Sirt1 activity in peripheral blood mononuclear cells from patients with rheumatoid arthritis

Wendling, Daniel; Vidon, Claire; Abbas, Wasim; Guillot, Xavier; Toussirot, Éric; Herbein, Georges

doi:10.1016/j.jbspin.2014.02.006

Cited by 10 publications

(12 citation statements)

References 10 publications

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“…We did not find significant difference in the cytoplasmic Sirt1 activity in PBMCs of RA patients compared to HC (283818±179670 versus 356069±194855, p = 0.15) ( Table 1 ) as reported previously [ 20 ]. Cytoplasmic Sirt1 activity was lower in RA patients with severe disease compared to HC (120063±147394 versus 356069±194855; P = 0.03) ( Fig.…”

Section: Resultssupporting

confidence: 88%

Dysregulated Serum IL-23 and SIRT1 Activity in Peripheral Blood Mononuclear Cells of Patients with Rheumatoid Arthritis

et al. 2015

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Sirtuin 1 (Sirt1) is a class III histone deacetylase (HDAC) that modulates gene expression and is involved in the regulation of proinflammatory cytokines. Interleukin-23 (IL-23) is produced by activated macrophages and dendritic cells and could fuel the progression of rheumatoid arthritis (RA). The goal of our study was to evaluate serum IL-23 levels and both Sirt1 activity and expression in peripheral blood mononuclear cells (PBMCs) in patients with RA compared to healthy controls (HC) and to determine the relationship between Sirt1 activity/expression and IL-23 levels. We assessed apoptosis in PBMCs of RA patients and its association with Sirt1 expression and serum IL-23. Serum IL-23 levels were increased in RA patients in comparison with controls. We found a positive correlation between the levels of serum IL-23 and serum IL-6 in RA patients. Decreased cytoplasmic Sirt1 activity was observed in RA patients with severe disease compared to HC. The expression of Sirt1 protein was significantly decreased in PBMCs of RA patients compared to HC using western blotting. Serum IL-23 levels correlated positively with the cytoplasmic Sirt1 activity in RA patients. Apoptosis rate of PBMCs isolated from RA patients was increased compared to HC and correlated negatively with the expression of Sirt1 protein and serum IL-23 levels. Levels of serum IL-23 and Sirt1 activity and expression were disturbed in RA parallel to increased PBMC apoptosis. Our findings might provide the rationale for the development of new therapeutic approaches in RA.

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Section: Resultssupporting

confidence: 88%

Dysregulated Serum IL-23 and SIRT1 Activity in Peripheral Blood Mononuclear Cells of Patients with Rheumatoid Arthritis

et al. 2015

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“…Reported epigenetic alterations include global hypomethylation [99, 100], local hypomethylation of LINE-1 and DR-3 promoters [101, 102], increased HDAC activity [103, 104], Sirt1 overexpression [105] and hyperacetylation [104], local H4 acetylation within MMP-1 promoter [106], sumoylation [107], and distinct pattern of microRNA expression [108]. …”

Section: The Nine Hallmarks Of Aging and Ramentioning

confidence: 99%

“…Moreover, RA patient derived PBMC demonstrated increased HDAC activity [112], but no specific change of Sirt1 activity [105]. The current available data suggest that histone acetylation is differently modulated in aging and RA.…”

Section: The Nine Hallmarks Of Aging and Ramentioning

confidence: 99%

Rheumatoid Arthritis, Immunosenescence and the Hallmarks of Aging

Chalan¹,

Berg²,

Kroesen

et al. 2015

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Age is the most important risk factor for the development of infectious diseases, cancer and chronic inflammatory diseases including rheumatoid arthritis (RA). The very act of living causes damage to cells. A network of molecular, cellular and physiological maintenance and repair systems creates a buffering capacity against these damages. Aging leads to progressive shrinkage of the buffering capacity and increases vulnerability. In order to better understand the complex mammalian aging processes, nine hallmarks of aging and their interrelatedness were recently put forward.RA is a chronic autoimmune disease affecting the joints. Although RA may develop at a young age, the incidence of RA increases with age. It has been suggested that RA may develop as a consequence of premature aging (immunosenescence) of the immune system. Alternatively, premature aging may be the consequence of the inflammatory state in RA. In an effort to answer this chicken and egg conundrum, we here outline and discuss the nine hallmarks of aging, their contribution to the pre-aged phenotype and the effects of treatment on the reversibility of immunosenescence in RA.

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“…In RA patients we found no differences in Sirt1 activity (nuclear or cytoplasmic) compared to controls, and Sirt1 activity was not correlated with disease activity of RA [7]. The increase of Sirt1 activity in patients treated with NSAIDs could favor increased IL-6 levels which were observed after ex vivo treatment with resveratrol; a possible relationship between Sirt1 and IL-6 is suggested in OA Fig.…”

Section: Introductionmentioning

confidence: 52%

“…Nuclear Sirt1 activity in SpA without (0) and with (1) NSAIDs. [5,8] and RA [7]; a relation between Sirt1 and Cox-2 is suggested in a mouse model [10].…”

Section: Introductionmentioning

confidence: 94%