RT² Profiler PCR Array (Rotor-Gene® Format) Human Lipoprotein Signaling & Cholesterol Metabolism
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
The Expression of the Human Apolipoprotein Genes and Their Regulation by Ppars
CORE Metadata, citation and similar papers at core.ac.uk Provided by UEF Electronic Publications The expression of the human apolipoprotein genes and their regulation by PPARs Juuso Uski M.Sc. Thesis Biochemistry Department of Biosciences University of Kuopio June 2008 Abstract The expression of the human apolipoprotein genes and their regulation by PPARs. UNIVERSITY OF KUOPIO, the Faculty of Natural and Environmental Sciences, Curriculum of Biochemistry USKI Juuso Oskari Thesis for Master of Science degree Supervisors Prof. Carsten Carlberg, Ph.D. Merja Heinäniemi, Ph.D. June 2008 Keywords: nuclear receptors; peroxisome proliferator-activated receptor; PPAR response element; apolipoprotein; lipid metabolism; high density lipoprotein; low density lipoprotein. Lipids are any fat-soluble, naturally-occurring molecules and one of their main biological functions is energy storage. Lipoproteins carry hydrophobic lipids in the water and salt-based blood environment for processing and energy supply in liver and other organs. In this study, the genomic area around the apolipoprotein genes was scanned in silico for PPAR response elements (PPREs) using the in vitro data-based computer program. Several new putative REs were found in surroundings of multiple lipoprotein genes. The responsiveness of those apolipoprotein genes to the PPAR ligands GW501516, rosiglitazone and GW7647 in the HepG2, HEK293 and THP-1 cell lines were tested with real-time PCR. The APOA1, APOA2, APOB, APOD, APOE, APOF, APOL1, APOL3, APOL5 and APOL6 genes were found to be regulated by PPARs in direct or secondary manners. Those results provide new insights in the understanding of lipid metabolism and so many lifestyle diseases like atherosclerosis, type 2 diabetes, heart disease and stroke. -
Proteomic Analysis of HDL from Inbred Mouse Strains Implicates APOE Associated with HDL in Reduced Cholesterol Effl Ux Capacity Via the ABCA1 Pathway
Supplemental Material can be found at: http://www.jlr.org/content/suppl/2015/12/15/jlr.M063701.DC1 .html ˔ Author’s Choice Proteomic analysis of HDL from inbred mouse strains implicates APOE associated with HDL in reduced cholesterol effl ux capacity via the ABCA1 pathway Nathalie Pamir , 1, * Patrick Hutchins , * Graziella Ronsein , * Tomas Vaisar , * Catherine A. Reardon , † Godfrey S. Getz , † Aldons J. Lusis , § and Jay W. Heinecke * Downloaded from Department of Medicine,* University of Washington , Seattle, WA ; Department of Pathology, † University of Chicago , Chicago, IL ; and Department of Genetics, § University of California at Los Angeles , Los Angeles, CA Abstract Cholesterol effl ux capacity associates strongly Supplementary key words atherosclerosis • cardiovascular risk • mass and negatively with the incidence and prevalence of human spectrometry • high density lipoprotein • apolipoprotein E • ATP bind- CVD. We investigated the relationships of HDL’s size and ing cassette transporter A1 www.jlr.org protein cargo with its cholesterol effl ux capacity using APOB-depleted serum and HDLs isolated from fi ve inbred mouse strains with different susceptibilities to atherosclero- Clinical and epidemiological studies show a robust at Univ of Washington Health Sciences Library SB-55, on February 5, 2016 sis. Like humans, mouse HDL carried >70 proteins linked to inverse association of HDL-cholesterol (HDL-C) levels lipid metabolism, the acute-phase response, proteinase inhi- with CVD risk ( 1 ). In randomized clinical trials, how- bition, and the immune system. HDL’s content of specifi c ever, two drugs, CETP inhibitors and niacin, that elevate proteins strongly correlated with its size and cholesterol ef- fl ux capacity, suggesting that its protein cargo regulates its HDL-C levels by different mechanisms, failed to reduce function. -
