Prostaglandin E2
 increases cyclic AMP and inhibits endothelin-1 production/secretion by guinea-pig tracheal epithelial cells through EP4
 receptors

We have studied the binding of endothelin-1 (ET-1) to cultured canine tracheal epithelial cells. A single specific binding site for 125I-labeled ET-1 was identified with an apparent dissociation constant (Kd) of 0.2 nM, maximal binding sites (Bmax) of 6.7 x 10(3) sites/cell, and half-maximal inhibition (IC50) of 0.3 nM during a 2-h incubation period. The binding of 125I-ET-1 to these cells was inhibited by the presence of unlabeled ET-1, ET-2, or BQ-123, whereas ET-3 and sarafotoxin S6c did not compete for this binding site. These binding characteristics are consistent with those of the ETA receptor. At 37 degrees C, specific binding continuously increased over 18 h, while at 4 degrees C, it reached a plateau by 2 h. The increase in binding at 37 degrees C was not associated with DNA synthesis but was dependent upon protein synthesis, suggesting that epithelial binding sites were produced continuously under these incubation conditions. Our results indicate that canine tracheal epithelial cells possess specific binding sites for ET-1 with characteristics similar to those of the ETA receptor subtype. Because these cells are demonstrated to both release and bind ET-1, the results further suggest that ET-1 is involved in paracrine and/or autocrine control mechanisms in the airway epithelium.

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Residual Oil Fly Ash Induces Cytotoxicity and Mucin Secretion by Guinea Pig Tracheal Epithelial Cells via an Oxidant-Mediated Mechanism

Toxicology and Applied Pharmacology ◽

10.1006/taap.1999.8886 ◽

2000 ◽

Vol 163 (3) ◽

pp. 221-230 ◽

Cited By ~ 39

Author(s):

Nanfei Jiang ◽

Kevin L. Dreher ◽

Janice A. Dye ◽

Yuehua Li ◽

Judy H. Richards ◽

...

Keyword(s):

Fly Ash ◽

Epithelial Cells ◽

Guinea Pig ◽

Residual Oil ◽

Mucin Secretion ◽

Tracheal Epithelial Cells ◽

Residual Oil Fly Ash ◽

Tracheal Epithelial ◽

Oil Fly Ash

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Release of reactive oxygen species by guinea pig tracheal epithelial cells in vitro

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1992.262.6.l708 ◽

1992 ◽

Vol 262 (6) ◽

pp. L708-L712 ◽

Cited By ~ 5

Author(s):

V. L. Kinnula ◽

K. B. Adler ◽

N. J. Ackley ◽

J. D. Crapo

Keyword(s):

Reactive Oxygen Species ◽

Protein Kinase C ◽

Protein Kinase ◽

Epithelial Cells ◽

Guinea Pig ◽

Oxygen Species ◽

Tracheal Epithelial Cells ◽

Kinase C ◽

Apical Side ◽

Tracheal Epithelial

Regulatory and stimulatory mechanisms of H2O2 release from guinea pig tracheal epithelial cells were investigated. Cells in primary culture maintained in a previously described air-liquid interface system released H2O2 to the extracellular space only from the apical side of the cells. The rate of release was 0.044 +/- 0.003 nmol.min-1.mg protein-1. H2O2 release could be stimulated significantly during a 30-min incubation period with phorbol myristate acetate (PMA) and platelet-activating factor (PAF). A stimulatory effect of PAF was achieved at concentrations greater than 100 nM and with PMA at concentrations greater than 10 ng (16 nM). When protein kinase C was inactivated with staurosporine, the responses to both PAF and PMA were abolished, whereas the cyclooxygenase inhibitor, indomethacin, did not affect H2O2 generation. When guinea pig tracheal epithelial cells were exposed to sublethal concentrations of extracellular H2O2 (30 microM), H2O2 was detoxified from both apical and basal sides, H2O2 removal being significantly more rapid from the apical side of the cells. These results suggest that tracheal epithelial cells can be stimulated to generate reactive oxygen species into the airway lumen and that this occurs in response to inflammatory mediators that act through protein kinase C. Luminal H2O2 release may have developed as a defense mechanism against microbes, and, similarly, luminal detoxification of H2O2 could represent an important mechanism of modulation of airway inflammation in response to oxidant stress.

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The Induction of cell Differentiation of Guinea PIG Tracheal Epithelial Cells Using the 3-Dimensional Co-Culture System with Fibroblasts

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)44601-5 ◽

1997 ◽

Vol 73 ◽

pp. 23

Author(s):

Y. Uchida

Keyword(s):

Cell Differentiation ◽

Epithelial Cells ◽

Guinea Pig ◽

Culture System ◽

3 Dimensional ◽

Tracheal Epithelial Cells ◽

Tracheal Epithelial

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Prostaglandin secretion by guinea pig tracheal epithelial cells caused by eosinophil major basic protein

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1993.265.3.l234 ◽

1993 ◽

Vol 265 (3) ◽

pp. L234-L242 ◽

Cited By ~ 5

Author(s):

S. R. White ◽

K. S. Sigrist ◽

S. M. Spaethe

Keyword(s):

Epithelial Cells ◽

Guinea Pig ◽

Basic Protein ◽

Primary Cultures ◽

Thromboxane B2 ◽

Major Basic Protein ◽

Tracheal Epithelial Cells ◽

Subsequent Response ◽

Tracheal Epithelial ◽

Eosinophil Major Basic Protein

We examined the effect of eosinophil major basic protein (MBP) on prostaglandin (PG) secretion from guinea pig tracheal epithelial (GPTE) cells. Primary cultures of GPTE cells were incubated with 10(-6) M MBP for up to 6 h and then stimulated with 10(-6) M bradykinin (BK). PGE2, 6-ketoprostaglandin F1 alpha (PGF1 alpha), PGF2 alpha, and thromboxane B2 (TxB2) concentrations in media were determined by enzyme-linked immunoabsorbent assay (EIA). Incubation with MBP for 6 h caused secretion of both PGE2 (17,614 +/- 4,416 vs. 1,426 +/- 555 pg/10(6) cells at baseline, P < 0.001, n = 7) and PGF2 alpha (20,303 +/- 5,724 vs. 3,790 +/- 1.075 pg/10(6) cells at baseline, P < 0.002, n = 7). Secretion of PGE2 and PGF2 alpha stimulated by MBP required at least 2 h. Incubation with MBP for 6 h also augmented the subsequent response to BK: PGE2 secretion was 29,215 +/- 6,853 vs. 3,445 +/- 1,041 pg/10(6) cells for BK alone (P < 0.0001), and PGF2 alpha secretion was 25,407 +/- 6,237 vs. 5,213 +/- 1,535 pg/10(6) cells for BK alone (P < 0.0001). MBP did not change 6-keto-PGF1 alpha and TxB2 secretion. Incubation of GPTE cells from seven animals with polylysine, a protein with mass and ion charge similar to MBP, for 2 h, both caused secretion of PGE2 (8,579 +/- 3,244 vs. 788 +/- 419 pg/10(6) cells at baseline, P < 0.01) and augmented the response to BK (12,732 +/- 4,788 vs. 1,653 +/- 680 pg/10(6) cells after BK alone, P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

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