Journal
GENES
Volume 12, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/genes12111829
Keywords
inflammation; apoptosis; circular RNA; miR-30e-3p/DENND1B axis; Lipopolysaccharide
Categories
Funding
- Natural Scientific Foundation of China [31761143014, U1901206]
- Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program [2019BT02N630]
- Ten-Thousand Talents Program [W03020593]
- China Agriculture Research System [CARS-41-G03]
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The study revealed that circNFIC promotes cell inflammation and apoptosis through the miR-30e-3p/DENND1B axis.
Disordered inflammation and apoptosis are closely related to diseases, and inflammation can also promote cell apoptosis, where growing evidence has shown that circular RNAs (circRNAs) play important roles. Lipopolysaccharide (LPS) is the main component of the cytoderm of gram-negative bacterium, which can cause inflammatory responses in macrophages. We constructed an inflammatory model by exposing chicken macrophage cell lines (also known as HD11) to LPS for in vitro experiments. In this study, we validated a novel circRNA-circNFIC-which was dramatically up-regulated in tissues infected by coccidia and cells exposed to LPS. Besides, circNFIC could significantly promote the expression levels of pro-inflammation factors, including (IL-1 beta, TNF alpha, and IFN gamma) and pro-apoptosis maker genes (caspase 3 and caspase 8) in HD11 exposed to LPS or not. In terms of mechanism, circNFIC exerted notable effects on DENND1B to regulate cell inflammation and apoptosis by sponging miR-30e-3p. The molecular functions played by miR-30e-3p and DENND1B have been explored, respectively. In addition, the effects of circNFIC knockdown suppressing the expression of pro-inflammatory and pro-apoptosis functions could be reversed by a miR-30e-3p inhibitor. On the whole, circNFIC promoted cell inflammation and apoptosis via the miR-30e-3p/DENND1B axis.
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