New candidate genes for ST-elevation myocardial infarction.
ATP Binding Cassette Transporter, Subfamily G, Member 1
/ genetics
Activin Receptors, Type I
/ genetics
Carotid Stenosis
/ metabolism
Carrier Proteins
/ genetics
Down-Regulation
Female
Gene Expression Profiling
Humans
Male
Membrane Proteins
/ genetics
Microtubule-Associated Proteins
/ genetics
Middle Aged
Nerve Tissue Proteins
/ genetics
Nuclear Proteins
/ genetics
RNA
/ metabolism
ST Elevation Myocardial Infarction
/ genetics
Up-Regulation
rab GTP-Binding Proteins
/ genetics
acute myocardial infarction
atherothrombosis
cardiovascular clinical research
plaque rupture
Journal
Journal of internal medicine
ISSN: 1365-2796
Titre abrégé: J Intern Med
Pays: England
ID NLM: 8904841
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
pubmed:
8
10
2019
medline:
18
8
2020
entrez:
8
10
2019
Statut:
ppublish
Résumé
Despite extensive research in atherosclerosis, the mechanisms of coronary atherothrombosis in ST-elevation myocardial infarction (STEMI) patients are undetermined. Our aim was to find candidate genes involved in STEMI by analysing leucocyte gene expression in STEMI patients, without the influence of secondary inflammation from innate immunity, which was assumed to be a consequence rather than the cause of coronary atherothrombosis. Fifty-one patients were included at coronary angiography because of STEMI. Arterial blood was sampled in the acute phase (P1), at 24-48 h (P2) and at 3 months (P3). Leucocyte RNA was isolated and gene expression analysis was performed by Affymetrix Human Transcriptome Array 2.0. By omission of up- or downregulated genes at P2, secondary changes from innate immunity were excluded. Genes differentially expressed in P1 when compared to the convalescent sample in P3 were determined as genes involved in STEMI. Three genes were upregulated at P1 compared to P3; ABCG1 (P = 5.81 × 10 We found seven genes involved in STEMI. The study is unique regarding the blood sampling in the acute phase and omission of secondary expressed genes from innate immunity. However, the results need to be replicated by future studies.
Sections du résumé
BACKGROUND
Despite extensive research in atherosclerosis, the mechanisms of coronary atherothrombosis in ST-elevation myocardial infarction (STEMI) patients are undetermined.
OBJECTIVES
Our aim was to find candidate genes involved in STEMI by analysing leucocyte gene expression in STEMI patients, without the influence of secondary inflammation from innate immunity, which was assumed to be a consequence rather than the cause of coronary atherothrombosis.
METHODS
Fifty-one patients were included at coronary angiography because of STEMI. Arterial blood was sampled in the acute phase (P1), at 24-48 h (P2) and at 3 months (P3). Leucocyte RNA was isolated and gene expression analysis was performed by Affymetrix Human Transcriptome Array 2.0. By omission of up- or downregulated genes at P2, secondary changes from innate immunity were excluded. Genes differentially expressed in P1 when compared to the convalescent sample in P3 were determined as genes involved in STEMI.
RESULTS
Three genes were upregulated at P1 compared to P3; ABCG1 (P = 5.81 × 10
CONCLUSIONS
We found seven genes involved in STEMI. The study is unique regarding the blood sampling in the acute phase and omission of secondary expressed genes from innate immunity. However, the results need to be replicated by future studies.
Substances chimiques
ABCG1 protein, human
0
ATP Binding Cassette Transporter, Subfamily G, Member 1
0
CEMIP2 protein, human
0
Carrier Proteins
0
Membrane Proteins
0
Microtubule-Associated Proteins
0
NFATC2IP protein, human
0
Nerve Tissue Proteins
0
Nuclear Proteins
0
SUN1 protein, human
0
TTC9 protein, human
0
RNA
63231-63-0
ACVR1 protein, human
EC 2.7.11.30
Activin Receptors, Type I
EC 2.7.11.30
Rab20 protein, human
EC 3.6.1-
rab GTP-Binding Proteins
EC 3.6.5.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
66-77Informations de copyright
© 2019 The Association for the Publication of the Journal of Internal Medicine.
Références
Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 2002; 360: 7-22.
Cannon CP, Braunwald E, McCabe CH et al. Intensive versus Moderate Lipid Lowering with Statins after Acute Coronary Syndromes. N Engl J Med 2004; 350: 1495-504.
