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PPARγ is a nexus controlling alternative activation of macrophages via glutamine metabolism.

Abstract：

:The nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ) is known to regulate lipid metabolism in many tissues, including macrophages. Here we report that peritoneal macrophage respiration is enhanced by rosiglitazone, an activating PPARγ ligand, in a PPARγ-dependent manner. Moreover, PPARγ is required for macrophage respiration even in the absence of exogenous ligand. Unexpectedly, the absence of PPARγ dramatically affects the oxidation of glutamine. Both glutamine and PPARγ have been implicated in alternative activation (AA) of macrophages, and PPARγ was required for interleukin 4 (IL4)-dependent gene expression and stimulation of macrophage respiration. Indeed, unstimulated macrophages lacking PPARγ contained elevated levels of the inflammation-associated metabolite itaconate and express a proinflammatory transcriptome that, remarkably, phenocopied that of macrophages depleted of glutamine. Thus, PPARγ functions as a checkpoint, guarding against inflammation, and is permissive for AA by facilitating glutamine metabolism. However, PPARγ expression is itself markedly increased by IL4. This suggests that PPARγ functions at the center of a feed-forward loop that is central to AA of macrophages.

journal_name

Genes Dev

journal_title

Genes & development

authors

Nelson VL,Nguyen HCB,Garcìa-Cañaveras JC,Briggs ER,Ho WY,DiSpirito JR,Marinis JM,Hill DA,Lazar MA

doi

10.1101/gad.312355.118

subject

Has Abstract

pub_date

2018-08-01 00:00:00

pages

1035-1044

issue

15-16

eissn

0890-9369

issn

1549-5477

pii

gad.312355.118

journal_volume

32

pub_type

杂志文章

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