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GWAS Study

Exome-chip meta-analysis identifies association between variation in ANKRD26 and platelet aggregation.

Chen MH, Yanek LR, Backman JD et al.

29185836 PubMed ID
GWAS Study Type
6010 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

CM
Chen MH
YL
Yanek LR
BJ
Backman JD
EJ
Eicher JD
HJ
Huffman JE
BY
Ben-Shlomo Y
BA
Beswick AD
YL
Yerges-Armstrong LM
SA
Shuldiner AR
OJ
O'Connell JR
MR
Mathias RA
BD
Becker DM
BL
Becker LC
LJ
Lewis JP
JA
Johnson AD
FN
Faraday N
Chapter II

Abstract

Summary of the research findings

Previous genome-wide association studies (GWAS) have identified several variants associated with platelet function phenotypes; however, the proportion of variance explained by the identified variants is mostly small. Rare coding variants, particularly those with high potential for impact on protein structure/function, may have substantial impact on phenotype but are difficult to detect by GWAS. The main purpose of this study was to identify low frequency or rare variants associated with platelet function using genotype data from the Illumina HumanExome Bead Chip. Three family-based cohorts of European ancestry, including ~4,000 total subjects, comprised the discovery cohort and two independent cohorts, one of European and one of African American ancestry, were used for replication. Optical aggregometry in platelet-rich plasma was performed in all the discovery cohorts in response to adenosine diphosphate (ADP), epinephrine, and collagen. Meta-analyses were performed using both gene-based and single nucleotide variant association methods. The gene-based meta-analysis identified a significant association (P = 7.13 × 10-7) between rare genetic variants in ANKRD26 and ADP-induced platelet aggregation. One of the ANKRD26 SNVs - rs191015656, encoding a threonine to isoleucine substitution predicted to alter protein structure/function, was replicated in Europeans. Aggregation increases of ~20-50% were observed in heterozygotes in all cohorts. Novel genetic signals in ABCG1 and HCP5 were also associated with platelet aggregation to ADP in meta-analyses, although only results for HCP5 could be replicated. The SNV in HCP5 intersects epigenetic signatures in CD41+ megakaryocytes suggesting a new functional role in platelet biology for HCP5. This is the first study to use gene-based association methods from SNV array genotypes to identify rare variants related to platelet function. The molecular mechanisms and pathophysiological relevance for the identified genetic associations requires further study.

3,664 European ancestry individuals, 549 Old Order Amish (founder/genetic isolate) individuals

Chapter III

Study Statistics

Key metrics and study information

6010
Total Participants
GWAS
Study Type
Yes
Replicated
1,184 European ancestry individuals, 613 African American individuals
Replication Participants
European, African American or Afro-Caribbean
Ancestry
U.S.
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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Analysis In Progress

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