crystalline spectral signature. We further profiled plaques from Ldlr-/- mice fed a high fat diet, and likewise, found CE-dominate crystals. Finally, macrophage exposure to CCs or AcLDL induced auto-fluorescent puncta that co-stained with the LC3B autophagy sensor. In aggregate, we show that atheromatous plaques from mice, macaques and humans, display necrotic cores dominated by esterified CCs, and that plaque macrophages may induce autophagic vesicle formation upon encountering CCs. These findings help inform our knowledge of plaque core lipid evolution and how the process may incite systemic inflammation.
慢性 HIV 感染可能会加剧动脉粥样硬化性血管疾病,在晚期,这种疾病表现为富含结晶胆固醇的坏死斑块。这种病变可能会灾难性地破裂,导致心肌梗死和中风,目前这些疾病是 HIV 感染者死亡的重要原因。然而,在这一人群中,人们对斑块结构相对于结晶含量及其化学成分知之甚少。在这里,我们首次使用非线性光学显微镜研究了动脉粥样硬化性 SIV 感染猕猴的斑块晶体结构和组成。通过受激拉曼散射和二次谐波产生方法,检测到了无定形和结晶斑块脂质,并且晶体光谱特征表明其组成主要为胆固醇酯 (CE)。与对照组相比,SIV+ 样本中的胆固醇晶体 (CCs) 数量更多,其中部分差异是由于晶体长度较小所致。鉴于酯的发现,我们对 HIV+ 斑块进行了分析,也观察到了 CE 结晶的光谱特征。我们进一步对高脂饮食喂养的 Ldlr-/- 小鼠的斑块进行了分析,同样发现了 CE 主导的晶体。最后,巨噬细胞暴露于 CCs 或 AcLDL 会诱导具有自动荧光的斑点,这些斑点与自噬传感器 LC3B 共染色。总之,我们表明,来自小鼠、猕猴和人类的动脉粥样硬化斑块显示出富含酯化 CCs 的坏死核心,并且斑块巨噬细胞在遇到 CCs 时可能会诱导自噬囊泡的形成。这些发现有助于我们了解斑块核心脂质的演变过程,以及这一过程如何引发全身炎症。