Table S1 List of Genes/Proteins Shared Between NAFLD, Fibrosis, and Inflammation Gene Symbol Description Gene ID
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Polymorphisms with Late-Onset Alzheimer Disease in Han Chinese
172 Original Article on Translational Neurodegeneration Page 1 of 8 Association of lectin-like oxidized low density lipoprotein receptor 1 (OLR1) polymorphisms with late-onset Alzheimer disease in Han Chinese Zuo-Teng Wang1#, Xiao-Ling Zhong2#, Meng-Shan Tan1, Hui-Fu Wang1, Chen-Chen Tan1, Wei Zhang1, Zhan-Jie Zheng3, Ling-Li Kong3, Lan Tan1, Li Sun2 1Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China; 2Department of Neurology, Qingdao Central Hospital, Qingdao University, Qingdao 266042, China; 3Department of Geriatric, Qingdao Mental Health Center, Qingdao 266034, China Contributions: (I) Conception and design: All authors; (II) Administrative support: All authors; (III) Provision of study materials or patients: All authors; (VI) Collection and assembly of data: All authors; (V) Data analysis and interpretation: All authors; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. #These authors should be regarded as co-first authors. Correspondence to: Dr. Lan Tan, MD, PhD. Department of Neurology, Qingdao Municipal Hospital, Qingdao University, No. 5 Donghai Middle Road, Qingdao 266071, China. Email: [email protected]; Dr. Li Sun, MD, PhD. Department of Neurology, Qingdao Central Hospital, Qingdao University, Qingdao 266042, China. Email: [email protected]. Background: Lectin-like oxidized low density lipoprotein receptor 1 (OLR1) locates within the area of chromosome 12p, which has been identified as the AD-susceptible region, and plays a role in lipid metabolism. Therefore, it has been suggested to be a good candidate gene for Alzheimer’s disease (AD). Several SNPs within OLR1 have been reported to have association with AD among Caucasians. Methods: We selected and genotyped three SNPs (rs1050283, rs1050286, rs17808009) in OLR1 to investigate its possible relationship with the onset of late-onset Alzheimer disease(LOAD) in 984 LOAD cases and 1,354 healthy controls among northern Han Chinese. -
Genome Wide Analysis of TLR1/2- and TLR4-Activated SZ95 Sebocytes
RESEARCH ARTICLE Genome wide analysis of TLR1/2- and TLR4- activated SZ95 sebocytes reveals a complex immune-competence and identifies serum amyloid A as a marker for activated sebaceous glands DaÂniel ToÈ rőcsik1,2*, DoÂra KovaÂcs1, SzilaÂrd PoÂliska3, Zita Szentkereszty-KovaÂcs1, a1111111111 Marianna LovaÂszi1, Katalin Hegyi1, Andrea Szegedi1,4, Christos C. Zouboulis5, a1111111111 Mona Ståhle2 a1111111111 a1111111111 1 Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary, 2 Unit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, a1111111111 Stockholm, Sweden, 3 Department of Biochemistry and Molecular Biology, Genomic Medicine and Bioinformatics Core Facility, Faculty of Medicine, University of Debrecen, Debrecen, Hungary, 4 Division of Dermatological Allergology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary, 5 Departments of Dermatology, Venereology, Allergology and Immunology, Dessau Medical Center, Brandenburg Medical School Theodore Fontane, Dessau, Germany OPEN ACCESS * [email protected] Citation: ToÈrőcsik D, KovaÂcs D, PoÂliska S, Szentkereszty-KovaÂcs Z, LovaÂszi M, Hegyi K, et al. (2018) Genome wide analysis of TLR1/2- and TLR4-activated SZ95 sebocytes reveals a complex Abstract immune-competence and identifies serum amyloid A as a marker for activated sebaceous glands. Toll-like receptors (TLR) 2 and 4 are active in sebaceous glands and play a central role in PLoS ONE 13(6): e0198323. https://doi.org/ the development of acne. Still, there is only limited knowledge on their effect on sebocytes. 10.1371/journal.pone.0198323 In this work we performed global gene expression profile analysis with functional clustering Editor: Mauro Picardo, San Gallicano Dermatologic of the differentially regulated genes of TLR1/2 (PAM3CSK4)- and TLR4 (lipopolysaccharide Institute, ITALY [LPS])-activated SZ95 sebocytes. -