Biomolecules
biomolecules Review High-Density Lipoproteins Are Bug Scavengers Olivier Meilhac 1,2,*, Sébastien Tanaka 1,3 and David Couret 1,4 1 Université de la Réunion, Inserm, UMR 1188 Diabète athérothrombose Thérapies Réunion Océan Indien (DéTROI), F-97490 Sainte-Clotilde, France; [email protected] (S.T.); [email protected] (D.C.) 2 CHU de La Réunion, Centre d’Investigations Clinique 1410, 97410 Saint-Pierre, France 3 AP-HP, Service d’Anesthésie-Réanimation, CHU Bichat-Claude Bernard, 75018 Paris, France 4 CHU de La Réunion, Neurocritical Care Unit, 97410 Saint-Pierre, France * Correspondence: [email protected]; Tel.: +33-262-93-88-11 Received: 7 March 2020; Accepted: 6 April 2020; Published: 12 April 2020 Abstract: Lipoproteins were initially defined according to their composition (lipids and proteins) and classified according to their density (from very low- to high-density lipoproteins—HDLs). Whereas their capacity to transport hydrophobic lipids in a hydrophilic environment (plasma) is not questionable, their primitive function of cholesterol transporter could be challenged. All lipoproteins are reported to bind and potentially neutralize bacterial lipopolysaccharides (LPS); this is particularly true for HDL particles. In addition, HDL levels are drastically decreased under infectious conditions such as sepsis, suggesting a potential role in the clearance of bacterial material and, particularly, LPS. Moreover, “omics” technologies have unveiled significant changes in HDL composition in different inflammatory states, ranging from acute inflammation occurring during septic shock to low-grade inflammation associated with moderate endotoxemia such as periodontal disease or obesity. In this review, we will discuss HDL modifications associated with exposure to pathogens including bacteria, viruses and parasites, with a special focus on sepsis and the potential of HDL therapy in this context. -
Cholesterol in the Pathogenesis of Alzheimer's
REVIEWS Cholesterol in the Pathogenesis of Alzheimer’s, Parkinson’s Diseases and Autism: Link to Synaptic Dysfunction A. M. Petrov*, M. R. Kasimov, A. L. Zefirov Kazan State Medical University, Normal Physiology department, Butlerova str. 49, Kazan, 420012, Russia *E-mail: [email protected] Received April 22, 2016; in final form, November 28, 2016 Copyright © 2017 Park-media, Ltd. This is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT In our previous review, we described brain cholesterol metabolism in control conditions and in the case of some rare neurological pathologies linked to defects in the genes which are directly involved in the syn- thesis and/or traffic of cholesterol. Here, we have analyzed disruptions in cholesterol homeostasis in widespread neurodegenerative diseases (Alzheimer’s and Parkinson’s diseases) and autism spectrum disorders. We particu- larly focused on the synaptic dysfunctions that could arise from changes in both membrane cholesterol availa- bility and oxysterol production. Notably, alterations in the brain cholesterol metabolism and neurotransmission occur in the early stages of these pathologies and the polymorphism of the genes associated with cholesterol homeostasis and synaptic communication affects the risk of onset and severity of these diseases. In addition, pharmacological and genetic manipulations of brain cholesterol homeostasis in animal models frequently have marked effects on the progression of neurodegenerative diseases. Thus, the development of Alzheimer’s, Parkin- son’s and autism spectrum disorders may be partially associated with an imbalance of cholesterol homeostasis that leads to changes in the membrane cholesterol and oxysterol levels that, in turn, modulates key steps in the synaptic transmission. -
