FGL1 as a modulator of plasma D-dimer levels: Exome-wide marker analysis of plasma tPA, PAI-1, and D-dimer

被引：3

作者：

Thibord, Florian ^{[1
]}

Song, Ci ^{[1
]}

Pattee, Jack ^{[2
]}

Rodriguez, Benjamin A. T. ^{[1
]}

Chen, Ming-Huei ^{[1
]}

O'Donnell, Christopher J. ^{[1
,3
]}

Kleber, Marcus E. ^{[4
,5
]}

Delgado, Graciela E. ^{[4
]}

Guo, Xiuqing ^{[6
]}

Yao, Jie ^{[6
]}

Taylor, Kent D. ^{[6
]}

Ozel, Ayse Bilge ^{[7
]}

Brody, Jennifer A. ^{[8
,9
,10
]}

McKnight, Barbara ^{[11
]}

Gyorgy, Beata ^{[12
]}

Simonsick, Eleanor ^{[13
]}

Leonard, Hampton L. ^{[13
]}

Carrasquilla, German D. ^{[14
]}

Guindo-Martinez, Marta ^{[14
]}

Silveira, Angela ^{[15
,16
]}

Temprano-Sagrera, Gerard ^{[17
]}

Yanek, Lisa R. ^{[18
]}

Becker, Diane M. ^{[18
]}

Mathias, Rasika A. ^{[18
,19
]}

Becker, Lewis C. ^{[18
,20
]}

Raffield, Laura M. ^{[21
]}

Kilpelainen, Tuomas O. ^{[14
]}

Grarup, Niels ^{[14
]}

Pedersen, Oluf ^{[14
]}

Hansen, Torben ^{[14
]}

Linneberg, Allan ^{[22
]}

Hamsten, Anders ^{[15
,16
]}

Watkins, Hugh ^{[23
]}

Sabater-Lleal, Maria ^{[15
,16
,17
]}

Nalls, Mike A. ^{[13
]}

Tregouet, David-Alexandre ^{[12
,24
]}

Morange, Pierre-Emmanuel ^{[25
]}

Psaty, Bruce M. ^{[8
,9
,10
]}

Tracy, Russel P. ^{[26
,27
]}

Smith, Nicholas L. ^{[8
,9
,10
,28
,29
,30
]}

Desch, Karl C. ^{[31
]}

Cushman, Mary ^{[26
,27
]}

Rotter, Jerome I. ^{[6
]}

de Vries, Paul S. ^{[32
]}

Pankratz, Nathan D. ^{[33
]}

Folsom, Aaron R. ^{[34
]}

Morrison, Alanna C. ^{[32
]}

Maerz, Winfried ^{[4
,35
]}

Tang, Weihong ^{[34
]}

Johnson, Andrew D. ^{[1
]}

机构：

[1] Natl Heart Lung & Blood Inst, Framingham Heart Study, Framingham, MA USA

[2] Univ Minnesota, Sch Publ Hlth, Div Biostat, Minneapolis, MN USA

[3] US Dept Vet Affairs, Boston, MA USA

[4] Heidelberg Univ, Med Fac Mannheim, Vth Dept Med, Mannheim, Germany

[5] SYNLAB MVZ Humangenet Mannheim GmbH, Mannheim, Germany

[6] UCLA Med Ctr, Lundquist Inst BioMed Innovat Harbor, Inst Translat Gen & Populat Sci, Dept Pediat, Torrance, CA USA

[7] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA

[8] Univ Washington, Cardiovasc Hlth Res Unit, Dept Med, Seattle, WA 98195 USA

[9] Univ Washington, Cardiovasc Hlth Res Unit, Dept Epidemiol, Seattle, WA 98195 USA

[10] Univ Washington, Cardiovasc Hlth Res Unit, Dept Hlth Serv, Seattle, WA 98195 USA

[11] Univ Washington, Dept Biostat, Seattle, WA 98195 USA

[12] Sorbonne Univ, Inst Cardiometab & Nutr, INSERM UMRS1166, ICAN, Paris, France

[13] NIA, NIH, Bethesda, MD 20892 USA

[14] Univ Copenhagen, Novo Nord Fdn Ctr Basic Metab Res, Fac Hlth & Med Sci, Copenhagen, Denmark

[15] Karolinska Inst, Dept Med Solna, Cardiovasc Med Unit, Ctr Mol Med, Stockholm, Sweden

[16] Karolinska Univ Hosp Solna, Stockholm, Sweden

[17] IIB St Pau, Res Inst Hosp Santa Creu & St Pau, Genom Complex Dis, Barcelona, Spain

