Inflammation-regulated mRNA stability and the progression of vascular inflammatory diseases

Cardiovascular disease remains a major medical and socioeconomic burden in developed and developing societies, and will increase with an aging and increasingly sedentary society. Vascular disease and atherosclerotic vascular syndromes are essentially inflammatory disorders, and transcriptional and p...

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Vydáno v:Clinical science (1979) Ročník 131; číslo 22; s. 2687
Hlavní autoři: Herman, Allison B, Autieri, Michael V
Médium: Journal Article
Jazyk:angličtina
Vydáno: England 15.11.2017
Témata:
3' Untranslated Regions
Animals
Cytokines - genetics
Cytokines - immunology
Cytokines - metabolism
Gene Expression Regulation
Humans
Inflammation - genetics
Inflammation - immunology
Inflammation - metabolism
Inflammation Mediators - immunology
Inflammation Mediators - metabolism
RNA Stability
RNA, Messenger - genetics
RNA, Messenger - metabolism
RNA-Binding Proteins - genetics
RNA-Binding Proteins - metabolism
Signal Transduction
Vasculitis - genetics
Vasculitis - immunology
Vasculitis - metabolism
cardiovascular disease
inflammation
mRNA stability
ISSN:1470-8736, 1470-8736
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Popis
Shrnutí:Cardiovascular disease remains a major medical and socioeconomic burden in developed and developing societies, and will increase with an aging and increasingly sedentary society. Vascular disease and atherosclerotic vascular syndromes are essentially inflammatory disorders, and transcriptional and post-transcriptional processes play essential roles in the ability of resident vascular and inflammatory cells to adapt to environmental stimuli. The regulation of mRNA translocation, stability, and translation are key processes of post-transcriptional regulation that permit these cells to rapidly respond to inflammatory stimuli. For the most part, these processes are controlled by elements in the 3'-UTR of labile, proinflammatory transcripts. Since proinflammatory transcripts almost exclusively contain AU-rich elements (AREs), this represents a tightly regulated and specific mechanism for initiation and maintenance of the proinflammatory phenotype. RNA-binding proteins (RBPs) recognize cis elements in 3'-UTR, and regulate each of these processes, but there is little literature exploring the concept that RBPs themselves can be directly regulated by inflammatory stimuli. Conceptually, inflammation-responsive RBPs represent an attractive target of rational therapies to combat vascular inflammatory syndromes. Herein we briefly describe the cellular and molecular etiology of atherosclerosis, and summarize our current understanding of RBPs and their specific roles in regulation of inflammatory mRNA stability. We also detail RBPs as targets of current anti-inflammatory modalities and how this may translate into better treatment for vascular inflammatory diseases.
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ISSN:1470-8736
1470-8736
DOI:10.1042/CS20171373