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Increased tight junction (TJ) barrier permeability, induced by tumour necrosis factor (TNF)-α, may lead to the defects in TJ barrier and subsequent development of inflammation. Recent evidence suggests that miR-21 is implicated in inflammatory diseases. However, the physiological role of miR-21 in intestinal permeability remains elusive. This study aimed to explore the role of miR-21 in intestinal epithelial tight junction permeability. The filter-grown Caco-2 monolayers model system was established to mimic intestinal barrier defect. The tight junction proteins were detected by immunofluorescence and western blot analysis. The expression of miR-21 was assessed by real-time polymerase chain reaction (PCR). We found that the expression of miR-21 was increased significantly in TNF-α induced intestinal TJ barrier defect model. miR-21 overexpression significantly enhanced while miR-21 knockdown significantly decreased intestinal permeability. In addition, miR-21 overexpression significantly increased while miR-21 knockdown significantly decreased the levels of interleukin-6, interleukin-8 and prostaglandin E2 in cell culture medium. Furthermore, miR-21 positively regulated Akt phosphorylation and negatively regulated Phosphatase and tensin homolog (PTEN) expression in Caco-2 cells. Our results suggest that miR-21 may regulate intestinal epithelial tight junction permeability through PTEN/PI3K/Akt signalling pathway. This promotes the feasibility of targeting miR-21 in the clinical to preserve the intestinal barrier.
Zhang et al. (2015) studied this question.