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[PMID]: 29524862
[Au] Autor:Damen MSMA; Dos Santos JC; Hermsen R; Adam van der Vliet J; Netea MG; Riksen NP; Dinarello CA; Joosten LAB; Heinhuis B
[Ad] Address:Department of Internal Medicine and Radboud Center for Infectious Diseases (RCI), Nijmegen, The Netherlands.
[Ti] Title:Interleukin-32 upregulates the expression of ABCA1 and ABCG1 resulting in reduced intracellular lipid concentrations in primary human hepatocytes.
[So] Source:Atherosclerosis;271:193-202, 2018 Mar 02.
[Is] ISSN:1879-1484
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:BACKGROUND AND AIMS: The role of interleukin (IL-)32 in inflammatory conditions is well-established, however, the mechanism behind its role in atherosclerosis remains unexplained. Our group reported a promoter single nucleotide polymorphism in IL-32 associated with higher high-density lipoprotein (HDL) concentrations. We hypothesize that endogenous IL-32 in liver cells, a human monocytic cell line and carotid plaque tissue, can affect atherosclerosis by regulating (HDL) cholesterol homeostasis via expression of cholesterol transporters/mediators. METHODS: Human primary liver cells were stimulated with recombinant human (rh)TNFα and poly I:C to study the expression of IL-32 and mediators in cholesterol pathways. Additionally, IL-32 was overexpressed in HepG2 cells and overexpressed and silenced in THP-1 cells to study the direct effect of IL-32 on cholesterol transporters expression and function. RESULTS: Stimulation of human primary liver cells resulted in induction of IL-32α, IL-32ß and IL-32γ mRNA expression (p < 0.01). A strong correlation between the expression of IL-32γ and ABCA1, ABCG1, LXRα and apoA1 was observed (p < 0.01), and intracellular lipid concentrations were reduced in the presence of endogenous IL-32 (p < 0.05). Finally, IL32γ and ABCA1 mRNA expression was upregulated in carotid plaque tissue and when IL-32 was silenced in THP-1 cells, mRNA expression of ABCA1 was strongly reduced. CONCLUSIONS: Regulation of IL-32 in human primary liver cells, HepG2 and THP-1 cells strongly influences the mRNA expression of ABCA1, ABCG1, LXRα and apoA1 and affects intracellular lipid concentrations in the presence of endogenous IL-32. These data, for the first time, show an important role for IL32 in cholesterol homeostasis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 862598 MEDLINE  
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[PMID]: 29524728
[Au] Autor:Han T; Tian K; Pan H; Liu Y; Xu F; Li Z; Uchita T; Gao M; Hua H; Li D
[Ad] Address:Key Laboratory of Structure-Based Drug Design & Discovery, Ministry of Education, and School of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, PR China.
[Ti] Title:Novel hybrids of brefeldin A and nitrogen mustards with improved antiproliferative selectivity: Design, synthesis and antitumor biological evaluation.
[So] Source:Eur J Med Chem;150:53-63, 2018 Mar 01.
