期刊
CELLULAR IMMUNOLOGY
卷 295, 期 2, 页码 137-143出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2015.03.004
关键词
1 alpha,25-Dihydroxyvitamin D-3; Cigarette smoke extracts; ERK; Calpain-1; E-cadherin
Cigarette smoke extracts (CSE) alter calpain-1 expression via ERK signaling pathway in bronchial epithelial cells. 1 alpha,25-dihydroxyvitamin D-3 (1,25D(3)) inhibits cigarette smoke-induced epithelial barrier disruption. This study was aimed to explore whether the 1,25D(3) counteracted the CSE effects in a human bronchial epithelial cell line (16HBE). In particular, transepithelial electrical resistance (TER) and permeability, expression and distribution of E-cadherin and beta-catenin, calpain-1 expression, and ERR phosphoiylation were assessed in the CSE-stimulated 16HBE cells. The CSE induced the ERK phosphorylation, improved the calpain-1 expression, increased the distribution anomalies and the cleaving of E-cadherin and beta-catenin, and resulted in the TER reduction and the permeability increase. The 1,25D(3) reduced these pathological changes. The 1,25D(3) mediated effects were associated with a reduced ERK phosphorylation. In conclusion, the present study provides compelling evidences that the 1,25D(3) may be considered a possible valid therapeutic option in controlling the cigarette smoke-induced epithelial barrier disruption. (C) 2015 Elsevier Inc. All rights reserved.
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