Endogenous peroxidase activity was destroyed in 0.03% hydrogen peroxide in methanol for 30 minutes at room temperature. Slides were heated to 4☌ for five minutes, then to room temperature before washing in phosphate buffered saline (PBS) twice for five minutes each. Nasal polyps from steroid treated and steroid naive subjects were examined by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR).Ĭryostat sections (4 μm) were cut onto silanated glass slides and stored at –20☌. It was hypothesised that c-fos-irm would be expressed as a marker of cellular activation in polyps, but that glucocorticoid treatment would reduce the levels of expression. Since Emery et al 1 noted the presence of c-fos, c-jun, and c-myc mRNA in human nasal polyps it has been of interest to determine the distribution of c-fos immunoreactive material ( c-fos-irm) in nasal polyps and the effects of glucocorticoids on c-fos-irm and mRNA expression in vivo. 9, 10Ī human model would be useful for studying this postulated interaction between glucocorticoid and c-fos and to learn its relevance to the actions of glucocorticoids in vivo. 3-5, 7, 8 Hence, synthesis of mRNAs for many proinflammatory products may become reduced.
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This reduction in the amount of free activated AP-1 may lead to a “default” reduction in the expression of genes that require AP-1 for activation. These activated receptors are thought to bind to activated AP-1, leading to mutual inactivation of both protein factors. 3-6 Glucocorticoids enter cells and bind to glucocorticoid receptors.
One mechanism of glucocorticoid action is postulated to be an interaction with c-fos or AP-1. AP-1 helps initiate transcription of many proinflammatory genes, including those for cytokines. AP-1moves from the cytoplasm into the nucleus where it binds to AP-1 promoter sites on a wide variety of genes. 2 c-Fos combines with members of the c-jun family to form the transcription factor activation protein 1 ( AP-1). 1 The c-fos oncogene participates in transduction cascades that are initiated by many proinflammatory mediators. Nasal polyps are known to express high levels of proinflammatory transcription factors such as c-fos.
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