[Is] ISSN:1768-3254
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:A series of novel conjugates of brefeldin A (11a-c, 12a-c and 13a-c) were obtained by introducing a variety of nitrogen mustards at 4-OH or 7-OH position to explore more efficacious and less toxic antitumor agents. The antiproliferative activities were tested against three cancer cell lines (HL-60, PC-3 and Bel-7402) and one multidrug resistant cell line Bel-7402/5-FU. Among them, compound 11a was the strongest derivative with IC values of 4.48, 9.37, 0.2 and 0.84 µM, respectively, and more potent than nitrogen mustards. Though the antiproliferative potency was weaker than the lead compound brefeldin A, 11a displayed lower toxicity than brefeldin A (IC < 0.001 µM) with an IC of 9.74 µM against normal human liver L-O2 cells, showing good selectivity between normal and malignant liver cells. The mechanism studies confirmed that 11a could induce apoptosis, arrest cell cycle at the G1 phase and lead to mitochondrial dysfunction in Bel-7402 cells at submicromolar concentrations. Furthermore, 11a induced the intrinsic apoptotic mitochondrial pathway in Bel-7402 cells, evidenced by the enhanced expression of the pro-apoptotic protein Bax, cyto-c and p53, and the reduced expression of the anti-apoptotic protein Bcl-2. The caspase-9 and -3 levels were also up-regulated.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 862598 MEDLINE  
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[PMID]: 29524598
[Au] Autor:Mitran RA; Matei C; Berger D; Bajenaru L; Moisescu MG
[Ad] Address:"Ilie Murgulescu" Institute of Physical Chemistry, Romanian Academy of Sciences, 202 Splaiul Indepedentei, Bucharest, 060021, Romania; University "Politehnica" of Bucharest, Faculty of Applied Chemistry and Material Science, 1-7 Polizu street, Bucharest, 011061, Romania.
[Ti] Title:Controlling drug release from mesoporous silica through an amorphous, nanoconfined 1-tetradecanol layer.
[So] Source:Eur J Pharm Biopharm;, 2018 Mar 07.
[Is] ISSN:1873-3441
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Mesoporous silica materials are promising nano-carriers for drug delivery systems. Even though there are many strategies for controlling the drug release kinetics, these must be adapted through trial and error on a case-by-case basis. Here we explore the possibility of tailoring the release kinetics of hydrophilic, water soluble therapeutic agents from mesoporous silica through addition of a hydrophobic excipient, 1-tetradecanol. In vitro drug release experiments performed at 37 °C, in phosphate buffer solution (pH 7.4) show that the addition of tetradecanol yields slower drug release kinetics, which was correlated with the presence of a liquid fatty alcohol interfacial layer. The layer mass is 11-23 % wt. of the metoprolol-loaded silica sample, and it causes up to 1.6 times decrease of initial release rate with respect to materials without the fatty alcohol. This effect does not depend of carrier pore arrangement, being noticed for both hexagonal MCM-41 and cubic KIT-5 mesoporous silica. The toxicity of tetradecanol-containing materials was evaluated by formazan-based viability assay on Opossum kidney epithelial cell line, and no significant toxicity was observed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 862598 MEDLINE  
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[PMID]: 29524566
[Au] Autor:Uchida N; Haro-Mora JJ; Demirci S; Fujita A; Raines L; Hsieh MM; Tisdale JF
[Ad] Address:Molecular and Clinical Hematology Branch, National Heart Lung and Blood Institutes (NHLBI) / National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, Maryland (MD) USA. Electronic address: uchidan@nhlbi.nih.gov.
[Ti] Title:High-level embryonic globin production with efficient erythroid differentiation from a k562 erythroleukemia cell line.
[So] Source:Exp Hematol;, 2018 Mar 07.
[Is] ISSN:1873-2399
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:A reliable cell line capable of robust in vitro erythroid differentiation would be useful to investigate red blood cell (RBC) biology and genetic strategies for RBC diseases. K562 cells are widely utilized for erythroid differentiation; however, current differentiation methods are insufficient to analyze globin proteins. In this study, we sought to improve erythroid differentiation from K562 cells to enable protein-level globin analysis. K562 cells were exposed to a variety of reagents including hemin, rapamycin, imatinib, and/or decitabine (known erythroid inducers), and cultured in basic culture media or erythropoietin-based differentiation media. All single reagents induced observable erythroid differentiation with higher glycophorin A (GPA) expression, but were insufficient to produce detectable globin proteins. We then evaluated various combinations of these reagents, and developed a method incorporating imatinib pre-exposure and an erythropoietin-based differentiation culture containing both rapamycin and decitabine capable of efficient erythroid differentiation, high-level GPA expression (>90%), and high-level globin production at protein levels detectable by hemoglobin electrophoresis and high performance liquid chromatography. Additionally, ß-globin gene transfer resulted in detectable adult hemoglobin. In summary, we developed an in vitro K562 erythroid differentiation model with high-level globin production. This model provides a practical evaluation tool for hemoglobin production in human erythroid cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 862598 MEDLINE  
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[PMID]: 29524539
[Au] Autor:Lejal N; Truchet S; Bechor E; Bouguyon E; Khedkar V; Bertho N; Vidic J; Adenot P; Solier S; Pick E; Slama-Schwok A
[Ad] Address:Paris Saclay University, U892 INRA, Jouy en Josas, France.