Basic Science * Drug X Is Used for Ongoing IP/Patent Assessment Heart: First Published As 10.1136/Heartjnl-2021-BCS.199 on 4 June 2021
Abstracts Basic science * Drug X is used for ongoing IP/patent assessment Heart: first published as 10.1136/heartjnl-2021-BCS.199 on 4 June 2021. Downloaded from Conflict of Interest No BS1 REPROGRAMMING HUMAN MACROPHAGES WITH DRUG X: POTENTIAL MECHANISMS FOR STABILISATION OF ATHEROSCLEROTIC PLAQUES BS2 MECHANOSENSOR PIEZO1 IN SKELETAL MUSCLE PERICYTES 1Klaudia Kocsy, 1Endre Kiss-Toth, 2Jessica Redgrave, 2Arshad Majid, 3Sheila Francis. 1Department of Infection, Immunity & Cardiovascular Disease, The University of Sheffield, 1Yilizila Abudushalamu, 1Hema Viswambharan, 2Romana Mughal, 1Richard Cubbon, Sheffield, UK; 2Department of Neuroscience, The University of Sheffield, Sheffield, UK; 3The 1Mark Kearney, 1David Beech, 1Piruthivi Sukumar. 1Discovery and Translational Science University of Sheffield, Sheffield, UK Department Leeds Institute of Cardiovascular and Metabolic Medic, Leeds, UK; 2Department of Optometry and Vision Sciences School of Applied Sciences University of Huddersfield 10.1136/heartjnl-2021-BCS.199 10.1136/heartjnl-2021-BCS.200 Introduction Ischemic stroke is commonly caused by large artery atherosclerosis. Patients with a high atherosclerotic bur- Introduction Pericytes (PC) are mural cells which are present den (stenosis) and inflamed or ulcerated plaque are at in blood microvessels. They play an important part in the for- increased risk of early recurrent ischaemic events. Treatment mation and stabilization of new blood vessels. They are essen- with anti-inflammatory agents may therefore reduce stroke tial for vascular development and cardiovascular homeostasis. incidence and recurrence in patients with this condition, but They wrap around the endothelial cells (EC) and endothelial- in vitro human studies of the possible mechanisms are lacking. pericyte communication is both via physical contact and para- 1 We hypothesised that an anti-inflammatory compound crine signalling. -
MOUSE INTERLEUKIN-28B/INTERFERON-LAMBDA 3, CARRIER FREE Product Number: 12821-1 Lot Number: 5559 Size: 25 Μg
MOUSE INTERLEUKIN-28B/INTERFERON-LAMBDA 3, CARRIER FREE Product Number: 12821-1 Lot Number: 5559 Size: 25 µg Description: Mouse Interleukin-28B/Interferon-lambda 3, Carrier Free Source: A DNA sequence encoding the mature mouse IL-28B/IFN-λ3 (Asp 20 - Val 193) (Kotenko, S.V. et al., 2003, Nat. Immunol. 4(1):69 - 77) was expressed in E. coli. Form: Lyophilized Buffer: Phosphate-buffered saline (PBS) Reconstitution: It is recommended that sterile PBS be added to the vial to prepare a stock solution of no less than 100 μg/mL. Endotoxin: < 1 EU/µg Molecular Weight: The 175 amino acid residue methionyl form of recombinant mouse IL-28B has a predicted molecular mass of approximately 19.7 kDa. Purity: > 95% Synonyms: Mu IL-28B; Mu IFN-λ3 Accession #: NP_796370 Assays Used to Measure Bioactivity: Human HepG2 cells infected with encephalomyocarditis virus (Sheppard, P. et al., 2003, Nature Immunol. 