LaRosa JC, Grundy SM, Waters DD et al. Intensive Lipid Lowering with Atorvastatin in Patients with Stable Coronary Disease. N Engl J Med 2005; 352: 1425-35.
Ridker PM, Everett BM, Thuren T et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med 2017; 377: 1119-31.
Iannaccone M, Quadri G, Taha S et al. Prevalence and predictors of culprit plaque rupture at OCT in patients with coronary artery disease: a meta-analysis. Eur Heart J - Cardiovasc Imaging 2016; 17: 1128-37.
Brasier AR. The nuclear factor-κB-interleukin-6 signalling pathway mediating vascular inflammation. Cardiovasc Res 2010; 86: 211-8.
Valen G, Yan Z-q, Hansson GK. Nuclear factor kappa-B and the heart. J Am Coll Cardiol 2001; 38: 307-14.
Kiliszek M, Burzynska B, Michalak M et al. Altered gene expression pattern in peripheral blood mononuclear cells in patients with acute myocardial infarction. PLoS ONE 2012; 7: e50054.
Members ATF, Reviewers D, Guidelines ECfP et al. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. Eur Heart J 2008; 29: 2909-45.
Irizarry RA, Hobbs B, Collin F et al. Exploration, normalization, and summaries of high density oligonucleotide array probe level data. Biostatistics (Oxford, England) 2003; 4: 249-64.
Folkersen L, Persson J, Ekstrand J et al. Prediction of ischemic events on the basis of transcriptomic and genomic profiling in patients undergoing carotid endarterectomy. Mol Med (Cambridge, Mass) 2012; 18: 669-75.
Razuvaev A, Ekstrand J, Folkersen L et al. Correlations between clinical variables and gene-expression profiles in carotid plaque instability. Eur J Vasc Endovasc Surg 2011; 42: 722-30.
Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovasc Res 2002; 53: 31-47.
Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. New England J Med 2005; 352: 1685-95.
Ruparelia N, Godec J, Lee R et al. Acute myocardial infarction activates distinct inflammation and proliferation pathways in circulating monocytes, prior to recruitment, and identified through conserved transcriptional responses in mice and humans. Eur Heart J 2015; 36: 1923-34.
Li AC, Binder CJ, Gutierrez A et al. Differential inhibition of macrophage foam-cell formation and atherosclerosis in mice by PPARα, β/δ, and γ. J Clin Invest 2004; 114: 1564-76.
Hardy LM, Frisdal E, Le Goff W. Critical role of the human ATP-binding cassette G1 transporter in cardiometabolic diseases. Int J Mol Sci 2017; 18: 1892.
Fielding CJ, Fielding PE. Cellular cholesterol efflux. Biochem Biophys Acta 2001; 1533: 175-89.
Anastasius M, Kockx M, Jessup W, Sullivan D, Rye K-A, Kritharides L. Cholesterol efflux capacity: An introduction for clinicians. Am Heart J 2016; 180: 54-63.
Meurs I, Lammers B, Zhao Y et al. The effect of ABCG1 deficiency on atherosclerotic lesion development in LDL receptor knockout mice depends on the stage of atherogenesis. Atherosclerosis 2012; 221: 41-7.
Münch G, Bültmann A, Li Z et al. Overexpression of ABCG1 protein attenuates arteriosclerosis and endothelial dysfunction in atherosclerotic rabbits. Heart Int 2012; 7: e12.
Wang N, Silver DL, Costet P, Tall AR. Specific binding of ApoA-I, enhanced cholesterol efflux, and altered plasma membrane morphology in cells expressing ABC1. J Biol Chem 2000; 275: 33053-8.
Yvan-Charvet L, Ranalletta M, Wang N et al. Combined deficiency of ABCA1 and ABCG1 promotes foam cell accumulation and accelerates atherosclerosis in mice. J Clin Invest 2007; 117: 3900-8.
Sivapalaratnam S, Basart H, Watkins NA et al. Monocyte gene expression signature of patients with early onset coronary artery disease. PLoS ONE 2012; 7: e32166.
Schou J, Frikke-Schmidt R, Kardassis D et al. Genetic variation in ABCG1 and risk of myocardial infarction and ischemic heart disease. Arterioscler Thromb Vasc Biol 2012; 32: 506-15.
