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Dysfunction of cholesterol sensor SCAP promotes inflammation activation in THP-1 macrophages

Ouyang, Nan, Gan, Hua, He, Quan, Lei, Han, Wang, Stephen Y., Liu, Qing, Zhou, Chao·2018·Experimental Cell Research
DOI 10.1016/j.yexcr.2018.03.032
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Abstract

Crosstalk occurs between dyslipidemia and chronic inflammation, which are both precipitants of atherosclerosis. Sterol regulatory element binding proteins cleavage-activating protein (SCAP) plays a key role in regulating cholesterol homeostasis. The present study investigated the effects of SCAP dysfunction on the expression of inflammatory cytokines and lipid metabolism in THP-1 macrophages. Intracellular cholesterol content was assessed by Oil Red O staining and quantitative assays. The expression of SCAP, HMGCR, pro-IL-1β and N-SREBP2, p65(N) in the nucleus were examined by real-time quantitative RT-PCR and Western blotting. The level of secretary proteins IL-1β, TNF-α and MCP-1 in the supernatants were determined by ELISA. The translocation of SCAP from the endoplasmic reticulum (ER) to the Golgi was detected by confocal microscopy. Our results demonstrated that over-expression of SCAP significantly increased the expression of HMGCR, pro-IL-1β in the cytoplasm, and mature IL-1β, TNF-α, MCP-1 in the supernatants, while knocking down SCAP dramatically decreased the expression of these molecules. Betulin effectively suppressed the accumulation of intracellular cholesterol in the SCAP over-expressed THP-1 macrophages, but did not affect the expression of inflammatory cytokines, indicating that the pro-inflammatory effect of SCAP was independent of its routine role in regulating cholesterol homeostasis. Furthermore, we investigated the molecular mechanisms mediating the crosst…

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Metadata

Authors
Ouyang, N., Gan, H., He, Q., Lei, H., Wang, S. Y., Liu, Q., & Zhou, C.
Venue
Experimental Cell Research
Publisher
Elsevier BV
Published
2018-06
Volume
367
Issue
2
Pages
162-169
ISSN
0014-4827
DOI
10.1016/j.yexcr.2018.03.032
Cited by
14
References
4
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
National Natural Science Foundation of China (81500341)

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