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Transcript and Protein Analysis Reveals Better Survival Skills of Monocyte-Derived Dendritic Cells Compared to Monocytes During Oxidative Stress Transcript and Protein Analysis Reveals Better Survival Skills of Monocyte-Derived Dendritic Cells Compared to Monocytes during Oxidative Stress Ilse Van Brussel1*, Dorien M. Schrijvers2, Wim Martinet2, Isabel Pintelon3, Maartje Deschacht4, Kathy Schnorbusch3, Louis Maes4, Johan M. Bosmans1,5, Christiaan J. Vrints1,5, Dirk Adriaensen3, Paul Cos4, Hidde Bult6 1 Laboratory of Cellular and Molecular Cardiology, University of Antwerp, Wilrijk, Antwerp, Belgium, 2 Laboratory of Physiopharmacology, University of Antwerp, Wilrijk, Antwerp, Belgium, 3 Laboratory of Cell Biology and Histology, University of Antwerp, Antwerp, Antwerp, Belgium, 4 Laboratory of Microbiology, Parasitology and Hygiene (LMPH), University of Antwerp, Wilrijk, Antwerp, Belgium, 5 Department of Cardiology, University Hospital of Antwerp, Edegem, Antwerp, Belgium, 6 Laboratory of Pharmacology, University of Antwerp, Wilrijk, Antwerp, Belgium Abstract Background: Dendritic cells (DCs), professional antigen-presenting cells with the unique ability to initiate primary T-cell responses, are present in atherosclerotic lesions where they are exposed to oxidative stress that generates cytotoxic reactive oxygen species (ROS). A large body of evidence indicates that cell death is a major modulating factor of atherogenesis. We examined antioxidant defence systems of human monocyte-derived (mo)DCs and monocytes in response to oxidative stress. Methods: Oxidative stress was induced by addition of tertiary-butylhydroperoxide (tert-BHP, 30 min). Cellular responses were evaluated using flow cytometry and confocal live cell imaging (both using 5-(and-6)-chloromethyl-2,7- dichlorodihydrofluorescein diacetate, CM-H2DCFDA). Viability was assessed by the neutral red assay. Total RNA was extracted for a PCR profiler array. Five genes were selected for confirmation by Taqman gene expression assays, and by immunoblotting or immunohistochemistry for protein levels. Results: Tert-BHP increased CM-H2DCFDA fluorescence and caused cell death. Interestingly, all processes occurred more slowly in moDCs than in monocytes. The mRNA profiler array showed more than 2-fold differential expression of 32 oxidative stress–related genes in unstimulated moDCs, including peroxiredoxin-2 (PRDX2), an enzyme reducing hydrogen peroxide and lipid peroxides. PRDX2 upregulation was confirmed by Taqman assays, immunoblotting and immunohis- tochemistry. Silencing PRDX2 in moDCs by means of siRNA significantly increased CM-DCF fluorescence and cell death upon tert-BHP-stimulation. Conclusions: Our results indicate that moDCs exhibit higher intracellular antioxidant capacities, making them better equipped to resist oxidative stress than monocytes. Upregulation of PRDX2 is involved in the neutralization of ROS in moDCs. Taken together, this points to better survival skills of DCs in oxidative stress environments, such as atherosclerotic plaques. Citation: Van Brussel I, Schrijvers DM, Martinet W, Pintelon I, Deschacht M, et al. (2012) Transcript and Protein Analysis Reveals Better Survival Skills of Monocyte- Derived Dendritic Cells Compared to Monocytes during Oxidative Stress. PLoS ONE 7(8): e43357. doi:10.1371/journal.pone.0043357 Editor: T. Mark Doherty, Statens Serum Institute, Denmark Received October 20, 2011; Accepted July 23, 2012; Published August 15, 2012 Copyright: ß 2012 Van Brussel et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: This work was supported by the University of Antwerp (GOA-BOF 2407; http://www.ua.ac.be/main.aspx?c = ONDERZK&n = 86348), and the agency of Innovation by Science and Technology (IWT-TBM; http://www.iwt.be/subsidies/tbm). Paul Cos is a postdoctoral researcher awarded by the Fund for Scientific Research (FWO; www.fwo.be) – Flanders (Belgium). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist. * E-mail: [email protected] Introduction Dendritic cells (DCs) are highly specialized antigen-presenting cells involved in both innate and adaptive immune responses. Oxidative stress is believed to contribute to the development of Under (oxidative) stress conditions, such as inflammation, infection several chronic human diseases, including atherosclerosis [1–5], and tissue damage, DCs rapidly take up foreign antigens to process and results from an imbalance between production of reactive and present them as soluble antigens in complexes with either class oxygen species (ROS) and antioxidant defences [2]. Accumulating I or class II major histocompatibility complex (MHC) molecules evidence has shown that ROS mediate innate