Allyl Isothiocyanate Increases MRP1 Function and Expression in a Human Bronchial Epithelial Cell Line

Multidrug resistance-associated protein 1 (MRP1), a member of the ATP-binding cassette (ABC) superfamily of transporters, plays an important role in normal lung physiology by protecting cells against oxidative stress and toxic xenobiotics. The present study investigates the effects of allyl isothiocyanate (AITC) onMRP1mRNA and MRP1 protein expression and transporter activity in the immortalised human bronchial epithelial cell line 16HBE14o-.MRP1mRNA and MRP1 protein expression in 16HBE14o- cells that were treated with allyl isothiocyanate were analysed by real-time PCR assay and Western blotting. The transport of carboxyfluorescein, a known MRP1 substrate, was measured by functional flow cytometry to evaluate MRP1 activity. Treatment with AITC at concentrations of 5–40 μM increased MRP1 protein levels in a concentration-dependent manner. AITC treatments at concentrations of 1–40 μM caused concentration-dependent increases inMRP1mRNA levels that were up to seven times greater than the levels found in control cells. Finally, AITC treatment at concentrations of 5–40 μM significantly increased MRP1-dependent efflux in 16HBE14o- cells. These results suggest that AITC can increase the expression and activity of MRP1 in 16HBE14o- cells in a concentration-dependent manner. The upregulation of MRP1 activity and expression by AITC could produce therapeutic effects in the treatment of lung disease.

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Interleukin-9 and Interleukin-13 augment UTP-induced Cl ion transport via hCLCA1 expression in a human bronchial epithelial cell line

Clinical & Experimental Allergy ◽

10.1111/j.1365-2222.2007.02646.x ◽

2007 ◽

Vol 37 (2) ◽

pp. 219-224 ◽

Cited By ~ 5

Author(s):

Y. Endo ◽

K. Isono ◽

M. Kondo ◽

J. Tamaoki ◽

A. Nagai

Keyword(s):

Epithelial Cell ◽

Ion Transport ◽

Cell Line ◽

Bronchial Epithelial Cell ◽

Human Bronchial Epithelial Cell ◽

Epithelial Cell Line ◽

Bronchial Epithelial ◽

Interleukin 13 ◽

Interleukin 9

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In vitro genotoxicity assay of sidestream smoke using a human bronchial epithelial cell line

Food and Chemical Toxicology ◽

10.1016/s0278-6915(02)00034-0 ◽

2002 ◽

Vol 40 (6) ◽

pp. 845-850 ◽

Cited By ~ 37

Author(s):

L. Wolz ◽

G. Krause ◽

G. Scherer ◽

M. Aufderheide ◽

U. Mohr

Keyword(s):

Epithelial Cell ◽

Cell Line ◽

Bronchial Epithelial Cell ◽

Human Bronchial Epithelial Cell ◽

Epithelial Cell Line ◽

Bronchial Epithelial ◽

Sidestream Smoke ◽

In Vitro Genotoxicity

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Gene profiles of a human bronchial epithelial cell line after in vitro exposure to respiratory (non-)sensitizing chemicals: Identification of discriminating genetic markers and pathway analysis

Toxicology ◽

10.1016/j.tox.2008.10.014 ◽

2009 ◽

Vol 255 (3) ◽

pp. 151-159 ◽

Cited By ~ 23

Author(s):

Sandra Verstraelen ◽

Inge Nelissen ◽

Jef Hooyberghs ◽

Hilda Witters ◽

Greet Schoeters ◽

...

Keyword(s):

Epithelial Cell ◽

Cell Line ◽

Genetic Markers ◽

Pathway Analysis ◽

Bronchial Epithelial Cell ◽

Epithelial Cell Line ◽

Bronchial Epithelial ◽

Gene Profiles ◽

In Vitro Exposure

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Retinoic acid inhibits interleukin-4-induced eotaxin production in a human bronchial epithelial cell line

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00289.2003 ◽

2004 ◽

Vol 286 (4) ◽

pp. L777-L785 ◽

Cited By ~ 14

Author(s):

Kei Takamura ◽

Yasuyuki Nasuhara ◽

Motoko Kobayashi ◽

Tomoko Betsuyaku ◽

Yoko Tanino ◽

...

Keyword(s):

Retinoic Acid ◽

Epithelial Cell ◽

Cell Line ◽

Nuclear Translocation ◽

Bronchial Epithelial Cell ◽

Inhibitory Effect ◽

Human Bronchial Epithelial Cell ◽

Epithelial Cell Line ◽

Transcriptional Level ◽

Bronchial Epithelial

Retinoic acid (RA) is known to accelerate wound healing and induce cell differentiation. All- trans RA (ATRA) exerts its effect by binding retinoic acid receptors, which are members of the nuclear receptor family. We investigated whether RA can alter expression of eotaxin, a potent eosinophil chemoattractant that is regulated by the transcription factors signal transducer and activator of transcription 6 (STAT6) and NF-κB. We examined the effects of RA on eotaxin expression in a human bronchial epithelial cell line BEAS-2B. ATRA and its stereodimer 9- cis retinoic acid (9- cis RA) inhibited IL-4-induced release of eotaxin at 10-6M by 78.0 and 52.0%, respectively ( P < 0.05). ATRA and 9- cis RA also significantly inhibited IL-4-induced eotaxin mRNA expression at 10-6M by 52.3 and 53.5%, respectively ( P < 0.05). In contrast, neither ATRA nor 9- cis RA had any effects on TNF-α-induced eotaxin production. In transfection studies using eotaxin promoter luciferase plasmids, the inhibitory effect of ATRA on IL-4-induced eotaxin production was confirmed at the transcriptional level. Interestingly, ATRA had no effects on IL-4-induced tyrosine phosphorylation, nuclear translocation, or DNA binding activity of STAT6. Activating protein-1 was not involved in ATRA-mediated transrepression of eotaxin with IL-4 stimulation. The mechanism of the inhibitory effect of ATRA on IL-4-induced eotaxin production in human bronchial epithelial cells has not been elucidated but does not appear to be due to an effect on STAT6 activation. These findings raise the possibility that RA may reduce eosinophilic airway inflammation, one of the prominent pathological features of allergic diseases such as bronchial asthma.

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