[Ti] Title:Turning off NADPH oxidase-2 by impeding p67 activation in infected mouse macrophages reduced viral entry and inflammation.
[So] Source:Biochim Biophys Acta;, 2018 Mar 07.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Targeting cells of the host immune system is a promising approach to fight against Influenza A virus (IAV) infection. Macrophage cells use the NADPH oxidase-2 (NOX2) enzymatic complex as a first line of defense against pathogens by generating superoxide ions O and releasing H O . Herein, we investigated whether targeting membrane -embedded NOX2 decreased IAV entry via raft domains and reduced inflammation in infected macrophages. METHODS: Confocal microscopy and western blots monitored levels of the viral nucleoprotein NP and p67 , NOX2 activator subunit, Elisa assays quantified TNF-α levels in LPS or IAV-activated mouse or porcine alveolar macrophages pretreated with a fluorescent NOX inhibitor, called nanoshutter NS1. RESULTS: IAV infection in macrophages promoted p67 translocation to the membrane, rafts clustering and activation of the NOX2 complex at early times. Disrupting rafts reduced intracellular viral NP. NS1 markedly reduced raft clustering and viral entry by binding to the C-terminal of NOX2 also characterized in vitro. NS1 decrease of TNF-α release depended on the cell type. CONCLUSION: NOX2 participated in IAV entry and raft-mediated endocytosis. NOX2 inhibition by NS1 reduced viral entry. NS1 competition with p67 for NOX2 binding shown by in silico models and cell-free assays was in agreement with NS1 inhibiting p67 translocation to membrane-embedded NOX2 in mouse and porcine macrophages. GENERAL SIGNIFICANCE: We introduce NS1 as a compound targeting NOX2, a critical enzyme controlling viral levels and inflammation in macrophages and discuss the therapeutic relevance of targeting the C-terminal of NADPH oxidases by probes like NS1 in viral infections.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 862598 MEDLINE  
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[PMID]: 29515105
[Au] Autor:Rani B; Malfettone A; Dituri F; Soukupova J; Lupo L; Mancarella S; Fabregat I; Giannelli G
[Ad] Address:School of Medicine, University of Bari, Bari, Italy.
[Ti] Title:Galunisertib suppresses the staminal phenotype in hepatocellular carcinoma by modulating CD44 expression.
