Abstract
The 10% of patients with the most severe asthma are responsible for a large part of healthcare expenditure and morbidity. Understanding the processes involved is key if new therapeutic approaches are to be developed. Evidence is accumulating that chronic diseases such as asthma are associated with temporal and spatial alterations in the pattern of inflammatory gene expression within the airways. Expression of these genes can be regulated by transcriptional, posttranscriptional, translational and epigenetic mechanisms. It is well established that binding of activated transcription factors to specific inducible gene promoter sites is tightly controlled by chromatin state as a result of histone modifications, particularly the balance between histone acetylation and deacetylation [1]. The interaction between transcription factors and the promoter is key to the diversification of gene expression in a time dependent manner leading to altered gene expression profiles. Alterations of the accessibility of transcription factors to the DNA can have residing effects upon gene transcription. This review will focus on the regulation of several groups of key genes which are involved in chronic airway inflammation and remodelling in asthma drawing mainly from our experience of studying these processes in airway smooth muscle cells. An overview is shown in Fig. 1.
Keywords: Transcription, asthma, smooth muscle, epigenetic, chromatin, prostanoids, chemokines, growth factors, H2A/H2B, N-terminal, acetyltransferase, proteins, cyclic peptides, polyadenylation, COX-2, NF-IL-6, chemoattractant, cytokines, mRNA, angiogenesis
Current Pharmaceutical Design
Title: Transcriptional Regulation of Inflammatory Genes Associated with Severe Asthma
Volume: 17 Issue: 7
Author(s): Rachel L. Clifford, William R. Coward, Alan J. Knox and Alison E. John
Affiliation:
Keywords: Transcription, asthma, smooth muscle, epigenetic, chromatin, prostanoids, chemokines, growth factors, H2A/H2B, N-terminal, acetyltransferase, proteins, cyclic peptides, polyadenylation, COX-2, NF-IL-6, chemoattractant, cytokines, mRNA, angiogenesis
Abstract: The 10% of patients with the most severe asthma are responsible for a large part of healthcare expenditure and morbidity. Understanding the processes involved is key if new therapeutic approaches are to be developed. Evidence is accumulating that chronic diseases such as asthma are associated with temporal and spatial alterations in the pattern of inflammatory gene expression within the airways. Expression of these genes can be regulated by transcriptional, posttranscriptional, translational and epigenetic mechanisms. It is well established that binding of activated transcription factors to specific inducible gene promoter sites is tightly controlled by chromatin state as a result of histone modifications, particularly the balance between histone acetylation and deacetylation [1]. The interaction between transcription factors and the promoter is key to the diversification of gene expression in a time dependent manner leading to altered gene expression profiles. Alterations of the accessibility of transcription factors to the DNA can have residing effects upon gene transcription. This review will focus on the regulation of several groups of key genes which are involved in chronic airway inflammation and remodelling in asthma drawing mainly from our experience of studying these processes in airway smooth muscle cells. An overview is shown in Fig. 1.
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Cite this article as:
L. Clifford Rachel, R. Coward William, J. Knox Alan and E. John Alison, Transcriptional Regulation of Inflammatory Genes Associated with Severe Asthma, Current Pharmaceutical Design 2011; 17 (7) . https://dx.doi.org/10.2174/138161211795429000
DOI https://dx.doi.org/10.2174/138161211795429000 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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