Aggravated Intestinal Apoptosis by ClC-3 Deletion is Lethal to Mice Endotoxemia.

Aggravated Intestinal Apoptosis by ClC-3 Deletion is Lethal to Mice Endotoxemia. Cell Biol Int. 2018 Jul 04;: Authors: Huang LY, Li YJ, Li PP, Li HC, Ma P Abstract Our previous study found that ClC-3 chloride channel functioned differently in the vascular and intestinal inflammation, the loss of ClC-3 reduced vascular inflammation but exacerbated intestinal inflammation. To furtherly clarify the role of ClC-3 chloride channels in systemic inflammation, we used LPS-induced endotoxemia model to investigate the response of wild-type and ClC-3 knockout mice to systemic inflammation. The results showed that in the LPS-induced endotoxemia model, the mortality of mice with ClC-3 deletion was significantly higher than that of wild-type mice. The liver and lung inflammations in mice with ClC-3 deletion were significantly less than those in wild-type mice, and the levels of TNF-α and MIP-2 in serum were lower than those of wild-type mice. However, intestinal inflammatory cytokines contents and intestinal permeability were higher than wild-type mice. After transfection of THP-1 cells with ClC-3 siRNA, the contents of TNF-α and IL-8 in LPS-induced cell supernatants were significantly decreased. Further experiments revealed that the level of Bax and Cleaved Caspase 3 in intestinal tissue of mice with ClC-3 deletion was significantly increased, while the level of Bcl2 didn't change, which indicated that the intestinal apoptosis was increased aft...
Source: Cell Biology International - Category: Cytology Authors: Tags: Cell Biol Int Source Type: research