Journal
CELL BIOCHEMISTRY AND FUNCTION
Volume 33, Issue 4, Pages 235-240Publisher
WILEY-BLACKWELL
DOI: 10.1002/cbf.3109
Keywords
intestinal epithelial barrier; microRNA-21; PI3K; Akt pathway; tumour necrosis factor
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Funding
- Science and Technology Commission of Shanghai Municipality [11ZR1405700]
- Key Clinical Discipline Construction of Shanghai Municipality [ZK2012B20]
- Shanghai Municipal Commission of Health and Family planning [20144Y0193]
- Science and Technology Commission in Jinshan district [2014-3-18]
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Increased tight junction (TJ) barrier permeability, induced by tumour necrosis factor (TNF)-, 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- 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. Copyright (c) 2015 John Wiley & Sons, Ltd.
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