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      CRP-level-associated polymorphism rs1205 within the CRP gene is associated with 2-hour glucose level: The SAPPHIRe study

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          Abstract

          C-reactive protein (CRP) encoded by CRP gene is a reflection of systemic inflammation. Many studies associated CRP level with diabetes and glucose levels, but the association of CRP gene with these traits is unclear. We conducted a cross-sectional study consisting of 945 siblings from 330 families collected by the Stanford Asian Pacific Program in Hypertension and Insulin Resistance (SAPPHIRe) to investigate associations between CRP polymorphisms, circulating CRP, diabetes, and glucose levels. Five single-nucleotide polymorphisms were analyzed: rs3093059, rs2794521, rs1417938, rs1800947, and rs1205. The generalized estimating equation approach was used to deal with correlated data within families. CRP level was positively correlated with diabetes prevalence and levels of fasting and 2-hour glucose (each P < 0.008). Alleles C at rs3093059 and G at rs1205 were associated with elevated CRP level (each P < 1.2 × 10 −6). Allele C at rs3093059 was associated with fasting glucose ( β = 0.20, P = 0.045) and G at rs1205 was associated with 2-hour glucose ( β = 0.46, P = 0.00090) post oral glucose tolerance test, but only the latter passed Bonferroni correction. No polymorphism was associated with diabetes. Since 2-hour glucose is an indicator of glucose tolerance, this study indicated CRP gene is associated with glucose intolerance.

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          Direct proinflammatory effect of C-reactive protein on human endothelial cells.

          The acute-phase reactant C-reactive protein (CRP) is an important risk factor for coronary heart disease. However, the possible effects of CRP on vascular cells are not known. We tested the effects of CRP on expression of adhesion molecules in both human umbilical vein and coronary artery endothelial cells. Expression of vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM-1), and E-selectin was assessed by flow cytometry. Incubation with recombinant human CRP (10 microg/mL) for 24 hours induced an approximately 10-fold increase in expression of ICAM-1 and a significant expression of VCAM-1, whereas a 6-hour incubation induced significant E-selectin expression. Adhesion molecule induction was similar to that observed in endothelial cells activated with interleukin-1beta. In coronary artery endothelial cells, induction of ICAM-1 and VCAM-1 was already present at 5 microg/mL and reached a maximum at 50 microg/mL, at which point a substantial increase in expression of E-selectin was also evident. The CRP effect was dependent on presence of human serum in the culture medium, because no effect was seen in cells cultured with serum-free medium. In contrast, interleukin-1beta was able to induce adhesion molecule expression in the absence of human serum. CRP induces adhesion molecule expression in human endothelial cells in the presence of serum. These findings support the hypothesis that CRP may play a direct role in promoting the inflammatory component of atherosclerosis and present a potential target for the treatment of atherosclerosis.
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            Genetically elevated C-reactive protein and ischemic vascular disease.

            Elevated levels of C-reactive protein (CRP) are associated with increased risks of ischemic heart disease and ischemic cerebrovascular disease. We tested whether this is a causal association. We studied 10,276 persons from a general population cohort, including 1786 in whom ischemic heart disease developed and 741 in whom ischemic cerebrovascular disease developed. We examined another 31,992 persons from a cross-sectional general population study, of whom 2521 had ischemic heart disease and 1483 had ischemic cerebrovascular disease. Finally, we compared 2238 patients with ischemic heart disease with 4474 control subjects and 612 patients with ischemic cerebrovascular disease with 1224 control subjects. We measured levels of high-sensitivity CRP and conducted genotyping for four CRP polymorphisms and two apolipoprotein E polymorphisms. The risk of ischemic heart disease and ischemic cerebrovascular disease was increased by a factor of 1.6 and 1.3, respectively, in persons who had CRP levels above 3 mg per liter, as compared with persons who had CRP levels below 1 mg per liter. Genotype combinations of the four CRP polymorphisms were associated with an increase in CRP levels of up to 64%, resulting in a theoretically predicted increased risk of up to 32% for ischemic heart disease and up to 25% for ischemic cerebrovascular disease. However, these genotype combinations were not associated with an increased risk of ischemic vascular disease. In contrast, apolipoprotein E genotypes were associated with both elevated cholesterol levels and an increased risk of ischemic heart disease. Polymorphisms in the CRP gene are associated with marked increases in CRP levels and thus with a theoretically predicted increase in the risk of ischemic vascular disease. However, these polymorphisms are not in themselves associated with an increased risk of ischemic vascular disease. 2008 Massachusetts Medical Society
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              Implementing a unified approach to family-based tests of association.

