The Role of KLF4 in Lps-Induced Intestinal Epithelial Cell Injury Through the MIR-1306-5P/HIPK2 Signaling Axis.

Sepsis-induced acute intestinal cell injury disrupts the normal barrier function of the intestine and leads to systemic inflammation and organ dysfunction. This study aims to investigate the molecular mechanism of Kruppel-like factor 4 (KLF4) in lipopolysaccharide (LPS)-induced intestinal epithelial cell injury. A human colonic mucosal epithelial cell line was treated with LPS to establish a model of intestinal epithelial injury. Real-time quantitative polymerase chain reaction and Western blot assay were performed to detect the expression of KLF4/microRNA (miR)-1306-5p/homeodomain interacting protein kinase 2 (HIPK2). Cell injury and apoptosis were detected. The levels of Occludin and zonula occludens-1 (ZO-1) were measured. The permeability was evaluated. The binding between KLF4 and the miR-1306-5p promoter, and between miR-1306-5p and HIPK2, was analyzed. The role of the miR-1306-5p/HIPK2 axis in cells was demonstrated by co-experiments. KLF4 and HIPK2 were downregulated, while miR-1306-5p was upregulated in LPS-treated cells. Overexpression of KLF4 increased cell viability and reduced apoptosis. Mechanistically, KLF4 could bind to the miR-1306-5p promoter, suppressing miR-1306-5p expression and thereby promoting HIPK2 expression. Overexpression of miR-1306-5p or downregulation of HIPK2 attenuated the protective effect of KLF4 overexpression on LPS-induced intestinal epithelial cell injury. In conclusion, KLF4 inhibits LPS-induced intestinal epithelial cell injury through the miR-1306-5p/HIPK2 axis.