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Wolverhampton Intellectual Repository and E-Theses > Research Institutes > Research Institute in Healthcare Science > Food Biology, Medical Microbiology and Disinfection Research Group > Anti-beta2GPI-antibody-induced endothelial cell gene expression profiling reveals induction of novel pro-inflammatory genes potentially involved in primary antiphospholipid syndrome.

Please use this identifier to cite or link to this item: http://hdl.handle.net/2436/29438
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Title: Anti-beta2GPI-antibody-induced endothelial cell gene expression profiling reveals induction of novel pro-inflammatory genes potentially involved in primary antiphospholipid syndrome.
Authors: Hamid, Colleen G.
Norgate, K.
D'Cruz, D.P.
Khamashta, M.A.
Arno, M.
Pearson, J.D.
Frampton, Geoffrey
Murphy, John J.
Citation: Annals of the Rheumatic Diseases, 66 (8): 1000-7
Publisher: BMJ Publishing & European League Against Rheumatism
Journal: Annals of the Rheumatic Diseases
Issue Date: 2007
URI: http://hdl.handle.net/2436/29438
DOI: 10.1136/ard.2006.063909
PubMed ID: 17223652
Additional Links: http://ard.bmj.com/cgi/content/full/66/8/1000
Abstract: OBJECTIVE: To determine the effects of primary antiphospholipid syndrome (PAPS)-derived anti-beta(2)GPI antibodies on gene expression in human umbilical vein endothelial cells (HUVEC) by gene profiling using microarrays. METHODS: Anti-beta(2)GPI antibodies purified from sera of patients with PAPS or control IgG isolated from normal subjects were incubated with HUVEC for 4 h before isolation of RNA and processing for hybridisation to Affymetrix Human Genome U133A-2.0 arrays. Data were analysed using a combination of the MAS 5.0 (Affymetrix) and GeneSpring (Agilent) software programmes. For selected genes microarray data were confirmed by real-time PCR analysis or at the protein level by ELISA. RESULTS: A total of 101 genes were found to be upregulated and 14 genes were downregulated twofold or more in response to anti-beta(2)GPI antibodies. A number of novel genes not previously associated with APS were induced, including chemokines CCL20, CXCL3, CX3CL1, CXCL5, CXCL2 and CXCL1, the receptors Tenascin C, OLR1, IL-18 receptor 1, and growth factors CSF2, CSF3 IL-6, IL1beta and FGF18. The majority of downregulated genes were transcription factors/signalling molecules including ID2. Quantitative real-time RT-PCR analysis confirmed the microarray results for selected genes (CSF3, CX3CL1, FGF18, ID2, SOD2, Tenascin C). CONCLUSIONS: This study reveals a complex gene expression response in HUVEC to anti-beta(2)GPI antibodies with multiple chemokines, pro-inflammatory cytokines, pro-thrombotic and pro-adhesive genes regulated by these antibodies in vitro. Some of these newly identified anti-beta(2)GPI antibody-regulated genes could contribute to the vasculopathy associated with this disease.
Type: Article
Language: en
MeSH: Adult
Antigen-Antibody Reactions
Antiphospholipid Syndrome
Autoantibodies
Case-Control Studies
Down-Regulation
E-Selectin
Endothelial Cells
Female
Gene Expression Profiling
Humans
Immunoglobulin G
Interleukin-8
Middle Aged
Oligonucleotide Array Sequence Analysis
beta 2-Glycoprotein I
ISSN: 0003-4967
Appears in Collections: Food Biology, Medical Microbiology and Disinfection Research Group

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