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Posttranscriptional control of airway inflammation

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Acute inflammation in the lungs is a vital protective response, efficiently and swiftly eliminating inciters of tissue injury. However, in respiratory diseases characterized by chronic inflammation, such as chronic obstructive pulmonary disease and asthma, enhanced expression of inflammatory mediators leads to tissue damage and impaired lung function. Although transcription is an essential first step in the induction of proinflammatory genes, tight regulation of inflammation requires more rapid, flexible responses. Increasing evidence shows that such responses are achieved by posttranscriptional mechanisms directly affecting mRNA stability and translation initiation. RNA‐binding proteins, microRNAs, and long noncoding RNAs interact with messenger RNA and each other to impact the stability and/or translation of mRNAs implicated in lung inflammation. Recent research has shown that these biological processes play a central role in the pathogenesis of several important pulmonary conditions. This review will highlight several posttranscriptional control mechanisms that influence lung inflammation and the known associations of derangements in these mechanisms with common respiratory diseases.

Schematic representation of human antigen R (HuR).
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Posttranscriptional regulation of chemokines CCL2 and CCL7. In addition to binding directly to the chemokine mRNA, glucocorticoids also decrease inflammation by positively upregulating TTP mRNA expression, which then decreases CCL2 mRNA stability and translation. CCL2, C‐C motif ligand 2; CCL7, C‐C motif ligand 7; GR, glucocorticoid receptor; HuR, human antigen R; miRNA, microRNA; TTP, tristetraprolin.
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Browse by Topic

RNA Structure and Dynamics > Influence of RNA Structure in Biological Systems
RNA Interactions with Proteins and Other Molecules > Protein–RNA Interactions: Functional Implications
RNA Turnover and Surveillance > Regulation of RNA Stability

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