[So] Source:Cell Death Dis;9(3):373, 2018 Mar 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cancer stem cells (CSCs) niche in the tumor microenvironment is responsible for cancer recurrence and therapy failure. To better understand its molecular and biological involvement in hepatocellular carcinoma (HCC) progression, one can design more effective therapies and tailored then to individual patients. While sorafenib is currently the only approved drug for first-line treatment of advanced stage HCC, its role in modulating the CSC niche is estimated to be small. By contrast, transforming growth factor (TGF)-ß pathway seems to influence the CSC and thus may impact hallmarks of HCC, such as liver fibrosis, cirrhosis, and tumor progression. Therefore, blocking this pathway may offer an appealing and druggable target. In our study, we have used galunisertib (LY2157299), a selective ATP-mimetic inhibitor of TGF-ß receptor I (TGFßI/ALK5) activation, currently under clinical investigation in HCC patients. Because the drug resistance is mainly mediated by CSCs, we tested the effects of galunisertib on stemness phenotype in HCC cells to determine whether TGF-ß signaling modulates CSC niche and drug resistance. Galunisertib modulated the expression of stemness-related genes only in the invasive (HLE and HLF) HCC cells inducing a decreased expression of CD44 and THY1. Furthermore, galunisertib also reduced the stemness-related functions of invasive HCC cells decreasing the formation of colonies, liver spheroids and invasive growth ability. Interestingly, CD44 loss of function mimicked the galunisertib effects on HCC stemness-related functions. Galunisertib treatment also reduced the expression of stemness-related genes in ex vivo human HCC specimens. Our observations are the first evidence that galunisertib effectiveness overcomes stemness-derived aggressiveness via decreased expression CD44 and THY1.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0384-5

  7 / 862598 MEDLINE  
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[PMID]: 29514102
[Au] Autor:Tovar-Díaz J; Pomrenze MB; Kan R; Pahlavan B; Morikawa H
[Ad] Address:Department of Neuroscience, University of Texas at Austin, Austin, TX 78712, USA; Waggoner Center for Alcohol and Addiction Research, University of Texas at Austin, Austin, TX 78712, USA.
[Ti] Title:Cooperative CRF and α1 Adrenergic Signaling in the VTA Promotes NMDA Plasticity and Drives Social Stress Enhancement of Cocaine Conditioning.
[So] Source:Cell Rep;22(10):2756-2766, 2018 Mar 06.
[Is] ISSN:2211-1247
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Stressful events rapidly trigger activity-dependent synaptic plasticity, driving the formation of aversive memories. However, it remains unclear how stressful experience affects plasticity mechanisms to regulate appetitive learning, such as intake of addictive drugs. Using rats, we show that corticotropin-releasing factor (CRF) and α1 adrenergic receptor (α1AR) signaling enhance the plasticity of NMDA-receptor-mediated glutamatergic transmission in ventral tegmental area (VTA) dopamine (DA) neurons through distinct effects on inositol 1,4,5-triphosphate (IP )-dependent Ca signaling. We find that CRF amplifies IP -Ca signaling induced by stimulation of α1ARs, revealing a cooperative mechanism that promotes glutamatergic plasticity. In line with this, acute social defeat stress engages similar cooperative CRF and α1AR signaling in the VTA to enhance learning of cocaine-paired cues. These data provide evidence that CRF and α1ARs act in concert to regulate IP -Ca signaling in the VTA and promote learning of drug-associated cues.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  8 / 862598 MEDLINE  
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[PMID]: 29511371
[Au] Autor:Manzano-Moreno FJ; Ramos-Torrecillas J; Melguizo-Rodríguez L; Illescas-Montes R; Ruiz C; García-Martínez O
[Ad] Address:Biomedical Group (BIO277), Department of Stomatology, School of Dentistry, University of Granada, Spain.
[Ti] Title:Bisphosphonate Modulation of the Gene Expression of Different Markers Involved in Osteoblast Physiology: Possible Implications in Bisphosphonate-Related Osteonecrosis of the Jaw.
[So] Source:Int J Med Sci;15(4):359-367, 2018.
