Interleukin-33 promotes the epithelial-mesenchymal transition of renal tubular epithelial cells via the NF-κB/Twist1 signalling pathway

Objectives: Epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells (RTECs) is a pathogenic factor for interstitial fibrosis (RIF). Interleukin-33 (IL-33) related to the occurrence and development RIF, but underlying mechanism remains unclear. Here, we investigated whether IL-33 mediates EMT RTECs by activating NF-κB/Twist1 signalling pathway. Methods: In vivo, RIF animal model induced unilateral ureteral obstruction (UUO) was established. The effects exogenous anti-IL-33 antibodies were evaluated. vitro, IL-33. inhibition nuclear kappa-B (NF-κB) pyrrolidine dithiocarbamate (PDTC) knockdown suppression tumorigenicity 2 (ST2) small interference RNA used observe through signaling Results: significantly aggravated UUO-induced pathological damage collagen deposition, down-regulated E-cadherin expression, up-regulated α-smooth muscle actin Vimentin expressions. Moreover, increased levels phospho-IκB-α (p-IκB-α) phospho-NF-κB p65 (p-NF-κB p65), NF-κB translocation, Twist1 expression. However, these reversed antibody. vitro , increases in p-IκB-α, p-NF-κB p65, expression inhibited PDTC or ST2. IL-33-mediated also reversed. inhibitor had no significant effect on ST2 Conclusions: IL-33/ST2 axis may up-regulate pathway, thereby inducing leading RIF.