Xu Y, Wang W, Zhang L et al. A polymorphism in the ABCG1 promoter is functionally associated with coronary artery disease in a Chinese Han population. Atherosclerosis 2011; 219: 648-54.
Rouillard AD, Gundersen GW, Fernandez NF et al. The harmonizome: a collection of processed datasets gathered to serve and mine knowledge about genes and proteins. Database: J Biol Databases Curation 2016; 2016: baw100.
Wennerberg K, Rossman KL, Der CJ. The Ras superfamily at a glance. J Cell Sci 2005; 118: 843-6.
Zerial M, McBride H. Rab proteins as membrane organizers. Nat Rev Mol Cell Biol 2001; 2: 107-17.
Prashar A, Schnettger L, Bernard EM, Gutierrez MG. Rab GTPases in Immunity and Inflammation. Front Cell Infect Microbiol 2017; 7: 435.
Lopez de Armentia MM, Amaya C, Colombo MI. Rab GTPases and the autophagy pathway: bacterial targets for a suitable biogenesis and trafficking of their own vacuoles. Cells 2016; 5: 11.
Schnettger L, Rodgers A, Repnik U et al. A Rab20-dependent membrane trafficking pathway controls M. tuberculosis replication by regulating phagosome spaciousness and integrity. Cell Host Microbe 2017; 21: 619-28.e5.
Gustafsson ÅB, Gottlieb RA. Autophagy in Ischemic heart disease. Circ Res 2009; 104: 150-8.
Valentim L, Laurence KM, Townsend PA et al. Urocortin inhibits Beclin1-mediated autophagic cell death in cardiac myocytes exposed to ischaemia/reperfusion injury. J Mol Cell Cardiol 2006; 40: 846-52.
Yamaguchi Y, Yamamoto H, Tobisawa Y, Irie F. TMEM2: A missing link in hyaluronan catabolism identified? Matrix Biol 2018;78-79:139-46.
Totong R, Schell T, Lescroart F et al. The novel transmembrane protein Tmem2 is essential for coordination of myocardial and endocardial morphogenesis. Development (Cambridge, England) 2011; 138: 4199-205.
Yao Y, Shao ES, Jumabay M, Shahbazian A, Ji S, Bostrom KI. High-density lipoproteins affect endothelial BMP-signaling by modulating expression of the activin-like kinase receptor 1 and 2. Arterioscler Thromb Vasc Biol 2008; 28: 2266-74.
van Dinther M, Visser N, de Gorter DJ et al. ALK2 R206H mutation linked to fibrodysplasia ossificans progressiva confers constitutive activity to the BMP type I receptor and sensitizes mesenchymal cells to BMP-induced osteoblast differentiation and bone formation. J Bone Miner Res 2010; 25: 1208-15.
Wahl S, Drong A, Lehne B et al. Epigenome-wide association study of body mass index, and the adverse outcomes of adiposity. Nature 2017; 541: 81-6.
Sun D, Heianza Y, Li X et al. Genetic, epigenetic and transcriptional variations at NFATC2IP locus with weight loss in response to diet interventions: The POUNDS Lost Trial. Diabetes Obes Metab 2018; 20: 2298-303.
Lu W, Gotzmann J, Sironi L et al. Sun1 forms immobile macromolecular assemblies at the nuclear envelope. Biochem Biophys Acta 2008; 1783: 2415-26.
Luo X, Yang W, Gao G. SUN1 regulates HIV-1 nuclear import in a manner dependent on the interaction between the viral capsid and cellular cyclophilin A. J Virol 2018;92:e00229-18.
Xu Y, Cao J, Huang S et al. Characterization of tetratricopeptide repeat-containing proteins critical for cilia formation and function. PLoS ONE 2015; 10: e0124378.
Sinnaeve PR, Donahue MP, Grass P et al. Gene expression patterns in peripheral blood correlate with the extent of coronary artery disease. PLoS ONE 2009;4:e7037-e.
Reilly SJ, Odeberg J, Tornvall P. Use of the whole leucocyte population in the study of the NFkappaB pathway. Scand J Immunol 2011; 73: 338-43.
Wong J, Quinn CM, Gelissen IC, Jessup W, Brown AJ. The effect of statins on ABCA1 and ABCG1 expression in human macrophages is influenced by cellular cholesterol levels and extent of differentiation. Atherosclerosis 2008; 196: 180-9.