Curcumin does not stimulate cAMP-mediated chloride transport in cystic fibrosis airway epithelial cells

被引:53
作者
Dragomir, A
Björstad, J
Hjelte, L
Roomans, GM
机构
[1] Uppsala Univ, Dept Med Cell Biol, SE-75123 Uppsala, Sweden
[2] Karolinska Univ Hosp, CF Ctr, SE-14186 Huddinge, Sweden
关键词
cystic fibrosis; chloride transport; CFTR; curcumin; airway epithelium;
D O I
10.1016/j.bbrc.2004.07.146
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It has been suggested that curcumin and other sarcoplasmic/endoplasmic reticulum Ca2+-pump inhibitors could correct the defect in the most common mutation (DeltaF508) in cystic fibrosis (CF), and restore normal chloride transport. In the present study, the effect of curcumin was tested on baby hamster kidney (BHK) cells transfected with DeltaF508-CFTR, a CF airway epithelial cell line (CFBE), and cells isolated from the nasal epithelium of CF-patient homozygous for the DeltaF508-mutation. Curcumin had a small effect on basal (non-CFTR-mediated) chloride efflux in CFBE and CF nasal epithelial cells, but did not increase the net cAMP-activated (CFTR-mediated) chloride efflux. Curcumin caused a small increase in net cAMP-activated chloride efflux from DeltaF508-CFTR BHK cells. Immunocytochemical analysis failed to show significant movement of DeltaF508-CFTR to the plasma membrane in DeltaF508-CFTR BHK cells or CFBE cells. It is concluded that it is unlikely that curcumin has a significant positive effect on CFTR-mediated chloride transport in airway epithelial cells. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:447 / 451
页数:5
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