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The National Institute of Biotechnology in the Negev (NIBN), Ben-Gurion University, Beer-Sheva, Israel
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The National Institute of Biotechnology in the Negev (NIBN), Ben-Gurion University, Beer-Sheva, Israel
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The National Institute of Biotechnology in the Negev (NIBN), Ben-Gurion University, Beer-Sheva, Israel
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The National Institute of Biotechnology in the Negev (NIBN), Ben-Gurion University, Beer-Sheva, Israel
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The National Institute of Biotechnology in the Negev (NIBN), Ben-Gurion University, Beer-Sheva, Israel
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inflammation (particularly macrophage infiltration) characterizes obese persons who develop insulin resistance ( Harman-Boehm et al . 2007 ), but to a much lesser degree age, sex and BMI-matched obese persons who remain insulin sensitive ( Kloting et al
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cytokine production in macrophages ( Distelhorst 2002 , Frankfurt & Rosen 2004 ). Macrophages also play a key role in the immune and inflammatory process, mainly acting as antigen-processing/presenting cells and sources of inflammatory cytokines. Although
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local inflammation ( Brown & Goldstein 1983 ). Recruited monocytes differentiate into macrophages and begin to take up oxidized lipoproteins, leading to the formation of foam cells. Foam cells are a primary component of early atheroma lesion formation
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Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute
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(Arg1; Rh02826373_m1) M1- and M2-activated macrophages respectively from the same cDNA as mentioned earlier. Quantitative PCRs were run on an ABI 7300 (Applied Biosystems), using TaqMan universal PCR master mix TaqMan master mix in a 10 μl reaction
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) ( Ruderman & Prentki 2004 ). Based on the requirement for AMPK to alleviate hepatic steatosis, there is growing demand to identify mediators of AMPK activation in response to dynamic physiological activity. Although macrophage migration inhibitory factor (MIF
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Surgical Research Unit, Department of Surgery, Laboratory of Metabolism, Infectious Diseases Service, Clinical Diabetes Unit, Radiology, Cell Physiology and Metabolism, Internal Medicine, Department of Surgery
Surgical Research Unit, Department of Surgery, Laboratory of Metabolism, Infectious Diseases Service, Clinical Diabetes Unit, Radiology, Cell Physiology and Metabolism, Internal Medicine, Department of Surgery
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Introduction Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in both innate and adaptive immunity. Originally described as a T-cell-derived product, MIF has now been shown to be released by numerous cell types and
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Departments of, Vascular Medicine, Medical Biochemistry, Pathology, Experimental Immunology, INSERM, Department of Internal Medicine, Academic Medical Center, 1105 AZ Amsterdam, The Netherlands
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by inflammatory cell infiltration, accumulation of heterogeneous macrophage populations, T-cell activation, cytokine production, and cell death, is also an integral part of the atherosclerotic process ( Packard & Libby 2008 ). In fact, all stages of
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). In the last decade, there has been a groundswell of interest in understanding the interrelationship between Leydig cells and testicular macrophages ( Haider 2004 , Hutson 2006 ). Moreover, lymphocytes and low number of mast cells are also present
Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
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Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
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Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
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Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
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Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
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Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
Department of Specialty Medicine, Appalachian Rural Health Institute, Edison Biotechnology Institute, Department of Biomedical Sciences, Biomedical Engineering Program, Interthyr Corporation, Diabetes Research Center
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adipocytes and associated inflammatory cells (macrophages) produce and release excessive amounts of biologically active ‘cytokines/adipokines’ (TNF-α, resistin, IL6, and PAI-1, etc.), which circulate via the portal and systemic vascular system to other
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Dehydroepiandrosterone (DHEA) is a ubiquitous adrenal hormone with immunomodulatory effects such as inhibition of the production of monokines. Whether DHEA itself or the downstream steroids are the immunomodulatory effector hormones in target cells is not known. In this study, we investigated the conversion of DHEA to downstream steroid hormones in target macrophages. Within 1 day of culture with radiolabeled DHEA, monocyte-derived macrophages converted DHEA to significant amounts of Delta5-derivatives such as 16OH-DHEA, 3beta, 17beta-androstenediol (A'diol), and 3beta,16alpha, 17beta-androstenetriol (A'triol). However, the production of Delta4-steroids (androstenedione (A'dione), testosterone (T), and 16OH-T) and estrogens (estrone, estradiol, and estriol) was relatively low. Further cultivation of macrophages for 5 days with radiolabeled DHEA resulted in a significant (P<0.05) increase of the molar amounts of A'triol (P=0.012), 16OH-T (P=0.008), and estriol (P=0.003). In contrast to monocyte-derived macrophages, monocytes did not express aromatase mRNA, which was demonstrated by RT-PCR (P<0.01). Furthermore, DHEA in macrophages significantly inhibited one of the downstream converting enzymes, the aromatase, which was not demonstrated in the presence of the typical macrophage activator, lipopolysaccharide (LPS) (P<0.01). In conclusion, conversion of DHEA to physiologically relevant amounts of Delta5- and Delta4-steroids and estrogens was demonstrated in monocyte-derived macrophages. The conversion depends on maturation of monocytes and local factors such as the presence of LPS. The conversion of DHEA leads to an increase of downstream effector hormones in target macrophages which may be an important factor for local immunomodulation.