Chromosome 1q21.1 contiguous gene deletion is associated with congenital heart disease

被引:124
作者
Christiansen, J
Dyck, JD
Elyas, BG
Lilley, M
Bamforth, JS
Hicks, M
Sprysak, KA
Tomaszewski, R
Haase, SM
Vicen-Wyhony, LM
Somerville, MJ
机构
[1] Univ Alberta, Dept Med Genet, Edmonton, AB T6G 2H7, Canada
[2] Univ Alberta, Dept Pediat, Edmonton, AB T6G 2H7, Canada
关键词
congenital heart disease; contiguous deletion syndrome; connexin40;
D O I
10.1161/01.RES.0000130528.72330.5c
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Congenital heart disease (CHD), comprising structural or functional abnormalities present at birth, is the most common birth defect in humans. Reduced expression of connexin40 (Cx40) has been found in association with atrial fibrillation, and deletion of Cx40 in a mouse model causes various structural heart abnormalities in 18% of heterozygotes. We screened 505 unrelated CHD cases for deletions or duplications of the Cx40 gene (GJA5) by real-time quantitative PCR, in order to determine whether altered copy number of this gene may be associated with a cardiac phenotype in humans. Dosage of Cx40 flanking genes (ACPL1 and Cx50 gene, GJA8) was determined by real-time PCR for all apparent positive cases. In total, 3 cases were found to carry deletions on chromosome 1q21.1 spanning ACPL1, Cx40, and Cx50 genes. Absence of heterozygosity was observed in all 3 index cases over a 1.5- to 3-Mb region. Samples from the parents of two cases were obtained, and microsatellites across 1q21.1 were genotyped. One of the apparently unaffected parents was found to carry this deletion. All 3 index cases presented with obstruction of the aortic arch as the common structural cardiac malformation, and had no consistent dysmorphic features. Genotyping of 520 unrelated normal controls for this deletion was negative. We hypothesize that this 1q21.1 multigene deletion is associated with a range of cardiac defects, with anomalies of the aortic arch being a particular feature.
引用
收藏
页码:1429 / 1435
页数:7
相关论文
共 41 条
  • [1] Positional identification of microdeletions with genetic markers
    Amos, CI
    Shete, S
    Chen, JF
    Yu, RK
    [J]. HUMAN HEREDITY, 2003, 56 (1-3) : 107 - 118
  • [2] Benson D. Woodrow, 2002, Cardiology Clinics, V20, P385, DOI 10.1016/S0733-8651(02)00009-7
  • [3] BENSON DW, 2002, CARDIOL CLIN, V20, pR6
  • [4] SHONES ANOMALY - OPERATIVE RESULTS AND LATE OUTCOME
    BOLLING, SF
    IANNETTONI, MD
    DICK, M
    ROSENTHAL, A
    BOVE, EL
    [J]. ANNALS OF THORACIC SURGERY, 1990, 49 (06) : 887 - 893
  • [5] Pathogenetic mechanisms of congenital cardiovascular malformations revisited
    Clark, EB
    [J]. SEMINARS IN PERINATOLOGY, 1996, 20 (06) : 465 - 472
  • [6] Collins-Nakai Ruth, 2002, Cardiology Clinics, V20, P367, DOI 10.1016/S0733-8651(02)00008-5
  • [7] COLLINSNAKAI R, 2002, CARDIOL CLIN, V20, pR5
  • [8] Impaired conduction of vasodilation along arterioles in connexin40-deficient mice
    de Wit, C
    Roos, F
    Bolz, SS
    Kirchhoff, S
    Krüger, O
    Willecke, K
    Pohl, U
    [J]. CIRCULATION RESEARCH, 2000, 86 (06) : 649 - 655
  • [9] Turner syndrome and the heart: Cardiovascular complications and treatment strategies
    Gravholt C.H.
    [J]. American Journal of Cardiovascular Drugs, 2002, 2 (6) : 401 - 413
  • [10] Development gone awry - Congenital heart disease
    Gruber, PJ
    Epstein, JA
    [J]. CIRCULATION RESEARCH, 2004, 94 (03) : 273 - 283