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Probing inflammasome activation in atherosclerosis

Chan, Yee-Hung and Ramji, Dipak P. ORCID: 2022. Probing inflammasome activation in atherosclerosis. Ramji, Dipak, ed. Atherosclerosis: Methods and Protocols, Vol. 2419. Methods in Molecular Biology, New York, NY: Springer, pp. 313-331. (10.1007/978-1-0716-1924-7_20)

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Atherosclerosis is driven by chronic inflammation in all stages of the disease. Inflammation is fueled by elevated levels of pro-inflammatory cytokines. Interleukins (IL) are cytokines of particular importance in atherosclerosis, due to their key involvement in various pro-atherogenic processes, including infiltration of immune cells to the lesion, stimulation of the production of other pro-inflammatory mediators by other sources, and generation of lipid laden foam cells, all of which contribute to plaque development and progression. Various stimuli that are abundant in atherosclerotic plaques, including oxidized low-density lipoprotein, cholesterol crystals and reactive oxygen species can trigger inflammasome activation. Importantly, activation of the nucleotide oligomerization domain leucine-rich repeat and pyrin domain containing protein 3 (NLRP3) inflammasome activates the caspase-1 protease and results in the generation and release of potent pro-inflammatory cytokines, IL-1β and IL-18. Both cytokines are influential in driving chronic inflammation and atherogenesis. This chapter describes the use of enzyme-linked immunosorbent assay (ELISA) and Western blot to quantify these cytokines in cell supernatant and lysate respectively, after stimulating inflammasome activation in cultured cells.

Item Type: Book Section
Date Type: Publication
Status: Published
Schools: Biosciences
Publisher: Springer
ISBN: 9781071619230
ISSN: 1064-3745
Last Modified: 06 Jan 2024 02:39

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