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GWAS Study

Genome-wide association study of erythrocyte density in sickle cell disease patients.

Ilboudo Y, Bartolucci P, Rivera A et al.

28552477 PubMed ID
GWAS Study Type
317 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

IY
Ilboudo Y
BP
Bartolucci P
RA
Rivera A
SJ
Sedzro JC
BM
Beaudoin M
TM
Trudel M
AS
Alper SL
BC
Brugnara C
GF
Galactéros F
LG
Lettre G
Chapter II

Abstract

Summary of the research findings

Deoxy-hemoglobin S polymerization into rigid fibers is the direct cause of the clinical sequelae observed in sickle cell disease (SCD). The rate of polymerization of sickle hemoglobin is determined primarily by intracellular hemoglobin concentration, itself dependent on the amount of sickle hemoglobin and on red blood cell (RBC) volume. Dense, dehydrated RBC (DRBC) are observed in SCD patients, and their number correlates with hemolytic parameters and complications such as renal dysfunction, leg ulcers and priapism. To identify new genes involved in RBC hydration in SCD, we performed the first genome-wide association study for DRBC in 374 sickle cell anemia (HbSS) patients. We did not find genome-wide significant results, indicating that variants that modulate DRBC have modest-to-weak effects. A secondary analysis demonstrated a nominal association (P=0.003) between DRBC in SCD patients and a variant associated with mean corpuscular hemoglobin concentration (MCHC) in non-anemic individuals. This intronic variant controls the expression of ATP2B4, the main calcium pump in erythrocytes. Our study highlights ATP2B4 as a promising target for modulation of RBC hydration in SCD patients.

317 cases

Chapter III

Study Statistics

Key metrics and study information

317
Total Participants
GWAS
Study Type
No
Replicated
African unspecified, NR
Ancestry
France
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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