[Is] ISSN:1449-1907
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:The aim of the present study was to elucidate the role of osteoblasts in bisphosphonates-related osteonecrosis of the jaw (BRONJ). The specific objective was to evaluate the effect on osteoblasts of two nitrogen-containing BPs (zoledronate and alendronate) and one non-nitrogen-containing BP (clodronate) by analyzing modulations in their expression of genes essential for osteoblast physiology. Real-time polymerase chain reaction (RT-PCR) was used to study the effects of zoledronate, alendronate, and clodronate at doses of 10 , 10 , or 10 M on the expression of Runx-2, OSX, ALP, OSC, OPG, RANKL, Col-I, BMP-2, BMP-7, TGF-ß1, VEGF, TGF-ßR1, TGF-ßR2, and TGF-ßR3 by primary human osteoblasts (HOBs) and MG-63 osteosarcoma cells. Expression of these markers was found to be dose-dependent, with no substantive differences between these cell lines. In general, results demonstrated a significant increase in TFG-ß1, TGF-ßR1, TGF-ßR2, TGF-ßR3, and VEGF expressions and a significant reduction in RUNX-2, Col-1, OSX, OSC, BMP-2, BMP-7, ALP, and RANKL expressions, while OPG expression varied according to the dose and cell line. The results of this study of HOBS and MG-63 cell lines indicate that low BP doses can significantly affect the expression of genes essential for osteoblast growth and differentiation and of genes involved in regulating osteoblast-osteoclast interaction, possibly by increasing TGF-ß1 production. These findings suggest that osteoblasts may play an important role in BRONJ development, without ruling out other factors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.7150/ijms.22627

  9 / 862598 MEDLINE  
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[PMID]: 29511364
[Au] Autor:Huang SF; Chu SC; Hsieh YH; Chen PN; Hsieh YS
[Ad] Address:Division of Chest Medicine, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung City, Taiwan, ROC.
[Ti] Title:Viola Yedoensis Suppresses Cell Invasion by Targeting the Protease and NF-κB Activities in A549 and Lewis Lung Carcinoma Cells.
[So] Source:Int J Med Sci;15(4):280-290, 2018.
[Is] ISSN:1449-1907
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:Cancer metastasis is a vital trait in malignancies with complicated early diagnosis and therapeutic management. Therefore, the development of new remedies and the utilization of natural medicines that target metastasis are of great interest and have been studied extensively. Chinese medicinal herbs have various anti-carcinogenesis properties; however, the in vitro effect and mechanism of on cancer cell metastasis remains poorly understood. extracts (VYE) can suppress the invasion of a highly metastatic human lung cancer cell line, A549 cells. According to gelatin zymography and casein zymography assays, VYE inhibited the activities of matrix metalloproteinases (MMPs) and urokinase-type plasminogen activator (u-PA). The results of reverse transcription-polymerase chain reaction and Western blotting revealed that VYE can alter the expression of proteinase inhibitor. VYE also suppressed the DNA binding activity of nuclear factor-kappa B. We concluded that VYE may inhibit tumor invasion by suppressing the activities of MMP and u-PA in lung cancer cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.7150/ijms.22793

  10 / 862598 MEDLINE  
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[PMID]: 29506649
[Au] Autor:Degrossoli A; Müller A; Xie K; Schneider JF; Bader V; Winklhofer KF; Meyer AJ; Leichert LI
[Ad] Address:Institute for Biochemistry and Pathobiochemistry - Microbial Biochemistry, Ruhr-Universität Bochum, Bochum, Germany.
[Ti] Title:Neutrophil-generated HOCl leads to non-specific thiol oxidation in phagocytized bacteria.
[So] Source:Elife;7, 2018 Mar 06.
[Is] ISSN:2050-084X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Phagocytic immune cells kill pathogens in the phagolysosomal compartment with a cocktail of antimicrobial agents. Chief among them are reactive species produced in the so-called oxidative burst. Here, we show that bacteria exposed to a neutrophil-like cell line experience a rapid and massive oxidation of cytosolic thiols. Using roGFP2-based fusion probes, we could show that this massive breakdown of the thiol redox homeostasis was dependent on phagocytosis, presence of NADPH oxidase and ultimately myeloperoxidase. Interestingly, the redox-mediated fluorescence change in bacteria expressing a glutathione-specific Grx1-roGFP2 fusion protein or an unfused roGFP2 showed highly similar reaction kinetics to the ones observed with roGFP2-Orp1, under all conditions tested. We recently observed such an indiscriminate oxidation of roGFP2-based fusion probes by HOCl with fast kinetics in vitro. In line with these observations, abating HOCl production in immune cells with a myeloperoxidase inhibitor significantly attenuated the oxidation of all three probes in bacteria.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review


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