4:63). The ED50 for this effect is typically 7.5 - 37.5 ng/mL. Shipping Conditions: Wet Ice Physical State of Product During Shipping: Lyophilized Special Conditions/Comments: After receipt, this product should be kept at -70˚C or below for retention of full activity. Upon reconstitution, this cytokine can be stored under sterile conditions at 2˚C to 8˚C for one month or at -20˚C to -70˚C in a manual defrost freezer for three months without detection loss of activity. Avoid repeated freeze-thaw cycles. For more information on protein handling, visit the PBL website at www.interferonsource.com . Product Information: Human IL-28A, IL-28B, and IL-29, also named interferon-λ2 (IFN-λ2), IFN-λ3, and IFN-λ1, respectively, are newly identified class II cytokine receptor ligands that are distantly related to members of the IL-10 family (11- 13% aa sequence identity) and type I IFN family (15 - 19% aa sequence identity).1 – 3 The genes encoding these three cytokines are localized to chromosome 19 and each is composed of multiple exons. -
Molecular Characterization of Tea Catechin Treated Human Prostate Cancer Cell Lines Yewseok Suh
Florida State University Libraries Electronic Theses, Treatises and Dissertations The Graduate School 2006 Molecular Characterization of Tea Catechin Treated Human Prostate Cancer Cell Lines Yewseok Suh Follow this and additional works at the FSU Digital Library. For more information, please contact [email protected] THE FLORIDA STATE UNIVERSITY COLLEGE OF ARTS AND SCIENCES MOLECULAR CHARACTERIZATION OF TEA CATECHIN TREATED HUMAN PROSTATE CANCER CELL LINES By YEWSEOK SUH A Dissertation submitted to the Department of Chemistry and Biochemistry in partial fulfillment of the requirements for the degree of Doctor of Philosophy Degree Awarded: Summer Semester, 2006 The members of the Committee approve the dissertation of Yewseok Suh defended on May 12, 2006. Qing-Xiang Amy Sang Professor Directing Dissertation Thomas C.S. Keller III Outside Committee Member Joseph B. Schlenoff Committee Member Hong Li Committee Member Approved: Naresh Dalal, Chair, Department of Chemistry and Biochemistry Joseph Travis, Dean, College of Arts and Sciences The Office of Graduate Studies has verified and approved the above named committee members. ii This dissertation is dedicated to my parents for their endless love and encouragement, to my lovely wife Inok Park for her support, and to our charming daughter, Tae-won. iii ACKNOWLEDGEMENTS I would like to express my gratitude to my major professor for her support throughout the research. Also thanks to all my committee members, Dr. Thomas C. S. Keller III, Dr. Hong Li, and Dr. Joseph B. Schlenoff, for their support, advice, and guidance. Special thanks to our lab members especially, Ziad Sahab and Robert G. Newcomer and former lab member Douglas R. -
2018 Chen Lingyan 1448129
This electronic thesis or dissertation has been downloaded from the King’s Research Portal at https://kclpure.kcl.ac.uk/portal/ Genetics and Epigenetics in Systemic Lupus Erythematosus Chen, Lingyan Awarding institution: King's College London The copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without proper acknowledgement. END USER LICENCE AGREEMENT Unless another licence is stated on the immediately following page this work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International licence. https://creativecommons.org/licenses/by-nc-nd/4.0/ You are free to copy, distribute and transmit the work Under the following conditions: Attribution: You must attribute the work in the manner specified by the author (but not in any way that suggests that they endorse you or your use of the work). Non Commercial: You may not use this work for commercial purposes. No Derivative Works - You may not alter, transform, or build upon this work. Any of these conditions can be waived if you receive permission from the author. Your fair dealings and other rights are in no way affected by the above. Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 03. Oct. 2021 GENETICS AND EPIGENETICS IN SYSTEMIC LUPUS ERYTHEMATOSUS Lingyan CHEN Department of Medical & Molecular Genetics Faculty of Life Sciences & Medicine King’s College London This thesis is submitted for the degree of DoCtor of Philosophy (PhD) 1 To my parents 2 DeClaration The work described in this thesis was carried out within the Vyse Immunogenetics Group in the Department of Medical and Molecular Genetics at King’s College London under the supervision of Professor Timothy James Vyse and Dr David Lester Morris and between the years of October 2014 and March 2018. -
