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

Liqun Sun, Meihua Sun, Ke Ma, Jiangtao Liu
American Journal of Physiology. Cell Physiology 2020 July 15
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, the measurement of the expression of let-7d-5p, galectin-3 (LGALS3), toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB) as well as proinflammatory cytokines (TNF-α, IL-1b and IL-6) was conducted. The interaction between let-7d-5p and LGALS3 or Argonaute2 (AGO2) was identified. Gain- and loss-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, while LGALS3, TLR4 and NF-κB were highly expressed in the intestinal tissues of NEC rats. Over-expression 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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