scholarly journals G Protein-Coupled Receptor 109A and Host Microbiota Modulate Intestinal Epithelial Integrity During Sepsis

2018 ◽  
Author(s):  
Guangxin Chen ◽  
Shoupeng Fu ◽  
Bingxu Huang ◽  
Liwei Xie ◽  
Xin Ran ◽  
...  
2004 ◽  
Vol 287 (4) ◽  
pp. R772-R779 ◽  
Author(s):  
Sónia Fraga ◽  
Pedro A. Jose ◽  
Patrício Soares-da-Silva

Dopamine-induced inhibition of Na+-K+-ATPase has been suggested to play a role in the regulation of Na+ absorption at the intestinal level, and these effects were mediated by dopamine D1-like receptors. The aim of this work was to evaluate the effect of the activation of the D1-like receptors on the activity of the Na+/H+ exchanger (NHE) in the rat intestinal epithelial cell line IEC-6. The presence of D1 receptors was confirmed by immunoblotting. The dopamine D1-like receptor agonist SKF-38393 produced a concentration-dependent inhibition of NHE activity and stimulation of adenylyl cyclase (AC), this being antagonized by the D1 selective antagonist SKF-83566. Effects of SKF-38393 on NHE and AC activities were maximal at 5 min of exposure to the agonist and rapidly diminished with no effect at 25 min. Exposure of cells for 25 min to dibutyryl-cAMP (0.5 mM) or to the AC activator forskolin (3 μM) effectively inhibited NHE activity. Pretreatment of cells with heparin (1 μM), a nonselective G protein-coupled receptor kinase (GRK) inhibitor, prevented the loss of effects on NHE activity after 25 min exposure to SKF-38393. The presence of GRK4, GRK6A, and GRK6B was confirmed by immunoblotting. Overnight treatment with the anti-GRK4–6 antibody complexed with Lipofectin was also effective in preventing loss of the effects of SKF-38393 on NHE and AC activities. It is concluded that dopamine D1 receptors in IEC-6 rapidly desensitize to D1-like agonist stimulation and GRK4 and 6 appear to be involved in agonist-mediated responsiveness and desensitization.


2012 ◽  
Vol 142 (5) ◽  
pp. S-809
Author(s):  
Cheryl de Valliere ◽  
Solange Vidal ◽  
Jyrki J. Eloranta ◽  
Silvia Lang ◽  
Irina Vetter ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2756
Author(s):  
Jinbiao Zhao ◽  
Jinhua Hu ◽  
Xi Ma

The study was conducted to explore actions of decanoic acid on regulating intestinal barrier and antioxidant functions in intestinal epithelium cells isolated from porcine jejunum (IPEC-J2) and C57/BL6 mice models. In vitro and vivo assays, mice and IPEC-J2 cells treated by H2O2 were disposed of sodium decanoate and sodium butyrate to determine intestinal barrier and antioxidant functions of the host. Results showed that sodium decanoate upregulated expression of tight junction proteins and improved antioxidant capacity in both IPEC-J2 cells treated by H2O2 and mice models (p < 0.05). Sodium decanoate increased weight gain and ileal villus height of mice compared with control and sodium butyrate treatments (p < 0.05). Sodium decanoate increased α-diversity of ileal microbiota, volatile fatty acids concentration, and G protein-coupled receptor-43 (GPR-43) expression in the ileum and colon of mice (p < 0.05). In conclusion, sodium decanoate improved antioxidant capacity, intestinal morphology, and gut physical barrier of intestinal epithelial cells, resulting in an increase growth performance of mice, which is mediated through activating GPR-43 signaling.


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