脂肪组织
小RNA
生物
胰岛素抵抗
脂质代谢
脂肪组织巨噬细胞
细胞生物学
细胞生长
基因
胰岛素
白色脂肪组织
内分泌学
遗传学
作者
Neil T. Sprenkle,Nathan C. Winn,Kaitlyn E. Bunn,Yang Zhao,D. Park,Birgitte Giese,John Karijolich,K. Mark Ansel,C. Henrique Serezani,Alyssa H. Hasty,Heather H. Pua
出处
期刊:Cell Reports
[Elsevier]
日期:2023-08-01
卷期号:42 (8): 112928-112928
被引量:2
标识
DOI:10.1016/j.celrep.2023.112928
摘要
Identifying molecular circuits that control adipose tissue macrophage (ATM) function is necessary to understand how ATMs contribute to tissue homeostasis and obesity-induced insulin resistance. In this study, we find that mice with a myeloid-specific knockout of the miR-23-27-24 clusters of microRNAs (miRNAs) gain less weight on a high-fat diet but exhibit worsened glucose and insulin tolerance. Analysis of ATMs from these mice shows selectively reduced numbers and proliferation of a recently reported subset of lipid-associated CD9+Trem2+ ATMs (lipid-associated macrophages [LAMs]). Leveraging the role of miRNAs to control networks of genes, we use RNA sequencing (RNA-seq), functional screens, and biochemical assays to identify candidate target transcripts that regulate proliferation-associated signaling. We determine that miR-23 directly targets the mRNA of Eif4ebp2, a gene that restricts protein synthesis and proliferation in macrophages. Altogether, our study demonstrates that control of proliferation of a protective subset of LAMs by noncoding RNAs contributes to protection against diet-induced obesity metabolic dysfunction.
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