| Literature DB >> 33604630 |
Ming Xu1, Xiao-Yong Li1, Laichun Song1, Chao Tao1, Jihui Fang1, Liang Tao1.
Abstract
Apoptosis and inflammation were the main hallmarks of sepsis-induced cardiomyopathy (SIC). Yes-associated protein isoform 1 (Yap1) and miR-484 were involved in mitochondrial fission and apoptosis, especially proapoptotic roles in SIC. Here, we investigated the role of Yap1 and miR-484 in lipopolysaccharide (LPS)-treated H9c2 cells. Yap1 was downregulated, while miR-484 was elevated by LPS treatment. Cell counting kit-8, flow cytometry, western blotting, and ELISA showed that miR-484 inhibitor significantly improved cell viability, decreased apoptosis, suppressed NLRP3 inflammasome formation, and reduced secretion of inflammatory cytokines TNF-α, IL-1β, and IL-6. Yap1, directly targeted by miR-484 shown in the luciferase assay, was more like a compensatory regulator of LPS stimulation. Knockdown of Yap1 inverted the effects of miR-484 inhibitor, including decreased cell viability, and promoted apoptosis and inflammation. These revealed miR-484 directly targeted mRNA of Yap1 to inhibit cell viability, and promote apoptosis and inflammation in LPS-treated H9c2 cells.Entities:
Keywords: SIC; apoptosis; cardiomyocyte; inflammation
Mesh:
Substances:
Year: 2021 PMID: 33604630 DOI: 10.1093/bbb/zbaa009
Source DB: PubMed Journal: Biosci Biotechnol Biochem ISSN: 0916-8451 Impact factor: 2.043