We have located links that may give you full text access.
Interferon-stimulated gene 15 promotes cholesterol efflux by activating autophagy via the miR-17-5p/Beclin-1 pathway in THP-1 macrophage-derived foam cells.
European Journal of Pharmacology 2018 May 16
Macrophage autophagy contributes to the hydrolysis of cholesteryl ester into free cholesterol mainly for ATP-binding cassette transporter A1 (ABCA1)-dependent efflux. Interferon-stimulated gene 15 (ISG15) has been shown to regulate autophagy in multiple types of cells. The present study aimed to examine the effects of ISG15 on autophagy and cholesterol efflux in THP-1 macrophage-derived foam cells and to explore the underlying molecular mechanisms. Our results showed that overexpression of ISG15 promoted autophagy and cholesterol efflux and inhibited lipid accumulation without impact on ABCA1 expression. Inhibition of autophagy by 3-methyladenine (3-MA) abrogated the enhancing effects of ISG15 on cholesterol efflux. Both bioinformatics analysis and dual luciferase reporter assay identified Beclin-1 as a direct target of miR-17-5p. Moreover, ISG15 overexpression markedly decreased miR-17-5p levels and upregulated Beclin-1 expression. ISG15-induced enhancement of autophagy and cholesterol efflux was reversed by pretreatment with either miR-17-5p mimic or Beclin-1 siRNA. In conclusion, these findings suggest that ISG15 reduces miR-17-5p levels and thereby promotes Beclin-1-mediated autophagy, resulting in increased cholesterol efflux from THP-1 macrophage-derived foam cells.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app