              We describe a broad class of family-based association tests that are adjusted for admixture; use either dichotomous or measured phenotypes; accommodate phenotype-unknown subjects; use nuclear families, sibships or a combination of the two, permit multiple nuclear families from a single pedigree; incorporate di- or multi-allelic marker data; allow additive, dominant or recessive models; and permit adjustment for covariates and gene-by-environment interactions. The test statistic is basically the covariance between a user-specified function of the genotype and a user-specified function of the trait. The distribution of the statistic is computed using the appropriate conditional distribution of offspring genotypes that adjusts for admixture.
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                Author and article information

                Contributors
                hsiung@nhri.org.tw
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                11 August 2017
                11 August 2017
                2017
                : 7
                : 7987
                Affiliations
                [1 ]ISNI 0000 0004 0573 0731, GRID grid.410764.0, Division of Endocrinology and Metabolism, Department of Internal Medicine, , Taichung Veterans General Hospital, ; Taichung, Taiwan
                [2 ]ISNI 0000 0001 0425 5914, GRID grid.260770.4, , College of Medicine, National Yang-Ming University, ; Taipei, Taiwan
                [3 ]ISNI 0000 0004 0532 3749, GRID grid.260542.7, Institute of Medical Technology, , National Chung-Hsing University, ; Taichung, Taiwan
                [4 ]ISNI 0000 0004 0634 0356, GRID grid.260565.2, , School of Medicine, National Defense Medical Center, ; Taipei, Taiwan
                [5 ]ISNI 0000 0000 9337 0481, GRID grid.412896.0, , The Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, ; Taipei, Taiwan
                [6 ]ISNI 0000000406229172, GRID grid.59784.37, Division of Biostatistics and Bioinformatics, Institute of Population Health Sciences, , National Health Research Institutes, Zhunan, ; Miaoli County, Taiwan
                [7 ]ISNI 0000 0004 0572 7815, GRID grid.412094.a, Department of Internal Medicine, , National Taiwan University Hospital, ; Taipei, Taiwan
                [8 ]ISNI 0000 0004 0638 9360, GRID grid.278244.f, Division of Endocrinology & Metabolism, , Tri-Service General Hospital, ; Taipei, Taiwan
                [9 ]ISNI 0000 0004 0604 5314, GRID grid.278247.c, Section of Endocrinology and Metabolism, Department of Medicine, , Taipei Veterans General Hospital, ; Taipei, Taiwan
                [10 ]ISNI 0000 0001 0425 5914, GRID grid.260770.4, Faculty of Medicine, School of Medicine, , National Yang-Ming University, ; Taipei, Taiwan
                [11 ]ISNI 0000000419368956, GRID grid.168010.e, Division of Cardiovascular Medicine, Falk Cardiovascular Research Building, , Stanford University School of Medicine, ; Stanford, CA USA
                [12 ]ISNI 0000 0004 0573 0731, GRID grid.410764.0, Department of Medical Research, , Taichung Veterans General Hospital, ; Taichung, Taiwan
                [13 ]ISNI 0000 0004 0573 0731, GRID grid.410764.0, Cardiovascular Center, , Taichung Veterans General Hospital, ; Taichung, Taiwan
                [14 ]Institute for Translational Genomics and Population Sciences and Department of Pediatrics, Los Angeles BioMedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USA
                Article
                8696
                10.1038/s41598-017-08696-2
                5554245
                28801571
                b202d8c9-0f04-46bb-bbac-4b385fc2357c
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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                : 15 February 2017
                : 12 July 2017
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