Ncounter® Autoimmune Discovery Consortium Panel
nCounter® Autoimmune Discovery Consortium Panel - Gene Details Official Symbol Accession Alias / Previous Symbol Official Full Name Other targets or Isoform Information AAMP NM_001087.3 angio associated migratory cell protein ABHD6 NM_020676.5 abhydrolase domain containing 6 ACKR2 NM_001296.3 CMKBR9,CCBP2;chemokine binding protein 2 atypical chemokine receptor 2 ACOXL NM_018308.1 acyl-Coenzyme A oxidase-like acyl-CoA oxidase like ACSL6 NM_001009185.1 FACL6;fatty-acid-Coenzyme A ligase, long-chain 6 acyl-CoA synthetase long chain family member 6 ADA NM_000022.2 adenosine deaminase ADAM30 NM_021794.2 a disintegrin and metalloproteinase domain 30 ADAM metallopeptidase domain 30 ADCY3 NM_004036.3 adenylate cyclase 3 ADCY7 NM_001114.4 adenylate cyclase 7 AFF3 NM_001025108.1 LAF4;lymphoid nuclear protein related to AF4,AF4/FMR2 family, member 3 AF4/FMR2 family member 3 AGAP2 NM_014770.3 CENTG1;centaurin, gamma 1 ArfGAP with GTPase domain, ankyrin repeat and PH domain 2 AHI1 NM_001134830.1 Abelson helper integration site Abelson helper integration site 1 AHR NM_001621.3 aryl hydrocarbon receptor AHSA2;AHA1, activator of heat shock 90kDa protein ATPase homolog 2 AHSA2 NM_152392.1 (yeast),activator of HSP90 ATPase homolog 2 activator of HSP90 ATPase homolog 2, pseudogene APECED;autoimmune regulator (autoimmune polyendocrinopathy candidiasis AIRE NM_000383.2 ectodermal dystrophy) autoimmune regulator AMIGO3 NM_198722.2 adhesion molecule with Ig like domain 3 ANKRD55 NM_024669.2 ankyrin repeat domain 55 ANTXR2 NM_058172.5 anthrax toxin receptor -
Evaluating the Effect of TLR4-Overexpressing on The
Guo et al. J of Biol Res-Thessaloniki (2020) 27:13 https://doi.org/10.1186/s40709-020-00124-3 Journal of Biological Research-Thessaloniki RESEARCH Open Access Evaluating the efect of TLR4-overexpressing on the transcriptome profle in ovine peripheral blood mononuclear cells Xiaofei Guo1†, Jinlong Zhang1,2†, Yao Li2, Jing Yang1, Yihai Li1, Chunxiao Dong1, Guoshi Liu2, Zhengxing Lian2 and Xiaosheng Zhang1* Abstract Background: Toll-like receptor 4 (TLR4) plays an important role in the elimination of Gram-negative bacteria infec- tions and the initiation of antiinfammatory response. Using the technology of pronuclear microinjection, genetically modifed (GM) sheep with TLR4 overexpression were generated. Previous studies have shown that these GM sheep exhibited a higher infammatory response to Gram-negative bacteria infection than wild type (WT) sheep. In order to evaluate the gene expression of GM sheep and study the co-expressed and downstream genes for TLR4, peripheral blood mononuclear cells (PBMC) from TLR4-overexpressing (Tg) and wild type (WT) sheep were selected to discover the transcriptomic diferences using RNA-Seq. Result: An average of 18,754 and 19,530 known genes were identifed in the Tg and WT libraries, respectively. A total of 338 known genes and 85 novel transcripts were found to be diferentially expressed in the two libraries (p < 0.01). A diferentially expressed genes (DEGs) enrichment analysis showed that the GO terms of infammatory response, cell recognition, etc. were signifcantly (FDR < 0.05) enriched. Furthermore, the above DEGs were signifcantly (FDR < 0.05) enriched in the sole KEGG pathway of the Phagosome. Real-time PCR showed the OLR1, TLR4 and CD14 genes to be diferentially expressed in the two groups, which validated the DEGs data. -
