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      Involvement of the Circadian Rhythm and Inflammatory Cytokines in the Pathogenesis of Rheumatoid Arthritis

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          Abstract

          Among the symptoms of patients with rheumatoid arthritis (RA), joint stiffness is influenced by diurnal rhythm and reaches peak in the morning, which is a common complaint and reflects the circadian nature of disease manifestation. In addition, inflammatory cytokines, which reach peak secretion early in the morning are major players causing the morning stiffness. In this review, we explore the link between the circadian clock and inflammation, focusing on the interactions of various clock genes with the immune-pathways underlying the pathology of rheumatoid arthritis.

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          Transcriptional architecture and chromatin landscape of the core circadian clock in mammals.

          Nobuya Koike, Seung-Hee Yoo, Hung-Chung Huang … (2012)
          The mammalian circadian clock involves a transcriptional feed back loop in which CLOCK and BMAL1 activate the Period and Cryptochrome genes, which then feedback and repress their own transcription. We have interrogated the transcriptional architecture of the circadian transcriptional regulatory loop on a genome scale in mouse liver and find a stereotyped, time-dependent pattern of transcription factor binding, RNA polymerase II (RNAPII) recruitment, RNA expression, and chromatin states. We find that the circadian transcriptional cycle of the clock consists of three distinct phases: a poised state, a coordinated de novo transcriptional activation state, and a repressed state. Only 22% of messenger RNA (mRNA) cycling genes are driven by de novo transcription, suggesting that both transcriptional and posttranscriptional mechanisms underlie the mammalian circadian clock. We also find that circadian modulation of RNAPII recruitment and chromatin remodeling occurs on a genome-wide scale far greater than that seen previously by gene expression profiling.
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            System-level identification of transcriptional circuits underlying mammalian circadian clocks.

            Yasufumi Shigeyoshi, Motoaki Sano, Masamitsu Iino … (2005)
            Mammalian circadian clocks consist of complexly integrated regulatory loops, making it difficult to elucidate them without both the accurate measurement of system dynamics and the comprehensive identification of network circuits. Toward a system-level understanding of this transcriptional circuitry, we identified clock-controlled elements on 16 clock and clock-controlled genes in a comprehensive surveillance of evolutionarily conserved cis elements and measurement of their transcriptional dynamics. Here we report the roles of E/E' boxes, DBP/E4BP4 binding elements and RevErbA/ROR binding elements in nine, seven and six genes, respectively. Our results indicate that circadian transcriptional circuits are governed by two design principles: regulation of E/E' boxes and RevErbA/ROR binding elements follows a repressor-precedes-activator pattern, resulting in delayed transcriptional activity, whereas regulation of DBP/E4BP4 binding elements follows a repressor-antiphasic-to-activator mechanism, which generates high-amplitude transcriptional activity. Our analysis further suggests that regulation of E/E' boxes is a topological vulnerability in mammalian circadian clocks, a concept that has been functionally verified using in vitro phenotype assay systems.
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              Differential control of Bmal1 circadian transcription by REV-ERB and ROR nuclear receptors.

              Fabienne Guillaumond, Hugues Dardente, Vincent Giguère … (2005)
              Circadian rhythms result from feedback loops involving clock genes and their protein products. In mammals, 2 orphan nuclear receptors, REV-ERBalpha and RORalpha, play important roles in the transcription of the clock gene Bmal1. The authors now considerably extend these findings with the demonstration that all members of the REV-ERB (alpha and beta) and ROR (alpha, beta, and gamma) families repress and activate Bmal1 transcription, respectively. The authors further show that transcription of Bmal1 is the result of competition between REV-ERBs and RORs at their specific response elements (RORE). Moreover, they demonstrate that Reverb genes are similarly expressed in the thymus, skeletal muscle, and kidney, whereas Ror genes present distinct expression patterns. Thus, the results indicate that all members of the REV-ERB and ROR families are crucial components of the molecular circadian clock. Furthermore, their strikingly different patterns of expression in nervous and peripheral tissues provide important insights into functional differences between circadian clocks within the organism.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Immunol Res
                Journal ID (iso-abbrev): J Immunol Res
                Journal ID (publisher-id): JIR
                Title: Journal of Immunology Research
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2314-8861
                ISSN (Electronic): 2314-7156
                Publication date (Print): 2014
                Publication date (Electronic): 8 May 2014
                Volume: 2014
                Electronic Location Identifier: 282495
                Affiliations
                1Faculty of Health Sciences, Kobe University School of Medicine, Kobe 654-0142, Japan
                2Department of General Internal Medicine, Kobe University School of Medicine, Kobe 650-0017, Japan
                3Division of Rehabilitation Medicine, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan
                4Clinical Immunology, Kobe University Graduate School of Health Sciences, 7-10-2, Tomogaoka, Suma, Kobe 654-0142, Japan
                Author notes
                *Akira Hashiramoto: hash@ 123456kobe-u.ac.jp

                Academic Editor: Mizuko Mamura

                Article
                DOI: 10.1155/2014/282495
                PMC ID: 4034483
                PubMed ID: 24901009
                SO-VID: f4eeaade-0b75-4b57-8745-bf607cfd9aed
                Copyright © Copyright © 2014 Kohsuke Yoshida et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 5 March 2014
                Date accepted : 24 April 2014
                Categories
                Subject: Review Article

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