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Acute Myocardial Infarction in Rats
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Acute Myocardial Infarction in Rats

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Microglial Mincle receptor in the PVN contributes to sympathetic hyperactivity in acute myocardial infarction rat

Yu Wang1, Jie Yin2, Cailing Wang3

  • 1School of Medicine, Shandong University, Jinan, China.

Journal of Cellular and Molecular Medicine
|October 25, 2018
PubMed

Insights

Macrophage-inducible C-type lectin (Mincle) in the brainstem promotes dangerous heart arrhythmias after heart attacks by increasing sympathetic nerve activity. Inhibiting Mincle reduces these arrhythmias and may offer new treatment strategies.

Area of Science:

  • Cardiovascular Research
  • Neuroscience
  • Immunology

Background:

  • Malignant ventricular arrhythmias (VAs) post-myocardial infarction (MI) are linked to sympathetic nerve hyperactivity.
  • Inflammation in the paraventricular nucleus (PVN) contributes to this sympathetic overactivity.

Purpose of the Study:

  • To investigate the role of Macrophage-inducible C-type lectin (Mincle) in the PVN in augmenting sympathetic activity after MI.
  • To determine if the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome/IL-1β axis is involved in Mincle-mediated sympathetic hyperactivity.

Main Methods:

  • Myocardial infarction induced by coronary artery ligation in rats.
  • Mincle expression, microglial activation, and sympathetic nerve activity (renal sympathetic nerve activity, norepinephrine levels) were measured.
  • Mincle-specific siRNA, NLRP3 siRNA, or IL-1β antagonist (gevokizumab) were administered to the PVN.
  • Arrhythmia scores were assessed using programmed electric stimulation.

Main Results:

  • Mincle expression in PVN microglia increased post-MI, correlating with sympathetic hyperactivity.
  • PVN-specific Mincle knockdown reduced microglial activation, sympathetic activity, and arrhythmia scores.
  • Mincle activation by its ligand (rSAP130) increased NLRP3 and IL-1β levels.
  • Inhibition of NLRP3 or IL-1β attenuated sympathetic hyperactivity.

Conclusions:

  • Mincle in PVN microglia exacerbates sympathetic hyperactivity and ventricular arrhythmias post-MI.
  • The Mincle-NLRP3/IL-1β axis plays a critical role in this process.
  • Targeting Mincle signaling offers a potential therapeutic strategy for preventing post-MI arrhythmias.
Keywords:
PVNIL-1βMincleNLRP3microgliamyocardial infarctionsympathetic hyperactivity

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