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- Title
LncRNA UCA1 remits LPS‐engendered inflammatory damage through deactivation of miR‐499b‐5p/TLR4 axis.
- Authors
Zhao, Yan‐jun; Chen, Yue‐e; Zhang, Hong‐jun; Gu, Xing
- Abstract
Neonatal pneumonia is a high neonatal mortality disease. The current research was designed to elucidate the modulatory function and feasible molecular mechanism of UCA1 in LPS‐induced injury in pneumonia. Herein, LPS was applied to induce WI‐38 cell inflammatory damage. We displayed that UCA1 was elevated in LPS‐injured WI‐38 cells. In the functional aspect, intervention of UCA1 evidently aggrandized cell viability in LPS‐triggered WI‐38 cells. In the meanwhile, elimination of UCA1 distinctly assuaged cell apoptosis concomitant with declined levels of proapoptotic proteins Bax and C‐caspase‐3, and ascended the expression of antiapoptotic protein Bcl‐2. Subsequently, disruption of UCA1 manifestly restrained inflammatory damage as characterized by declination of multiple pro‐inflammatory factors IL‐1β, IL‐6, and TNF‐α in WI‐38 cells under LPS circumstance. More importantly, we predicted and verified that UCA1 functioned as a ceRNA by efficaciously binding to miR‐499b‐5p thereby inversely adjusting miR‐499b‐5p expression. Interesting, TLR4 was identified as direct target of miR‐499b‐5p, and positively regulated by UCA1 through sponging miR‐499b‐5p. Mechanistically, absence of miR‐499b‐5p or restoration of TLR4 impeded the beneficial effects of UCA1 ablation on LPS‐stimulated apoptosis and inflammatory response. Collectively, these observations illuminated that UCA1 inhibition protected WI‐38 cells against LPS‐managed inflammatory injury and apoptosis process via miR‐499b‐5p/TLR4 crosstalk, which ultimately influencing the development of pneumonia.
- Subjects
LINCRNA; BAX protein; BCL-2 proteins; NEONATAL mortality; LIPOPOLYSACCHARIDES; PROTEIN expression; NEONATAL diseases
- Publication
IUBMB Life, 2021, Vol 73, Issue 2, p463
- ISSN
1521-6543
- Publication type
Article
- DOI
10.1002/iub.2443