Monocyte heterogeneity in obesity and subclinical atherosclerosis

Rogačev, Kyrill S.; Ulrich, Christof; Blömer, Lutz; Hornof, Florian; Oster, Katrin; Ziegelin, Maren; Cremers, Bodo; Grenner, Yvonne; Geisel, Jürgen; Schlitt, Axel; Köhler, Hans; Fliser, Danilo; Girndt, Matthias; Heine, Gunnar H.

doi:10.1093/eurheartj/ehp308

Cited by 169 publications

(164 citation statements)

References 22 publications

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“…Multiple studies in nondiabetics suggest a positive correlation between the proportion of circulating CD14 lo /CD16 ϩ monocytes and proinflammatory markers or carotid intimamedia thickness (3,4,48), but no significant differences are found in the mean percentages of CD14 lo /CD16 ϩ monocytes between patients with uncomplicated diabetes, diabetics with cardiovascular disease, and control subjects (5). In this study of diabetic patients, classification of monocyte subtypes based on CD14 and CD16 expression did not correlate with 25(OH)D level or with functional adhesion, suggesting that different monocyte markers could better characterize the functions con-FIGURE 6.…”

Section: Discussionmentioning

confidence: 99%

“…Nearly 26 million Americans suffer from type 2 diabetes mellitus (T2DM), 4 a disease with an increased risk of cardiovascular disease, the leading cause of morbidity and premature mortality in Western populations (1). Very little is known about the mechanisms by which insulin resistance and chronic inflammation promote vascular complications in patients with T2DM.…”

mentioning

confidence: 99%

“…Peripheral blood monocytes are typically defined by cell surface lipopolysaccharide receptor CD14 and Fc␥ receptor III CD16 as CD14 hi /CD16 Ϫ (classical) and CD14 lo /CD16 ϩ (nonclassical) (2). The proportion of CD14 lo / CD16 ϩ monocytes rises in patients with coronary artery disease compared with healthy controls and significantly correlates with carotid intimal medial thickness in healthy populations (3,4). In contrast, diabetic patients with coronary artery disease have no difference in the proportion of CD14 lo / CD16 ϩ monocytes compared with diabetics or healthy individuals without coronary artery disease, thus raising controversy regarding the importance of these monocyte phenotype markers in vascular disease (5).…”

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confidence: 99%

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Vitamin D Suppression of Endoplasmic Reticulum Stress Promotes an Antiatherogenic Monocyte/Macrophage Phenotype in Type 2 Diabetic Patients

Riek

Sprague

et al. 2012

Journal of Biological Chemistry

116

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Background:Interactions between environmental conditions and monocyte phenotype are critical for the development of vascular complications in diabetes. Results: Modulation of ER stress by vitamin D controls monocyte/macrophage phenotype and vascular adhesion. Conclusion: Vitamin D is a natural ER stress reliever that promotes an anti-inflammatory monocyte/macrophage phenotype. Significance: Vitamin D is a potential therapy to reduce vascular complications in diabetics.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Vitamin D Suppression of Endoplasmic Reticulum Stress Promotes an Antiatherogenic Monocyte/Macrophage Phenotype in Type 2 Diabetic Patients

Riek

Sprague

et al. 2012

Journal of Biological Chemistry

116

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“…The CD16 marker has been used to show the existence of two major subsets of monocyte/macrophage subpopulations with distinct roles in target tissues. 10,[46][47][48] …”

Section: Discussionmentioning

confidence: 99%

Dietary intervention-induced weight loss decreases macrophage content in adipose tissue of obese women

et al. 2010

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Objective: Accumulation of adipose tissue macrophages (ATMs) is observed in obesity and may participate in the development of insulin resistance and obesity-related complications. The aim of our study was to investigate the effect of long-term dietary intervention on ATM content in human adipose tissue. Design: We performed a multi-phase longitudinal study. Subjects and measurements: A total of 27 obese pre-menopausal women (age 39±2 years, body mass index 33.7±0.5 kg m -2 ) underwent a 6-month dietary intervention consisting of two periods: 4 weeks of very low-calorie diet (VLCD) followed by weight stabilization composed of 2 months of low-calorie diet and 3to 4 months of weight maintenance diet. At baseline and at the end of each dietary period, samples of subcutaneous adipose tissue (SAT) were obtained by needle biopsy and blood samples were drawn. ATMs were determined by flow cytometry using combinations of cell surface markers. Selected cytokine and chemokine plasma levels were measured using enzyme-linked immunosorbent assay. In addition, in a subgroup of 16 subjects, gene expression profiling of macrophage markers in SAT was performed using real-time PCR. Results: Dietary intervention led to a significant decrease in body weight, plasma insulin and C-reactive protein levels. After VLCD, ATM content defined by CD45 þ /14 þ /206 þ did not change, whereas it decreased at the end of the intervention. This decrease was associated with a downregulation of macrophage marker mRNA levels (CD14, CD163, CD68 and LYVE-1 (lymphatic vessel endothelial hyaluronan receptor-1)) and plasma levels of monocyte-chemoattractant protein-1 (MCP-1) and CXCL5 (chemokine (C-X-C motif) ligand 5). During the whole dietary intervention, the proportion of two ATM subpopulations distinguished by the CD16 marker was not changed. Conclusion: A 6-month weight-reducing dietary intervention, but not VLCD, promotes a decrease in the number of the whole ATM population with no change in the relative distribution of ATM subsets.

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“…Chez l'homme, des premiers travaux ont révélé que les cellules mononucléées circulantes expriment un statut pro-inflammatoire chez les sujets obèses [20]. Plus récemment, une étude clinique indique que la fréquence d'une sous-population de monocytes CD14 dim CD16 + récemment identifiée est augmentée chez des sujets en surpoids [21]. Cette souspopulation monocytaire pourrait contribuer préféren-tiellement à l'accumulation des macrophages dans le tissu adipeux.…”

Section: D'où Viennent Les Macrophages Du Tissu Adipeux ?unclassified