Analysis and Quantitation of Splicing Variants of the TPA-Inducible PGHS-1 mRNA in Rat Tracheal Epithelial Cells

Kitzler, Jeffrey W.; Hill, Elizabeth M.; Hardman, Ron C.; Reddy, Nagi G.; Philpot, Richard M.; Eling, Thomas E.

doi:10.1006/abbi.1995.1115

Cited by 20 publications

(19 citation statements)

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“…A second COX-1 variant, which lacks exon 1 and instead contains part of intron 2, was identified (Kitzler et al, 1995) in a rat tracheal cell line (EGV-6). This transcript was expressed at low levels; however, more than 90% of the COX-1 transcripts in this cell line are in this variant form.…”

Section: F Variants Of Cyclooxygenase Isoenzymesmentioning

confidence: 99%

“…Primary rat tracheal epithelial cells and fibroblasts were also found to contain the variant transcript, but at only 1% of the level of COX-1 mRNA. Because this transcript lacks exon 1, which contains the initiating codon for translation, it has been considered to encode a nonsense COX protein (Kitzler et al, 1995). Interestingly, however, studies of the rat gastrointestinal tract show differential expression of this variant relative to COX-1 in aging stomach (Vogiagis et al, 2000).…”

Section: F Variants Of Cyclooxygenase Isoenzymesmentioning

confidence: 99%

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Cyclooxygenase Isozymes: The Biology of Prostaglandin Synthesis and Inhibition

2004

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Section: F Variants Of Cyclooxygenase Isoenzymesmentioning

confidence: 99%

Section: F Variants Of Cyclooxygenase Isoenzymesmentioning

confidence: 99%

Cyclooxygenase Isozymes: The Biology of Prostaglandin Synthesis and Inhibition

2004

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“…Complementary deoxyribonucleic acids (cDNAs) encoding this enzyme have been isolated and sequenced from primary ovine tracheal epithelial cells [35], and from the rat tracheal epithelial cell line, EGV-6 [36]. Two interesting features of these mRNAs have emerged.…”

Section: Lipid Mediatorsmentioning

confidence: 99%

Airway epithelium as an effector of inflammation: molecular regulation of secondary mediators

Martin

Rochelle²,

Fischer³

et al. 1997

Eur Respir J

139

101

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Deleterious environmental stimuli cause the airway epithelium to respond with increased secretions of mucus, reaction of oxygen/nitrogen species, changes in ciliary beating, and the influx of inflammatory cells. The epithelium is a target for factors released by infiltrating inflammatory cells, and has recently been shown to serve as an effector of such inflammation. Molecular mechanisms regulating production of secondary inflammatory mediators (cytokines, lipid mediators, and reactive oxygen/nitrogen species) have yet to be fully described.This report reviews the production of secondary mediators by epithelial cells and by airway epithelium. Lipid mediators are enzymatically produced by the airway epithelium in response to primary mediators. Molecular mechanisms regulating the production of cyclo-oxygenase, lipoxygenase and prostaglandin synthase are discussed, along with the potential of lipid mediators to produce inflammation. The molecular regulation of nitric oxide production is also described in the context of its role as a signalling molecule in pathways regulating secretion of mucus, ciliary motion, and intercellular adhesion molecule-1 (ICAM-1) expression. The production of cytokines by the airway epithelium is shown to play a role in causing inflammation associated with respiratory diseases. Particular attention is paid to molecular mechanisms governing the expression of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-8 (IL-8).

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“…A splice variant of COX-1 lacking exon 9 was reported in human fibroblasts (Diaz et al, 1992), and recently it was shown that the mRNA transcript for this COX-1 variant is present in various human tissues; however, the corresponding protein is either not formed or subject to rapid proteolytic degradation (Schneider et al, 2005). Yet another COX-1 splice variant containing an intronic sequence was described in rat tracheal epithelial cells (Kitzler et al, 1995), rat stomach (Vogiagis et al, 2000), and rat colorectal tumors (Vogiagis et al, 2001). Another COX-1 splice variant was shown to be present in endothelial cells (Hla, 1996).…”

Section: Cox Splice Variantsmentioning

confidence: 99%

Acetaminophen and the Cyclooxygenase-3 Puzzle: Sorting out Facts, Fictions, and Uncertainties

Kis

Snipes²,

Busija³

2005

J Pharmacol Exp Ther

208

149

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Cyclooxygenase (COX)-3, a novel COX splice variant, was suggested as the key to unlocking the mystery of the mechanism of action of acetaminophen. Although COX-3 might have COX activity in canines, and this activity might be inhibited by acetaminophen, its low expression level and the kinetics indicate unlikely clinical relevance. In rodents and humans, COX-3 encodes proteins with completely different amino acid sequences than COX

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Analysis and Quantitation of Splicing Variants of the TPA-Inducible PGHS-1 mRNA in Rat Tracheal Epithelial Cells

Cited by 20 publications

References 0 publications

Cyclooxygenase Isozymes: The Biology of Prostaglandin Synthesis and Inhibition

Cyclooxygenase Isozymes: The Biology of Prostaglandin Synthesis and Inhibition

Airway epithelium as an effector of inflammation: molecular regulation of secondary mediators

Acetaminophen and the Cyclooxygenase-3 Puzzle: Sorting out Facts, Fictions, and Uncertainties

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