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Ischemic Heart-Derived Small Extracellular Vesicles Impair Adipocyte Function.

Lu Gan1,2, Demin Liu2,3, Dina Xie2

  • 1Laboratory of Emergency Medicine, Department of Emergency Medicine and National Clinical Research Center for Geriatrics, West China Hospital (L.G., L.L., H.H., P.Y., Y.H., Y.C.), Sichuan University, Chengdu, China.

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|November 12, 2021
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Summary
This summary is machine-generated.

Myocardial ischemia/reperfusion (MI/R) induces adipocyte endoplasmic reticulum (ER) stress and dysfunction through small extracellular vesicles (sEVs) carrying the miR-23-27-24 cluster. Targeting this sEV communication pathway may prevent metabolic dysfunction post-MI/R.

Keywords:
adipocytesadipokinesextracellular vesicleshomeostasistranscription factors

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Area of Science:

  • Cardiovascular Biology
  • Metabolic Homeostasis
  • Extracellular Vesicle Biology

Background:

  • Acute myocardial infarction (MI) leads to systemic metabolic dysfunction through incompletely understood mechanisms.
  • Adipocytes are crucial for metabolic homeostasis, but the impact of MI on adipocyte function remains unclear.
  • Small extracellular vesicles (sEVs) mediate organ-organ communication, yet their role in post-MI cardiomyocyte-adipocyte crosstalk is unknown.

Purpose of the Study:

  • To investigate the role of sEVs in mediating communication between cardiomyocytes and adipocytes following MI.
  • To elucidate the mechanisms by which MI affects adipocyte function via sEVs.
  • To identify potential therapeutic targets for metabolic dysfunction after MI.

Main Methods:

  • Isolated plasma sEVs from sham control and MI/R animals, and incubated them with adipocytes.
  • Assessed gene expression, endoplasmic reticulum (ER) stress pathways (PERK-CHOP, ATF6-EDEM), and adiponectin (APN) levels in adipocytes.
  • Utilized bioinformatic analysis and RT-qPCR to identify microRNAs (miRNAs) in sEVs and adipose tissue.
  • Employed cardiomyocyte-specific miRNA sponges and mimics/inhibitors to investigate the role of the miR-23-27-24 cluster and its target EDEM3.

Main Results:

  • MI/R-derived sEVs significantly altered adipocyte gene expression, including reduced APN, and activated ER stress pathways.
  • The miR-23-27-24 cluster was significantly increased in sEVs and adipose tissue of MI/R animals, originating from cardiomyocytes.
  • miR-27a activated ER stress pathways, while a miR-27a inhibitor attenuated MI/R-induced ER stress and restored APN production.
  • EDEM3 was identified as a novel downstream target of miR-27a; adipocyte EDEM3 deficiency mimicked MI/R effects, while overexpression attenuated ER stress.

Conclusions:

  • MI/R induces adipocyte ER stress and endocrine dysfunction via cardiomyocyte-derived sEVs enriched with the miR-23-27-24 cluster.
  • Targeting sEV-mediated cardiomyocyte-adipocyte communication presents a potential therapeutic strategy to prevent post-MI metabolic dysfunction.