[18] Johns Hopkins, GeneSTAR Res Program, Div Gen Internal Med, Sch Med, Baltimore, MD USA

[19] Johns Hopkins Sch Med, Div Allergy & Clin Immunol, Baltimore, MD USA

[20] Johns Hopkins Sch Med, Div Cardiol, Baltimore, MD USA

[21] Univ N Carolina, Dept Genet, Chapel Hill, NC 27515 USA

[22] Bispebjerg & Frederiksberg Hosp, Ctr Clin Res & Prevent, Frederiksberg, Denmark

[23] Univ Oxford, Radcliffe Dept Med, Oxford, England

[24] Univ Bordeaux, INSERM, BPH, Bordeaux, France

[25] Aix Marseille Univ, INSERM, INRAE, Marseille, France

[26] Univ Vermont, Larner Coll Med, Vermont Ctr Cardiovasc & Brain Hlth, Dept Pathol & Lab Med, Burlington, VT USA

[27] Univ Vermont, Larner Coll Med, Vermont Ctr Cardiovasc & Brain Hlth, Dept Med, Burlington, VT USA

[28] Kaiser Permanente Washington, Kaiser Permanente Washington Hlth Res Inst, Seattle, WA USA

[29] Univ Washington, Dept Epidmiol, Seattle, WA USA

[30] Seattle Epidmiol Res & Informat Ctr, Dept Vet Affairs Off Res & Dev, Seattle, WA USA

[31] Univ Michigan, Cell & Mol Biol Program, Dept Pediat, Ann Arbor, MI 48109 USA

[32] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Dept Epidemiol Human Genet & Environm Sci, Human Genet Ctr, Houston, TX 77030 USA

[33] Univ Minnesota, Sch Med, Dept Lab Med & Pathol, Minneapolis, MN USA

[34] Univ Minnesota, Sch Publ Hlth, Div Epidmiol & Community Hlth, Minneapolis, MN USA

[35] Synlab Holding Deutschland GmbH, Synlab Acad, Mannheim, Germany

来源：

JOURNAL OF THROMBOSIS AND HAEMOSTASIS | 2021年 / 19卷 / 08期

基金：

美国国家卫生研究院; 瑞典研究理事会;

关键词：

computational biology; exome; fibrinogen; fibrinolysis; genetic association study; TISSUE-PLASMINOGEN ACTIVATOR; CARDIOVASCULAR-DISEASE; LOW-FREQUENCY; ASSOCIATION; VARIANTS; FIBRINOGEN; RARE; HEART; METAANALYSIS; PROTEIN-1;

D O I：

10.1111/jth.15345

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Background Use of targeted exome-arrays with common, rare variants and functionally enriched variation has led to discovery of new genes contributing to population variation in risk factors. Plasminogen activator-inhibitor 1 (PAI-1), tissue plasminogen activator (tPA), and the plasma product D-dimer are important components of the fibrinolytic system. There have been few large-scale genome-wide or exome-wide studies of PAI-1, tPA, and D-dimer. Objectives We sought to discover new genetic loci contributing to variation in these traits using an exome-array approach. Methods Cohort-level analyses and fixed effects meta-analyses of PAI-1 (n = 15 603), tPA (n = 6876,) and D-dimer (n = 19 306) from 12 cohorts of European ancestry with diverse study design were conducted, including single-variant analyses and gene-based burden testing. Results Five variants located in NME7, FGL1, and the fibrinogen locus, all associated with D-dimer levels, achieved genome-wide significance (P < 5 x 10(-8)). Replication was sought for these 5 variants, as well as 45 well-imputed variants with P < 1 x 10(-4) in the discovery using an independent cohort. Replication was observed for three out of the five significant associations, including a novel and uncommon (0.013 allele frequency) coding variant p.Trp256Leu in FGL1 (fibrinogen-like-1) with increased plasma D-dimer levels. Additionally, a candidate-gene approach revealed a suggestive association for a coding variant (rs143202684-C) in SERPINB2, and suggestive associations with consistent effect in the replication analysis include an intronic variant (rs11057830-A) in SCARB1 associated with increased D-dimer levels. Conclusion This work provides new evidence for a role of FGL1 in hemostasis.

引用

页码：2019 / 2028

页数：10

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Navarro, Pau ;

Rose, Lynda M. ;

Oldmeadow, Christopher ;

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Basu, Saonli ;

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Liu, Dajiang J. ;

Deloukas, Panos ;

Samani, Nilesh J. ;

Schunkert, Heribert ;

Erdmann, Jeanette ;

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