Modulation of Cell-Mediated Immunity by HIV-1 Infection of Macrophages
Modulation of cell-mediated immunity by HIV-1 infection of macrophages Lucy Caitríona Kiernan Bell Division of Infection and Immunity University College London PhD Supervisor: Dr Mahdad Noursadeghi A thesis submitted for the degree of Doctor of Philosophy University College London August 2014 Declaration I, Lucy Caitríona Kiernan Bell, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis. 2 Abstract Cell-mediated immunity (CMI) is central to the host response to intracellular pathogens such as Mycobacterium tuberculosis (Mtb). The function of CMI can be modulated by human immunodeficiency virus (HIV)-1 via its pleiotropic effects on the immune response, including modulation of macrophages, which are parasitized by both HIV-1 and Mtb. HIV-1 infection is associated with increased risk of tuberculosis (TB), and so in this thesis I sought to explore the host/pathogen interactions through which HIV-1 dysregulates CMI, and thus changes the natural history of TB. Using an in vitro model of human monocyte-derived macrophages (MDMs), I characterise a phenotype wherein HIV-1 specifically attenuates production of the immunoregulatory cytokine interleukin (IL)-10 in response to Mtb and other innate immune stimuli. I show that this phenotype requires HIV-1 integration and gene expression, and may result from a function of the HIV-1 accessory proteins. I identify that the phosphoinositide 3-kinase (PI3K) pathway specifically regulates IL-10 production in human MDMs, and thus may be a target for HIV-1 to mediate IL-10 attenuation. -
Critical Role of Oxidized LDL Receptor-1 in Intravascular
www.nature.com/scientificreports OPEN Critical role of oxidized LDL receptor‑1 in intravascular thrombosis in a severe infuenza mouse model Marumi Ohno1, Akemi Kakino2, Toshiki Sekiya1, Naoki Nomura1, Masashi Shingai1, Tatsuya Sawamura2 & Hiroshi Kida1* Although coagulation abnormalities, including microvascular thrombosis, are thought to contribute to tissue injury and single‑ or multiple‑organ dysfunction in severe infuenza, the detailed mechanisms have yet been clarifed. This study evaluated infuenza‑associated abnormal blood coagulation utilizing a severe infuenza mouse model. After infecting C57BL/6 male mice with intranasal applications of 500 plaque‑forming units of infuenza virus A/Puerto Rico/8/34 (H1N1; PR8), an elevated serum level of prothrombin fragment 1 + 2, an indicator for activated thrombin generation, was observed. Also, an increased gene expression of oxidized low‑density lipoprotein (LDL) receptor‑1 (Olr1), a key molecule in endothelial dysfunction in the progression of atherosclerosis, was detected in the aorta of infected mice. Body weight decrease, serum levels of cytokines and chemokines, viral load, and infammation in the lungs of infected animals were similar between wild‑type and Olr1 knockout (KO) mice. In contrast, the elevation of prothrombin fragment 1 + 2 levels in the sera and intravascular thrombosis in the lungs by PR8 virus infection were not induced in KO mice. Collectively, the results indicated that OLR1 is a critical host factor in intravascular thrombosis as a pathogeny of severe infuenza. Thus, OLR1 is a promising novel therapeutic target for thrombosis during severe infuenza. Infuenza is a respiratory disease and remains a major health concern, causing approximately half a million deaths per year globally1. -
Review of Lambda Interferons in Hepatitis B Virus Infection: Outcomes and Therapeutic Strategies
