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Foam Cell Induction Activates AMPK But Uncouples Its Regulation of Autophagy and Lysosomal Homeostasis.

Abstract：

:The dysregulation of macrophage lipid metabolism drives atherosclerosis. AMP-activated protein kinase (AMPK) is a master regulator of cellular energetics and plays essential roles regulating macrophage lipid dynamics. Here, we investigated the consequences of atherogenic lipoprotein-induced foam cell formation on downstream immunometabolic signaling in primary mouse macrophages. A variety of atherogenic low-density lipoproteins (acetylated, oxidized, and aggregated forms) activated AMPK signaling in a manner that was in part due to CD36 and calcium-related signaling. In quiescent macrophages, basal AMPK signaling was crucial for maintaining markers of lysosomal homeostasis as well as levels of key components in the lysosomal expression and regulation network. Moreover, AMPK activation resulted in targeted upregulation of members of this network via transcription factor EB. However, in lipid-induced macrophage foam cells, neither basal AMPK signaling nor its activation affected lysosomal-associated programs. These results suggest that while the sum of AMPK signaling in cultured macrophages may be anti-atherogenic, atherosclerotic input dampens the regulatory capacity of AMPK signaling.

journal_name

Int J Mol Sci

journal_title

International journal of molecular sciences

authors

LeBlond ND,Nunes JRC,Smith TKT,O'Dwyer C,Robichaud S,Gadde S,Côté M,Kemp BE,Ouimet M,Fullerton MD

doi

10.3390/ijms21239033

subject

Has Abstract

pub_date

2020-11-27 00:00:00

issue

23

issn

1422-0067

pii

ijms21239033

journal_volume

21

pub_type

杂志文章

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