Association Between the APOA2 Rs3813627 Single Nucleotide Polymorphism and HDL and APOA1 Levels Through BMI
biomedicines Article Association between the APOA2 rs3813627 Single Nucleotide Polymorphism and HDL and APOA1 Levels Through BMI Hatim Boughanem 1 , Borja Bandera-Merchán 2, Pablo Hernández-Alonso 2,3,4 , Noelia Moreno-Morales 5, Francisco José Tinahones 2,3, José Lozano 6 , Sonsoles Morcillo 2,3,* and Manuel Macias-Gonzalez 2,3,* 1 Instituto de Investigación Biomédica de Málaga (IBIMA), Facultad de Ciencias, Universidad de Málaga, 29010 Málaga, Spain; [email protected] 2 Unidad de Gestión Clínica de Endocrinología y Nutrición del Hospital Virgen de la Victoria, Instituto de Investigación Biomédica de Málaga (IBIMA), Universidad de Málaga, 29010 Málaga, Spain; [email protected] (B.B.-M.); [email protected] (P.H.-A.); [email protected] (F.J.T.) 3 Centro de Investigación Biomédica en Red de Fisiopatología de la Obesidad y la Nutrición, CIBERObn, 28029 Madrid, Spain 4 Human Nutrition Unit, Faculty of Medicine and Health Sciences, Sant Joan Hospital, Institut d’Investigació Sanitària Pere Virgili, Rovira i Virgili University, 43201 Reus, Spain 5 Department of Physiotherapy, School of Health Sciences, University of Malaga-Instituto de Investigación Biomédica de Málaga (IBIMA), 29010 Málaga, Spain; [email protected] 6 Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias, Universidad de Málaga, 29010 Málaga, Spain; [email protected] * Correspondence: [email protected] (S.M.); [email protected] (M.M.-G.); Tel.: +34-951-032-648 (S.M. & M.M.-G.); Fax: +34-27-951-924-651 (S.M. & M.M.-G.) Received: 18 February 2020; Accepted: 25 February 2020; Published: 27 February 2020 Abstract: Background: The interaction between obesity and genetic traits on high density lipoprotein (HDL) levels has been extensively studied. -
Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the filtration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green fluorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in -
Downloaded Separately for CEU (Individuals of Western and Northern European Origin) and YRI (Yoruba in Nigeria) from Hapmap Phase 2
NIH Public Access Author Manuscript Int J Obes (Lond). Author manuscript; available in PMC 2013 September 11. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Int J Obes (Lond). 2013 September ; 37(9): 1211–1220. doi:10.1038/ijo.2012.215. Lipoprotein receptor-related protein 1 variants and dietary fatty acids: meta-analysis of European origin and African American studies CE Smith1, J Ngwa2, T Tanaka3, Q Qi4, MK Wojczynski5, RN Lemaitre6, JS Anderson7, A Manichaikul8, V Mikkilä9, FJA van Rooij10,11, Z Ye12, S Bandinelli13, AC Frazier-Wood14, DK Houston15, F Hu4,16, C Langenberg12, NM McKeown1, D Mozaffarian17,18, KE North19, J Viikari20, MC Zillikens11,21, L Djoussé22, A Hofman10,11, M Kähönen23, EK Kabagambe14, RJF Loos12, GB Saylor7, NG Forouhi12, Y Liu24, KJ Mukamal25, Y-DI Chen26, MY Tsai27, AG Uitterlinden10,11,21, O Raitakari28, CM van Duijn10,11, DK Arnett14, IB Borecki5, LA Cupples2,29, L Ferrucci3, SB Kritchevsky15, T Lehtimäki30, Lu Qi4,16, JI Rotter26, DS Siscovick31, NJ Wareham12, JCM Witteman10,11, JM Ordovás1,32,33, and JA Nettleton34 1Nutrition and Genomics Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA, USA 2Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA 3Clinical Research Branch, National Institute on Aging, Baltimore, MD, USA 4Department of Nutrition, Harvard School of Public Health, Boston, MA, USA 5Department of Genetics, Washington University School of Medicine, St. -
