IL-1β Plays an Important Role in Pressure Overload-Induced Atrial Fibrillation in Mice

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Author(s)

    • Matsushita Naoko Matsushita Naoko
    • Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University|Division of Cardiology, Department of Internal Medicine, School of Medicine, Iwate Medical University
    • Ishida Nanae Sawa Yohei
    • Division of Cardiology, Department of Internal Medicine, School of Medicine, Iwate Medical University
    • Ibi Miho Hirose Masamichi
    • Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University
    • Saito Maki Ishida Nanae
    • Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University
    • Takahashi Masafumi Ibi Miho
    • Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University
    • Taniguchi Shunichiro Saito Maki
    • Division of Molecular and Cellular Pharmacology, Department of Pathophysiology and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University

Abstract

<p>Hypertension is one risk for atrial fibrillation (AF) and induces cardiac inflammation. Recent evidence indicates that pressure overload-induced ventricular structural remodeling is associated with the activation of nucleotide binding-oligomerization domain (NOD)-like receptor P3 (NLRP3) inflammasomes, including an apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC). We hypothesized that NLRP3 inflammasomes are an initial sensor for danger signals in pressure overload-induced atrial remodeling, leading to AF. Transverse aortic constriction (TAC) or a sham procedure was performed in mice deficient for ASC<sup>−/−</sup> and interleukin-1β (IL-1β<sup>−/−</sup>). One week after the procedure, electrical left atrial burst pacing from the esophagus was performed for 30 s to induce AF. IL-1β, monocyte chemotactic protein 1 (MCP-1), connective tissue growth factor (CTGF), and collagen 1 gene expression were also examined. The electrical burst pacing induced AF in TAC-operated wild-type (WT) (<i>p</i> < 0.001) and ASC<sup>−/−</sup> (<i>p</i> < 0.05) mice, compared to no AF in the sham-operated WT and ASC<sup>−/−</sup> mice, respectively. In contrast, the number of mice in which sustained AF was induced was similar between TAC-operated IL-1β<sup>−/−</sup> and sham-operated IL-1β<sup>−/−</sup> mice (<i>p</i> > 0.05). The expression of all genes tested was increased in TAC-operated WT and ASC<sup>−/−</sup> mice compared with sham-operated WT and ASC<sup>−/−</sup> mouse atria, respectively. CTGF and collagen 1, but not MCP-1, gene expressions were increased in TAC-operated IL-1β<sup>−/−</sup> mouse atria compared with sham-operated WT and IL-1β<sup>−/−</sup> mouse atria. In contrast, the IL-1β gene was not detected in either TAC-operated or sham-operated IL-1β<sup>−/−</sup> mouse atria. These results suggest that an IL-1β activation pathway, different from NLRP3 inflammasomes, plays an important role in pressure overload-induced sustained AF.</p>

Journal

  • Biological and Pharmaceutical Bulletin

    Biological and Pharmaceutical Bulletin 42(4), 543-546, 2019

    The Pharmaceutical Society of Japan

Codes

  • NII Article ID (NAID)
    130007622152
  • NII NACSIS-CAT ID (NCID)
    AA10885497
  • Text Lang
    ENG
  • ISSN
    0918-6158
  • NDL Article ID
    029603971
  • NDL Call No.
    Z53-V41
  • Data Source
    NDL  J-STAGE 
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