Neuroendocrine-immune correlates of circadian physiology: studies in experimental models of arthritis, ethanol feeding, aging, social isolation, and calorie restriction

Esquifino, Ana I.; Cano, Pilar; Jiménez-Ortega, Vanesa; Fernández-Mateos, Pilar; Cardinali, Daniel P.

doi:10.1007/s12020-007-9009-y

Cited by 26 publications

(38 citation statements)

References 210 publications

(260 reference statements)

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“…1). In mammals, the master circadian pacemaker SCN orchestrates several clock genes expressed in a tissue-specific fashion (21,22), and delayed oscillation in the peripheral clock as compared with SCN is also reported (23). Previous study concerning the contribution of arthritis to circadian clock is not available; however, serum TNF-a has been shown to exhibit a delayed secretion rhythm in the patients with RA as compared with healthy controls, being highest at 6:00 AM and remained upregulated until 10:00 AM (7), which coincides with the sign of morning stiffness in RA (24)(25)(26).…”

Section: Discussionmentioning

confidence: 99%

Mammalian Clock Gene Cryptochrome Regulates Arthritis via Proinflammatory Cytokine TNF-α

Hashiramoto

Yamada

Tsumiyama

et al. 2009

The Journal of Immunology

153

142

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The mammalian clock genes, Period and Cryptochrome (Cry), regulate circadian rhythm. We show that circadian rhythmicity and rhythmic expression of Period in the nuclei of inflammatory synovial cells and spleen cells are disturbed in mouse models of experimental arthritis. Expressions of other clock genes, Bmal1 and Dbp, are also disturbed in spleen cells by arthritis induction. Deletion of Cry1 and Cry2 results in an increase in the number of activated CD3+ CD69+ T cells and a higher production of TNF-α from spleen cells. When arthritis is induced, Cry1−/−Cry2−/− mice develop maximal exacerbation of joint swelling, and upregulation of essential mediators of arthritis, including TNF-α, IL-1β and IL-6, and matrix metalloproteinase-3. Wee-1 kinase is solely upregulated in Cry1−/−Cry2−/− mice, in line with upregulation of c-Fos and Wee-1 kinase in human rheumatoid arthritis. The treatment with anti–TNF-α Ab significantly reduced the severity and halted the progression of the arthritis of Cry1−/−Cry2−/− mice and vice versa, ectopic expression of Cry1 in the mouse embryonic fibroblast from Cry1−/−Cry2−/− mice significantly reduced the trans activation of TNF-α gene. Thus, the biological clock and arthritis influence each other, and this interplay can influence human health and disease.

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Section: Discussionmentioning

confidence: 99%

Mammalian Clock Gene Cryptochrome Regulates Arthritis via Proinflammatory Cytokine TNF-α

Hashiramoto

Yamada

Tsumiyama

et al. 2009

The Journal of Immunology

153

142

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“…Variability of enzymatic activity in the circadian cycle depends on many factors including age, sexual maturity, and diet. Recent studies reveal that the circadian rhythms of physiology and behavior are controlled by clock genes; the effectiveness and toxicity of many drugs including alcohol vary depending on dosing time associated with 24 hour rhythms of biochemical, physiological, and behavioral processes under the control of the circadian clock [Esquifino et al, 2007; Moore et al, 2010; Arjona et al, 2004; Arjona and Sarkar, 2006]. Circadian rhythm is also linked to the autonomic nervous system and the neuroendocrine system.…”

Section: Choosing the Right Laboratory Model Of Alcohol Abusementioning

confidence: 99%

Laboratory Models Available to Study Alcohol‐Induced Organ Damage and Immune Variations: Choosing the Appropriate Model

El-Guindy

Kovacs

Witte

et al. 2010

Alcoholism Clin & Exp Res

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The morbidity and mortality resulting from alcohol-related diseases impose a substantive cost to society globally. To minimize the financial burden on society and improve the quality of life for individuals suffering from the ill effects of alcohol abuse, researchers in the alcohol field are focused on understanding the mechanisms by which alcohol-related diseases develop and progress. Since ethical concerns and inherent difficulties limit the amount of alcohol abuse research that can be performed in humans, most is performed in laboratory animals. This article summarizes the various laboratory models of alcohol abuse that are currently available and are used to study the mechanisms by which alcohol abuse induces organ damage and immune defects. The strengths and weaknesses of each of the models are discussed. Integrated into the review are the presentations that were made in the symposium “Methods of Ethanol Application in Alcohol Model – How Long is Long Enough” at the joint 2008 Research Society on Alcoholism (RSA) and International Society for Biomedical Research on Alcoholism (ISBRA) meeting, Washington, DC, emphasizing the importance not only of selecting the most appropriate laboratory alcohol model to address the specific goals of a project but also of ensuring that the findings can be extrapolated to alcohol-induced diseases in humans.

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“…Circadian variations in the circulation of T, B and NK lymphocyte subsets in peripheral blood and in the density of epitope molecules at their surface have also been reported (Esquifino et al 2007). Of interest, some of these circadian variations change with aging (Mazzoccoli et al 2010;Mazzoccoli et al 2011).…”

Section: Discussionmentioning

confidence: 94%

“…Accumulating evidence indicates that many immune parameters, including lymphocyte proliferation, antigen presentation and cytokine gene expression, oscillate around the clock (Esquifino et al 2007). Circadian variations in the circulation of T, B and NK lymphocyte subsets in peripheral blood and in the density of epitope molecules at their surface have also been reported (Esquifino et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Promoter methylation of seven clock genes in total leukocytes from different-aged healthy subjects

Zhang

Lin

Ding

et al. 2012

Biological Rhythm Research

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DNA methylation plays an important role in the regulation of the expression of clock genes during normal development and in the development of cancer. The methylation status of clock genes may also be associated with aging. However, it is unknown whether promoter methylation is also a regulator for the age-related change of clock expression in human total lymphocytes. In the present study, methylation-specific polymerase chain reaction assays were used to examine the methylation status of seven key clock promoters, namely Bmal1, Clock, Npas2, Per1, Per2, Cry1 and Cry2. The methylation status was examined in 298 healthy subjects categorised into three groups according to their age. Noticeable methylation was only detected in the Cry1 and Npas2 promoters, suggesting their epigenetic regulation may be involved in modulating the expression of clock genes and circadian rhythms in leukocytes. However, their methylation frequency did not differ with age or gender.

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Neuroendocrine-immune correlates of circadian physiology: studies in experimental models of arthritis, ethanol feeding, aging, social isolation, and calorie restriction

Cited by 26 publications

References 210 publications

Mammalian Clock Gene Cryptochrome Regulates Arthritis via Proinflammatory Cytokine TNF-α

Mammalian Clock Gene Cryptochrome Regulates Arthritis via Proinflammatory Cytokine TNF-α

Laboratory Models Available to Study Alcohol‐Induced Organ Damage and Immune Variations: Choosing the Appropriate Model

Promoter methylation of seven clock genes in total leukocytes from different-aged healthy subjects

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