scholarly journals Retraction Note: Mst1 facilitates hyperglycemia-induced retinal pigmented epithelial cell apoptosis by evoking mitochondrial stress and activating the Smad2 signaling pathway

2021 ◽  
Author(s):  
Bing Wei ◽  
Min Wang ◽  
Wei Hao ◽  
Xiangdong He
Keyword(s):  
Epithelial Cell ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Mitochondrial Stress ◽  
Epithelial Cell Apoptosis

Let-7d-5p suppresses inflammatory response in neonatal rats with necrotizing enterocolitis via LGALS3-mediated TLR4/NF-κB signaling pathway

2020 ◽  
Vol 319 (6) ◽  
pp. C967-C979
Author(s):  
Liqun Sun ◽  
Meihua Sun ◽  
Ke Ma ◽  
Jiangtao Liu
Keyword(s):  
Epithelial Cell ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Necrotizing Enterocolitis ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Neonatal Rats ◽  
Loss Of Function ◽  
Epithelial Cell Apoptosis

Necrotizing enterocolitis (NEC) is an acute intestinal condition accounting for severe mortality and morbidity in preterm infants. This study aimed to identify the possible roles of let-7d-5p in neonatal rats with NEC. The differentially expressed genes (DEGs) related to NEC were initially screened in silico. After establishment of NEC rat models, measurement of the expression of let-7d-5p, galectin-3 (LGALS3), Toll-like receptor 4 (TLR4), and nuclear factor-κB (NF-κB) as well as proinflammatory cytokines (TNF-α, IL-1β, and IL-6) was conducted. The interaction between let-7d-5p and LGALS3 or argonaute-2 (AGO2) was identified. Gain- and loss-of-function approaches were then performed in an attempt to investigate the regulatory roles of let-7d-5p and LGALS3 in inflammation and cell apoptosis in NEC neonatal rats. Let-7d-5p was poorly expressed, whereas LGALS3, TLR4, and NF-κB were highly expressed, in the intestinal tissues of NEC rats. Overexpression of let-7d-5p resulted in decreased levels of proinflammatory factors in the intestinal tissues of NEC rats. Through sequential experimentation, let-7d-5p was identified to target LGALS3 and bind to AGO2. In addition, LGALS3 silencing or LPS treatment blocked the TLR4/NF-κB signaling pathway, thereby suppressing intestinal epithelial cell apoptosis and inflammation in NEC. Collectively, let-7d-5p might exercise its inhibitory properties in the inflammatory response and intestinal epithelial cell apoptosis in NEC neonatal rats via inactivation of the LGALS3-dependent TLR4/NF-κB signaling pathway.

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