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MiR‐874 promotes intestinal barrier dysfunction through targeting AQP3 following intestinal ischemic injury
Author(s) -
Zhi Xiaofei,
Tao Jinqiu,
Li Zengliang,
Jiang Baofei,
Feng Jin,
Yang Li,
Xu Hao,
Xu Zekuan
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.01.022
Subject(s) - occludin , paracellular transport , claudin , tight junction , downregulation and upregulation , intestinal ischemia , intestinal permeability , aquaporin 3 , microbiology and biotechnology , intestinal mucosa , ischemia , medicine , chemistry , permeability (electromagnetism) , aquaporin , cancer research , biology , reperfusion injury , gene , biochemistry , membrane
Intestinal ischemic injury is a significant clinical problem arising from diseases or as a complication of abdominal surgery. Our previous study showed aquaporin 3 is involved in intestinal barrier impairment. Here, we revealed that intestinal ischemia induced a time‐dependent increase of miR‐874 expression and a time‐dependent decrease of AQP3 expression, and the level of miR‐874 expression was inversely related to AQP3 protein expression. In addition, miR‐874 promoted the paracellular permeability in vitro through targeting 3′UTR of AQP3 . Two of the tight junction proteins, Occludin and Claudin‐1, were found to be involved in miR‐874‐induced intestinal barrier dysfunction.