viruses Review Review of Lambda Interferons in Hepatitis B Virus Infection: Outcomes and Therapeutic Strategies Laura A. Novotny 1 , John Grayson Evans 1, Lishan Su 2, Haitao Guo 3 and Eric G. Meissner 1,4,* 1 Division of Infectious Diseases, Medical University of South Carolina, Charleston, SC 29525, USA; [email protected] (L.A.N.); [email protected] (J.G.E.) 2 Division of Virology, Pathogenesis, and Cancer, Institute of Human Virology, Departments of Pharmacology, Microbiology, and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, USA; [email protected] 3 Department of Microbiology and Molecular Genetics, Cancer Virology Program, UPMC Hillman Cancer Center, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA; [email protected] 4 Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29425, USA * Correspondence: [email protected]; Tel.: +1-843-792-4541 Abstract: Hepatitis B virus (HBV) chronically infects over 250 million people worldwide and causes nearly 1 million deaths per year due to cirrhosis and liver cancer. Approved treatments for chronic infection include injectable type-I interferons and nucleos(t)ide reverse transcriptase inhibitors. A small minority of patients achieve seroclearance after treatment with type-I interferons, defined as sustained absence of detectable HBV DNA and surface antigen (HBsAg) antigenemia. However, type-I interferons cause significant side effects, are costly, must be administered for months, and most patients have viral rebound or non-response. Nucleos(t)ide reverse transcriptase inhibitors reduce HBV viral load and improve liver-related outcomes, but do not lower HBsAg levels or impart Citation: Novotny, L.A.; Evans, J.G.; seroclearance. -
TDP43 Exacerbates Atherosclerosis Progression by Promoting Inflammation and Lipid Uptake of Macrophages
fcell-09-687169 July 2, 2021 Time: 12:55 # 1 ORIGINAL RESEARCH published: 05 July 2021 doi: 10.3389/fcell.2021.687169 TDP43 Exacerbates Atherosclerosis Progression by Promoting Inflammation and Lipid Uptake of Macrophages Ning Huangfu, Yong Wang, Zhenyu Xu, Wenyuan Zheng, Chunlan Tao, Zhenwei Li, Yewen Hu and Xiaomin Chen* Department of Cardiology, Ningbo First Hospital, Ningbo, China Objective: Atherosclerosis (AS), characterized by cholesterol overloaded-macrophages accumulation and plaque formation in blood vessels, is the major cause of cardiovascular disease. Transactive response DNA-binding protein∼43 kDa (TDP43) has recently been identified as an independent driver of neurodegenerative diseases Edited by: through triggering inflammatory response. This study investigated whether TDP43 is Yuxain Shen, involved in AS development, especially in macrophages-mediated-foam cell formation Anhui Medical University, China and inflammatory responses. Reviewed by: Juntang Shao, Methods: Transactive response DNA-binding protein∼43 kDa expressions in Anhui Medical University, China Heiko Lemcke, oxidized low-density lipoprotein (oxLDL)-treated macrophages and peripheral blood University Medical Center Rostock, mononuclear cells (PBMCs) from patients with coronary artery disease (CAD) were Germany detected by real time-polymerase chain reaction (RT-PCR), Western blot, and *Correspondence: immunofluorescence. Gene gain or loss of function was used to investigate the effects Xiaomin Chen [email protected] of TDP43 on macrophages-mediated lipid untake and inflammation with ELISA, protein immunoprecipitation, RT-PCR, Western blot, and immunofluorescence. Macrophage Specialty section: TDP43 specific knockout mice with ApoE−=− background were fed with western This article was submitted to Signaling, diet for 12 weeks to establish AS model, and used to explore the role of TDP43 a section of the journal on AS progression.