PMID- 30930414
OWN - NLM
STAT- MEDLINE
DCOM- 20190801
LR  - 20190801
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 42
IP  - 4
DP  - 2019
TI  - IL-1beta Plays an Important Role in Pressure Overload-Induced Atrial Fibrillation in 
      Mice.
PG  - 543-546
LID - 10.1248/bpb.b18-00363 [doi]
AB  - 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(-/-) and interleukin-1beta (IL-1beta(-/-)). One 
      week after the procedure, electrical left atrial burst pacing from the esophagus 
      was performed for 30 s to induce AF. IL-1beta, 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) (p < 0.001) and ASC(-/-) (p < 0.05) mice, compared to no AF in the 
      sham-operated WT and ASC(-/-) mice, respectively. In contrast, the number of mice 
      in which sustained AF was induced was similar between TAC-operated IL-1beta(-/-) and 
      sham-operated IL-1beta(-/-) mice (p > 0.05). The expression of all genes tested was 
      increased in TAC-operated WT and ASC(-/-) mice compared with sham-operated WT and 
      ASC(-/-) mouse atria, respectively. CTGF and collagen 1, but not MCP-1, gene 
      expressions were increased in TAC-operated IL-1beta(-/-) mouse atria compared with 
      sham-operated WT and IL-1beta(-/-) mouse atria. In contrast, the IL-1beta gene was not 
      detected in either TAC-operated or sham-operated IL-1beta(-/-) mouse atria. These 
      results suggest that an IL-1beta activation pathway, different from NLRP3 
      inflammasomes, plays an important role in pressure overload-induced sustained AF.
FAU - Matsushita, Naoko
AU  - Matsushita N
AD  - Division of Molecular and Cellular Pharmacology, Department of Pathophysiology 
      and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.
AD  - Division of Cardiology, Department of Internal Medicine, School of Medicine, 
      Iwate Medical University.
FAU - Ishida, Nanae
AU  - Ishida N
AD  - Division of Molecular and Cellular Pharmacology, Department of Pathophysiology 
      and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.
FAU - Ibi, Miho
AU  - Ibi M
AD  - Division of Molecular and Cellular Pharmacology, Department of Pathophysiology 
      and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.
FAU - Saito, Maki
AU  - Saito M
AD  - Division of Molecular and Cellular Pharmacology, Department of Pathophysiology 
      and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.
FAU - Takahashi, Masafumi
AU  - Takahashi M
AD  - Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical 
      University.
FAU - Taniguchi, Shunichiro
AU  - Taniguchi S
AD  - Department of Molecular Oncology, Graduate School of Medicine, Shinshu 
      University.
FAU - Iwakura, Yoichiro
AU  - Iwakura Y
AD  - Division of Experimental Animal Immunology, Research Institute for Biological 
      Sciences, Tokyo University of Science.
FAU - Morino, Yoshihiro
AU  - Morino Y
AD  - Division of Cardiology, Department of Internal Medicine, School of Medicine, 
      Iwate Medical University.
FAU - Taira, Eiichi
AU  - Taira E
AD  - Department of Molecular Oncology, Graduate School of Medicine, Shinshu 
      University.
FAU - Sawa, Yohei
AU  - Sawa Y
AD  - Division of Cardiology, Department of Internal Medicine, School of Medicine, 
      Iwate Medical University.
FAU - Hirose, Masamichi
AU  - Hirose M
AD  - Division of Molecular and Cellular Pharmacology, Department of Pathophysiology 
      and Pharmacology, School of Pharmaceutical Sciences, Iwate Medical University.
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (CARD Signaling Adaptor Proteins)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1beta)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (Nlrp3 protein, mouse)
RN  - 0 (Pycard protein, mouse)
MH  - Animals
MH  - Atrial Fibrillation/genetics/*metabolism
MH  - Blood Pressure
MH  - CARD Signaling Adaptor Proteins/genetics
MH  - Chemokine CCL2/genetics
MH  - Heart Atria/metabolism
MH  - Hypertension/genetics/*metabolism
MH  - Interleukin-1beta/genetics/*metabolism
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
OTO - NOTNLM
OT  - NLRP3 inflammasome
OT  - atrial fibrillation
OT  - hypertension
EDAT- 2019/04/02 06:00
MHDA- 2019/08/02 06:00
CRDT- 2019/04/02 06:00
PHST- 2019/04/02 06:00 [entrez]
PHST- 2019/04/02 06:00 [pubmed]
PHST- 2019/08/02 06:00 [medline]
AID - 10.1248/bpb.b18-00363 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2019;42(4):543-546. doi: 10.1248/bpb.b18-00363.