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Biochem Biophys Res Commun. 2015 May 8;460(3):873-8. doi: 10.1016/j.bbrc.2015.03.125. Epub 2015 Mar 31.

1,25-Dihydroxyvitamin D3 preserves intestinal epithelial barrier function from TNF-α induced injury via suppression of NF-kB p65 mediated MLCK-P-MLC signaling pathway.

Author information

1
Division of General Surgery, Peking University First Hospital, Peking University, 8 Xi ShiKu Street, Beijing 100034, People's Republic of China.
2
Division of Gastroenterology, Peking University First Hospital, Peking University, 8 Xi ShiKu Street, Beijing 100034, People's Republic of China.
3
Division of General Surgery, Peking University First Hospital, Peking University, 8 Xi ShiKu Street, Beijing 100034, People's Republic of China. Electronic address: wangpengyuan2014@126.com.

Abstract

Substantial studies have demonstrated the protective effect of 1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) on intestinal barrier function, but the mechanisms are not fully illustrated. In this study, the effect of 1,25(OH)2D3 on TNF-α induced barrier dysfunction was further investigated in Caco-2 cell monolayers. The barrier function of Caco-2 monolayers was evaluated by measuring trans-epithelial electrical resistance (TEER) and FITC-Dextran 40,000 Da (FD-40) trans-membrane flux. ZO-1 and Occludin were chosen as markers of the localization of tight junction (TJ) proteins for immunofluorescence. The expression of MLCK and phosphorylation level of myosin light chain (MLC) were measured by immunoblotting. The activation of NF-kB p65 was analyzed by EMSA and immunofluorescence. The results suggest that 1,25(OH)2D3 preserves intestinal epithelial barrier function from TNF-α induced injury via suppression of NF-kB p65 mediated activation of MLCK-P-MLC signaling pathway.

KEYWORDS:

1,25(OH)2D3; MLCK; TNF-α; Tight junction (TJ); Trans-epithelial electrical resistance (TEER)

PMID:
25838204
DOI:
10.1016/j.bbrc.2015.03.125
[Indexed for MEDLINE]

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