Over-expression of apolipoprotein J inhibits cholesterol crystal-induced inflammatory responses via suppressing NLRP3 inflammasome activation in THP-1 macrophages

Title:

Over-expression of apolipoprotein J inhibits cholesterol crystal-induced inflammatory responses via suppressing NLRP3 inflammasome activation in THP-1 macrophages

Creator:

Li, Y., Song, Y.-Q., Zhang, Y., Liu, T., and Qin, Qin

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:0886e2cf-828f-4baf-bd17-cf6caf6dc066
uuid:0886e2cf-828f-4baf-bd17-cf6caf6dc066

Subject:

apolipoprotein J (clusterin), interleukin 1β, tumour necrosis factor α, THP-1 macrophages, and inflammation

Type:

model:article and TEXT

Format:

bez média and svazek

Description:

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.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Coverage:

183-190

Source:

Folia biologica | 2021 Volume:67 | Number:5-6

Harvested from:

CDK

Metadata only:

false