Rôles des aquaporines dans le cerveau

Guérin, Céline F.; Regli, Luca; Badaut, Jérôme

doi:10.1051/medsci/2005218-9747

Cited by 6 publications

(2 citation statements)

References 32 publications

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“…TNF-α is an important regulator of intestinal inflammation that induces an increase in intestinal permeability via extracellular signal-regulated kinase 1/2-dependent activation of ETS transcription factor (Elk-1), which subsequently activates the MLCK gene in the nucleus by binding to the promoter region of MLCK ( 37 , 38 ). However, restoration of impaired mucosal barrier function may be achieved via downregulation of MLCK expression ( 7 , 8 ).…”

Section: Discussionmentioning

confidence: 99%

The possible association between AQP9 in the intestinal epithelium and acute liver injury‑induced intestinal epithelium damage

Xiang

Wen

et al. 2018

Mol Med Report

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The present study aimed to investigate the expression and function of aquaporin (AQP)9 in the intestinal tract of acute liver injury rat models. A total of 20 Sprague Dawley rats were randomly divided into four groups: Normal control (NC) group and acute liver injury groups (24, 48 and 72 h). Acute liver injury rat models were established using D-amino galactose, and the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (Tbil) and albumin were determined using an automatic biochemical analyzer. Proteins levels of myosin light chain kinase (MLCK) in rat intestinal mucosa were investigated via immunohistochemistry. Pathological features were observed using hematoxylin and eosin (H&E) staining. MLCK, AQP9 and claudin-1 protein expression levels were detected via western blotting. Levels of ALT and AST in acute liver injury rats were revealed to steadily increase between 24 and 48 h time intervals, reaching a peak level at 48 h. Furthermore, TBil levels increased significantly until 72 h. Levels of ALT were revealed to significantly increase until the 48 h time interval, and then steadily decreased until the 72 h time interval. The acute liver injury 72 h group exhibited the greatest levels of MLCK expression among the three acute liver injury groups; however, all three acute liver injury groups exhibited enhanced levels of MLCK expression compared with the NC group. Protein levels of AQP9 and claudin-1 were enhanced in the NC group compared with the three acute liver injury groups. H&E staining demonstrated that terminal ileum mucosal layer tissues obtained from the acute liver injury rats exhibited visible neutrophil infiltration. Furthermore, the results revealed that levels of tumor necrosis factor-α, interleukin (IL)-6 and IL-10 serum cytokines were significantly increased in the acute liver injury groups. In addition, AQP9 protein expression was suppressed in acute liver injury rats, which induced pathological alterations in terminal ileum tissues may be associated with changes of claudin-1 and MLCK protein levels.

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