Synthesis and Secretion of Procathepsin B and Cystatin C by Human Bronchial Epithelial Cells in Vitro: Modulation of Cathepsin B Activity by Neutrophil Elastase

1995 ◽  
Vol 317 (1) ◽  
pp. 305-310 ◽  
Author(s):  
D. Burnett ◽  
M. Abrahamson ◽  
J.L. Devalia ◽  
R.J. Sapsford ◽  
R.J. Davies ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cystatin C ◽  
Neutrophil Elastase ◽  
Cathepsin B ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial

scholarly journals Activation of MAPKs in human bronchial epithelial cells exposed to metals

1998 ◽  
Vol 275 (3) ◽  
pp. L551-L558 ◽  
Author(s):  
James M. Samet ◽  
Lee M. Graves ◽  
Jacqueline Quay ◽  
Lisa A. Dailey ◽  
Robert B. Devlin ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Subsequent Increase ◽  
Induced Expression ◽  
Bronchial Epithelial ◽  
Mitogen Activated Protein ◽  
Metallic Compounds ◽  
Factor Α

We have previously shown that in vitro exposure to metallic compounds enhances expression of interleukin (IL)-6, IL-8, and tumor necrosis factor-α in human bronchial epithelial cells. To characterize signaling pathways involved in metal-induced expression of inflammatory mediators and to identify metals that activate them, we studied the effects of As, Cr, Cu, Fe, Ni, V, and Zn on the mitogen-activated protein kinases (MAPK) extracellular receptor kinase (ERK), c-Jun NH2-terminal kinase (JNK), and P38 in BEAS cells. Noncytotoxic concentrations of As, V, and Zn induced a rapid phosphorylation of MAPK in BEAS cells. Activity assays confirmed marked activation of ERK, JNK, and P38 in BEAS cells exposed to As, V, and Zn. Cr and Cu exposure resulted in a relatively small activation of MAPK, whereas Fe and Ni did not activate MAPK under these conditions. Similarly, the transcription factors c-Jun and ATF-2, substrates of JNK and P38, respectively, were markedly phosphorylated in BEAS cells treated with As, Cr, Cu, V, and Zn. The same acute exposure to As, V, or Zn that activated MAPK was sufficient to induce a subsequent increase in IL-8 protein expression in BEAS cells. These data suggest that MAPK may mediate metal-induced expression of inflammatory proteins in human bronchial epithelial cells.

scholarly journals Expression of lipocortins in human bronchial epithelial cells: effects of IL-1β , TNF-α, LPS and dexamethasone

1996 ◽  
Vol 5 (3) ◽  
pp. 210-217
Author(s):  
M. M. Verheggen ◽  
H. I. M. de Bont ◽  
P. W. C. Adriaansen-Soeting ◽  
B. J. A. Goense ◽  
C. J. A. M. Tak ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelium ◽  
Northern Blotting ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Annexin I ◽  
Tnf Α

In this study, we investigated the expression of lipocortin I and II (annexin I and I in the human bronchial epithelium, bothin vivoandin vitro. A clear expression of lipocortin I and II protein was found in the epithelium in sections of bronchial tissue. In cultured human bronchial epithelial cells we demonstrated the expression of lipocortin I and II mRNA and protein using Northern blotting, FACScan analysis and ELISA. No induction of lipocortin I or II mRNA or protein was observed after incubation with dexamethasone. Stimulation of bronchial epithelial cells with IL-1β, TNF-α or LPS for 24 h did not affect the lipocortin I or II mRNA or protein expression, although PGE2and 6-keto-PGF1αproduction was significantly increased. This IL-1β- and LPS-mediated increase in eicosanoids could be reduced by dexamethasone, but was not accompanied by an increase in lipocortin I or II expression. In human bronchial epithelial cells this particular glucocorticoid action is not mediated through lipocortin I or II induction.

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