Megalin, an Endocytotic Receptor with Signalling Potential
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 116 Megalin, an Endocytotic Receptor with Signalling Potential MÅRTEN LARSSON ACTA UNIVERSITATIS UPSALIENSIS ISSN 1651-6206 UPPSALA ISBN 91-554-6483-1 2006 urn:nbn:se:uu:diva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o Dr. John Pemberton List of original papers This thesis is based on the following -
UC San Diego UC San Diego Electronic Theses and Dissertations
UC San Diego UC San Diego Electronic Theses and Dissertations Title Insights from reconstructing cellular networks in transcription, stress, and cancer Permalink https://escholarship.org/uc/item/6s97497m Authors Ke, Eugene Yunghung Ke, Eugene Yunghung Publication Date 2012 Peer reviewed|Thesis/dissertation eScholarship.org Powered by the California Digital Library University of California UNIVERSITY OF CALIFORNIA, SAN DIEGO Insights from Reconstructing Cellular Networks in Transcription, Stress, and Cancer A dissertation submitted in the partial satisfaction of the requirements for the degree Doctor of Philosophy in Bioinformatics and Systems Biology by Eugene Yunghung Ke Committee in charge: Professor Shankar Subramaniam, Chair Professor Inder Verma, Co-Chair Professor Web Cavenee Professor Alexander Hoffmann Professor Bing Ren 2012 The Dissertation of Eugene Yunghung Ke is approved, and it is acceptable in quality and form for the publication on microfilm and electronically ________________________________________________________________ ________________________________________________________________ ________________________________________________________________ ________________________________________________________________ Co-Chair ________________________________________________________________ Chair University of California, San Diego 2012 iii DEDICATION To my parents, Victor and Tai-Lee Ke iv EPIGRAPH [T]here are known knowns; there are things we know we know. We also know there are known unknowns; that is to say we know there -
Common Genetic Variations Involved in the Inter-Individual Variability Of
nutrients Review Common Genetic Variations Involved in the Inter-Individual Variability of Circulating Cholesterol Concentrations in Response to Diets: A Narrative Review of Recent Evidence Mohammad M. H. Abdullah 1 , Itzel Vazquez-Vidal 2, David J. Baer 3, James D. House 4 , Peter J. H. Jones 5 and Charles Desmarchelier 6,* 1 Department of Food Science and Nutrition, Kuwait University, Kuwait City 10002, Kuwait; [email protected] 2 Richardson Centre for Functional Foods & Nutraceuticals, University of Manitoba, Winnipeg, MB R3T 6C5, Canada; [email protected] 3 United States Department of Agriculture, Agricultural Research Service, Beltsville, MD 20705, USA; [email protected] 4 Department of Food and Human Nutritional Sciences, University of Manitoba, Winnipeg, MB R3T 2N2, Canada; [email protected] 5 Nutritional Fundamentals for Health, Vaudreuil-Dorion, QC J7V 5V5, Canada; [email protected] 6 Aix Marseille University, INRAE, INSERM, C2VN, 13005 Marseille, France * Correspondence: [email protected] Abstract: The number of nutrigenetic studies dedicated to the identification of single nucleotide Citation: Abdullah, M.M.H.; polymorphisms (SNPs) modulating blood lipid profiles in response to dietary interventions has Vazquez-Vidal, I.; Baer, D.J.; House, increased considerably over the last decade. However, the robustness of the evidence-based sci- J.D.; Jones, P.J.H.; Desmarchelier, C. ence supporting the area remains to be evaluated. The objective of this review was to present Common Genetic Variations Involved recent findings concerning the effects of interactions between SNPs in genes involved in cholesterol in the Inter-Individual Variability of metabolism and transport, and dietary intakes or interventions on circulating cholesterol concen- Circulating Cholesterol trations, which are causally involved in cardiovascular diseases and established biomarkers of Concentrations in Response to Diets: cardiovascular health. -
