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MiR-690, an exosomal-derived miRNA from M2-polarized macrophages, improves insulin sensitivity in obese mice

Cell metabolism, 2021-04, Vol.33 (4), p.781-790.e5 [Peer Reviewed Journal]

2021 Elsevier Inc. ;Copyright © 2021 Elsevier Inc. All rights reserved. ;ISSN: 1550-4131 ;EISSN: 1932-7420 ;DOI: 10.1016/j.cmet.2020.12.019 ;PMID: 33450179

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Title:
MiR-690, an exosomal-derived miRNA from M2-polarized macrophages, improves insulin sensitivity in obese mice
Author: Ying, Wei ; Gao, Hong ; Dos Reis, Felipe Castellani Gomes ; Bandyopadhyay, Gautam ; Ofrecio, Jachelle M. ; Luo, Zhenlong ; Ji, Yudong ; Jin, Zhongmou ; Ly, Crystal ; Olefsky, Jerrold M.
Subjects: Adipocytes - cytology ; Adipocytes - metabolism ; Animals ; Antagomirs - metabolism ; DEAD-box RNA Helicases - deficiency ; DEAD-box RNA Helicases - genetics ; Diet, High-Fat ; exosomes ; Exosomes - metabolism ; Hepatocytes - cytology ; Hepatocytes - metabolism ; Insulin - metabolism ; Insulin Resistance ; insulin sensitivity ; macrophages ; Macrophages - cytology ; Macrophages - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Obese ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR-690 ; Muscle Fibers, Skeletal - cytology ; Muscle Fibers, Skeletal - metabolism ; obesity ; Obesity - metabolism ; Obesity - pathology ; Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors ; Phosphotransferases (Alcohol Group Acceptor) - genetics ; Phosphotransferases (Alcohol Group Acceptor) - metabolism ; Ribonuclease III - deficiency ; Ribonuclease III - genetics ; RNA Interference ; RNA, Small Interfering - metabolism
Is Part Of: Cell metabolism, 2021-04, Vol.33 (4), p.781-790.e5
Description: Insulin resistance is a major pathophysiologic defect in type 2 diabetes and obesity, while anti-inflammatory M2-like macrophages are important in maintaining normal metabolic homeostasis. Here, we show that M2 polarized bone marrow-derived macrophages (BMDMs) secrete miRNA-containing exosomes (Exos), which improve glucose tolerance and insulin sensitivity when given to obese mice. Depletion of their miRNA cargo blocks the ability of M2 BMDM Exos to enhance insulin sensitivity. We found that miR-690 is highly expressed in M2 BMDM Exos and functions as an insulin sensitizer both in vivo and in vitro. Expressing an miR-690 mimic in miRNA-depleted BMDMs generates Exos that recapitulate the effects of M2 BMDM Exos on metabolic phenotypes. Nadk is a bona fide target mRNA of miR-690, and Nadk plays a role in modulating macrophage inflammation and insulin signaling. Taken together, these data suggest miR-690 could be a new therapeutic insulin-sensitizing agent for metabolic disease. [Display omitted] •IL4/IL13-induced macrophages produce M2 exosomes that can improve insulin resistance•miRNAs are responsible for the effects of M2 exosomes•miR-690 is an insulin-sensitizing miRNA within M2 exosomes•The miR-690-Nadk axis regulates inflammation and insulin signaling Miscommunication between adipose tissue macrophages (ATMs) and insulin target tissues is key to the development of insulin resistance, while it is known that lean ATM-derived exosomes promote insulin sensitivity. Here, Ying et. al show that miR-690 within ATM-derived exosomes directly increases insulin sensitivity both in vitro and in vivo.
Publisher: United States: Elsevier Inc
Language: English
Identifier: ISSN: 1550-4131
EISSN: 1932-7420
DOI: 10.1016/j.cmet.2020.12.019
PMID: 33450179
Source: Cell Press Free Archives
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MiR-690, an exosomal-derived miRNA from M2-polarized macrophages, improves insulin sensitivity in obese mice

2021 Elsevier Inc. ;Copyright © 2021 Elsevier Inc. All rights reserved. ;ISSN: 1550-4131 ;EISSN: 1932-7420 ;DOI: 10.1016/j.cmet.2020.12.019 ;PMID: 33450179

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