immune reactions [8]. We and others recently demonstrated that DC precursors, (direct killing of microbes by phagocytes) [6] and signal immature DCs and mature DCs accumulate in human athero- transduction from pathogen-recognition receptors [7]. sclerotic plaques [9–11], where they are exposed to oxidative stress PLOS ONE | www.plosone.org 1 August 2012 | Volume 7 | Issue 8 | e43357 Response of Dendritic Cells to Oxidative Stress [12,13] and oxidized low density lipoproteins (oxLDL) [14,15]. CM-DCF fluorescence measured by FCM Therefore, it can be assumed that immature DCs will show After harvesting and washing, cells were labelled with Alexa phenotypic adaptations in order to function under oxidative stress Fluor 647-conjugated anti-human CD14 (monocytes) or anti- situations. To investigate this hypothesis, monocytes and mono- human HLA-DR (moDCs), both from Biolegend (Uithoorn, The cyte-derived (mo)DCs were exposed to a well known inducer of Netherlands). After 25 min, excess antibody was removed by oxidative stress, namely tertiary-butylhydroperoxide (tert-BHP). centrifugation (6 min, 4506g) and cells were suspended in PBS Tert-BHP was selected since it acutely causes oxidative stress, with 10 mM CM-H2DCFDA (Molecular Probes, Invitrogen, resulting in cell toxicity [16]. Decomposition of tert-BHP to alkoxyl Merelbeke, Belgium). After 20 min, extracellular probe was or peroxyl radicals accelerates lipid peroxidation chain reactions removed by centrifugation (6 min, 4506g), and cells were [17]. suspended in 100 ml PBS. CM-DCF fluorescence was measured The effectiveness of the antioxidant defence systems was immediately or after incubation (30 min, 37uC) with 200 mM tert- assessed by measuring intracellular ROS, which carries a real BHP (Sigma, Bornem, Belgium) on a FacsCanto II flow cytometer challenge as most ROS are highly reactive and very short-lived. (BD, Erembodegem, Belgium) using automatic compensation We used 5-(and-6)-chloromethyl-2,7-dichlorodihydrofluorescein settings, and 20,000 events were analyzed with FacsDiva 6.1 diacetate acetyl ester (CM-H2DCFDA) to evaluate intracellular software. CM-DCF fluorescence was evaluated within the oxidative stress, since it detects a very broad spectrum of ROS, population of CD14bright cells for monocytes and HLA-DRbright including hydrogen peroxide (H2O2), alkoxyl radicals and cells for moDCs (figure 1). peroxynitrite anions [18]. CM-DCF fluorescence was measured by flow cytometry (FCM), but as this technique cannot correct for CM-DCF fluorescence measured by confocal LCI potential differences in probe load between monocytes and Culture medium was removed and replaced by 2 mL PBS with moDCs, we also measured CM-DCF fluorescence in situ using Alexa Fluor 647-conjugated anti-human CD14 (monocytes) or confocal live cell imaging (LCI). LCI has the added advantage that anti-human HLA-DR (moDCs). After 25 min, cells were rinsed cell scraping and isolation, which may induce different degrees of with PBS, and 10 mM CM-H2DCFDA in PBS was added. After oxidative stress in both cell types, is avoided. 20 min, the dish was placed on a Zeiss Axiovert 200 microscope Secondly, survival of monocytes and moDCs was assessed by a attached to an UltraVIEW spinning confocal Live Cell Imager neutral red viability assay. (Perkin Elmer, Seer Green, UK). After taking a bright field To elucidate potential differences, we thirdly examined snapshot (figure 2A), red light (excitation 647 nm) was used to expression of oxidative stress-related genes (OSRGs) using a visualize HLA-DR or CD14 fluorescence (figure 2B). Then, CM- commercial PCR profiler array platform with 84 probe sets. Five DCF fluorescence was imaged for 18 min by repeated exposure to genes with (1) direct pro-or antioxidant enzymatic activity, (2) blue light (excitation 488 nm; 500 msec exposure time) at 2 min more than 4-fold differential expression, and (3) a fairly high intervals to minimize exposure to laser light (figure 2C). First, basal expression level in monocytes were selected for validation at the CM-DCF fluorescence was studied for 10 min at 25uC, then mRNA level (Taqman assays), and protein level (Western blot and 200 mM tert-BHP was added and fluorescence was recorded for immunohistochemistry). another 8 min. Thereafter, cells were continuously illuminated Finally, we examined whether peroxiredoxin-2 (PRDX2), that during 4 min to determine the individual probe load of each cell showed strong upregulation in moDCs, was involved in the by causing photo-oxidation of remaining 5-(and-6)-chloromethyl- resistance of moDCs to tert-BHP-induced cell death. PRDX2 2,7-dichlorofluorescein and 2 images per second were recorded
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