Prdc Cdna Insert Product Line
mLRP-10 VersaClone cDNA Catalog Number: RDC1306 Specifications: Description This shuttle vector contains the complete ORF for the gene of interest, Gene: mLrp10 along with a Kozak consensus sequence for optimal translation initiation. It is inserted NotI to AscI. The gene insert is flanked with Accession: BAB20775 convenient multiple cloning sites which can be used to easily cut and transfer the gene cassette into your desired expression vector. Insert size: 2155bp Preparation and Storage Concentration: 10µg at 0.2μg/μL Formulation cDNA is provided in 10 mM Tris-Cl, pH 8.5 Shipping Ships at ambient temperature Stability 1 year from date of receipt when stored at -20°C to -80°C Storage Use a manual defrost freezer and avoid repeated mLRP-10 cDNA freeze-thaw cycles. Plasmid Lrp10 low-density lipoprotein receptor-related protein 10 ZraI BmgBI AatII BstAPI HpaI [ Mus musculus (house mouse) ] SspI NdeI HindIII XmnI BamHI EcoRV Also known as: Lrp9 ScaI BmtI StuI NheI NotI EcoNI EagI Summary: BtgI NcoI LRP10 is a member of the low AMP BsmI density lipoprotein (LDL) receptor gene family. LDL receptors are transmembrane cell surface proteins involved in receptor- RDC1306 mediated endocytosis of lipoprotein 4889 bps BsaAI SnaBI and protein ligands. LRP10 is highly Tth111I mLRP10 (1-713) expressed in heart, lung, and liver. COLE1 AvrII LRP10 may be involved in the uptake of lipoprotein APOE in liver. NaeI NgoMIV BtgZI XhoI PciI AarI PspXI SapI BbsI XmaI BglII SmaI ApaI SalI PspOMI XbaI PpuMI Bst1107I Van91I BssHII AscI FOR RESEARCH USE ONLY NOT -
Convergence of Genes Implicated in Alzheimer's Disease on the Cerebral
Neurochemistry International 50 (2007) 12–38 www.elsevier.com/locate/neuint Review Convergence of genes implicated in Alzheimer’s disease on the cerebral cholesterol shuttle: APP, cholesterol, lipoproteins, and atherosclerosis C.J. Carter 176 Downs Road, Hastings, East Sussex TN34 2DZ, UK Received 5 April 2006; received in revised form 30 June 2006; accepted 11 July 2006 Available online 12 September 2006 Abstract Polymorphic genes associated with Alzheimer’s disease (see www.polygenicpathways.co.uk) delineate a clearly defined pathway related to cerebral and peripheral cholesterol and lipoprotein homoeostasis. They include all of the key components of a glia/neurone cholesterol shuttle including cholesterol binding lipoproteins APOA1, APOA4, APOC1, APOC2, APOC3, APOD, APOE and LPA, cholesterol transporters ABCA1, ABCA2, lipoprotein receptors LDLR, LRP1, LRP8 and VLDLR, and the cholesterol metabolising enzymes CYP46A1 and CH25H, whose oxysterol products activate the liver X receptor NR1H2 and are metabolised to esters by SOAT1. LIPA metabolises cholesterol esters, which are transported by the cholesteryl ester transport protein CETP. The transcription factor SREBF1 controls the expression of most enzymes of cholesterol synthesis. APP is involved in this shuttle as it metabolises cholesterol to 7-betahydroxycholesterol, a substrate of SOAT1 and HSD11B1, binds to APOE and is tethered to LRP1 via APPB1, APBB2 and APBB3 at the cytoplasmic domain and via LRPAP1 at the extracellular domain. APP cleavage products are also able to prevent cholesterol binding to APOE. BACE cleaves both APP and LRP1. Gamma-secretase (PSEN1, PSEN2, NCSTN) cleaves LRP1 and LRP8 as well as APP and their degradation products control transcription factor TFCP2, which regulates thymidylate synthase (TS) and GSK3B expression.