| First Author | Matsushita N | Year | 2019 |
| Journal | Biol Pharm Bull | Volume | 42 |
| Issue | 4 | Pages | 543-546 |
| PubMed ID | 30930414 | Mgi Jnum | J:290968 |
| Mgi Id | MGI:6442248 | Doi | 10.1248/bpb.b18-00363 |
| Citation | Matsushita N, et al. (2019) IL-1beta Plays an Important Role in Pressure Overload-Induced Atrial Fibrillation in Mice. Biol Pharm Bull 42(4):543-546 |
| abstractText | 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. |
