Over-expression of Apolipoprotein J Inhibits Cholesterol Crystal-Induced Inflammatory Responses via Suppressing NLRP3 Inflammasome Activation in THP-1 Macrophages.

IF 0.8 4区 生物学 Q4 BIOLOGY Folia Biologica-Krakow Pub Date : 2021-01-01 DOI:10.14712/fb2021067050183
Y Li, Y-Q Song, Y Zhang, T Liu, Q Qin
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Abstract

Apolipoprotein J (clusterin) is a component of high-density lipoproteins, the high level of which is reversely correlated with the risk of coronary heart disease. In addition, it exerts anti-inflammatory and anti-apoptotic effects on endothelial cells and inhibits smooth muscle cell migration and proliferation, indicating that it may play a protective role in cardiovascular disease. However, the exact mechanisms by which this occurs remain unclear. This study aimed to clarify these underlying protective mechanisms by researching the inhibitory effects of apolipoprotein J via the NOD-like receptor protein 3 pathway on the inflammation induced by cholesterol crystals in THP‑1 macrophages. In culture, THP-1 macrophages were infected with adenoviral vectors containing apolipoprotein J genes and subsequently treated with cholesterol crystals. The inflammatory cytokines interleukin‑1β, interleukin 18 and tumour necrosis factor α were quantitatively measured with ELISA kits. NOD-like receptor protein 3, cysteinyl aspartate specific proteinase 1 and interleukin 1β were evaluated by Western blot and PCR analysis. As a result, apolipoprotein J expression was found to remarkably decrease the levels of inflammatory cytokines, including tumour necrosis factor α, interleukin 18 and interleukin 1β, secreted by THP‑1 macrophages. It was also found capable of inhibiting the levels of NOD-like receptor protein 3, cysteinyl aspartate-specific proteinase 1 and interleukin 1β both at the protein and mRNA levels. In the current study, we revealed that over-expression of apolipoprotein J attenuated the inflammation induced by cholesterol crystals through inhibition of the NOD-like receptor protein 3 inflammasome pathway.

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载脂蛋白J的过表达通过抑制THP-1巨噬细胞NLRP3炎性体激活抑制胆固醇晶体诱导的炎症反应
载脂蛋白J(聚簇蛋白)是高密度脂蛋白的一个组成部分,其高水平与冠心病的风险呈负相关。此外,它对内皮细胞具有抗炎和抗凋亡作用,抑制平滑肌细胞的迁移和增殖,表明它可能在心血管疾病中起保护作用。然而,发生这种情况的确切机制尚不清楚。本研究通过nod样受体蛋白3途径研究载脂蛋白J对THP‑1巨噬细胞胆固醇结晶诱导炎症的抑制作用,旨在阐明这些潜在的保护机制。在培养中,用含载脂蛋白J基因的腺病毒载体感染THP-1巨噬细胞,随后用胆固醇晶体处理。采用ELISA试剂盒定量检测炎症因子白介素1β、白介素18和肿瘤坏死因子α。Western blot和PCR检测nod样受体蛋白3、天冬氨酸半胱氨酸特异性蛋白酶1和白细胞介素1β。结果发现载脂蛋白J的表达显著降低THP - 1巨噬细胞分泌的炎性细胞因子水平,包括肿瘤坏死因子α、白细胞介素18和白细胞介素1β。还发现它能够抑制nod样受体蛋白3、半胱氨酸天冬氨酸特异性蛋白酶1和白细胞介素1β的蛋白和mRNA水平。在目前的研究中,我们发现载脂蛋白J的过度表达通过抑制nod样受体蛋白3炎症小体途径来减轻胆固醇晶体诱导的炎症。
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来源期刊
Folia Biologica-Krakow
Folia Biologica-Krakow 医学-生物学
CiteScore
1.10
自引率
14.30%
发文量
15
审稿时长
>12 weeks
期刊介绍: Folia Biologica (Kraków) is an international online open access journal accepting original scientific articles on various aspects of zoology: phylogeny, genetics, chromosomal studies, ecology, biogeography, experimental zoology and ultrastructural studies. The language of publication is English, articles are assembled in four issues per year.
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