Plasma Level of Growth Arrest-Specific 6 (GAS6) Protein and Genetic Variations in the GAS6 Gene in Patients With Acute Coronary Syndrome

Growth arrest-specific gene 6 (GAS6) encodes a vitamin K-dependent protein that regulates inflammation, angiogenesis, and atherosclerotic plaque formation. The level of GAS6 expression is associated with plaque stability and stroke. We explored the role of GAS6 in cardiovascular disease, particularl...

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Bibliographic Details
Published in:American journal of clinical pathology 2009-05, Vol.131 (5), p.738-743
Main Authors: Jiang, Lei, Liu, Cheng Yun, Yang, Qun Fang, Wang, Ping, Zhang, Wen
Format: Article
Language:English
Subjects:
Acute Coronary Syndrome - blood
Acute Coronary Syndrome - diagnosis
Acute Coronary Syndrome - genetics
Adult
Aged
Biological and medical sciences
Biomarkers - blood
Cardiology. Vascular system
Coronary heart disease
Female
Gene Frequency
Genetic Predisposition to Disease
Genetic Variation
Genotype
Heart
Humans
Intercellular Signaling Peptides and Proteins - blood
Intercellular Signaling Peptides and Proteins - genetics
Investigative techniques, diagnostic techniques (general aspects)
Male
Medical sciences
Middle Aged
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Polymorphism, Single Nucleotide
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Summary:Growth arrest-specific gene 6 (GAS6) encodes a vitamin K-dependent protein that regulates inflammation, angiogenesis, and atherosclerotic plaque formation. The level of GAS6 expression is associated with plaque stability and stroke. We explored the role of GAS6 in cardiovascular disease, particularly in acute coronary syndrome (ACS). We determined the plasma levels of GAS6 protein by using an enzyme-linked immunosorbent assay method and investigated the role of the single nucleotide polymorphism (c.834+7G>A) in ACS. The median (interquartile range) plasma GAS6 levels were 16.9 microg/L (13-28 microg/L) in healthy control subjects and 10.65 microg/L (5.7-27.5 microg/L) in patients with ACS. The genotype frequencies for GG, AG, and AA, respectively, in patients with ACS were 66% (37/56), 29% (16/56), and 5% (3/56) and were 35% (14/40), 45% (18/40), 20% (8/40) in the control group. The AA genotype and A allele were less frequent in patients with ACS than in control subjects (P < .001). Our study indicates that GAS6 plasma concentrations at admission reflect the presence of common cardiovascular risk factors and can predict cardiovascular events. In addition, the AA genotype and A allele of the GAS6 gene relate to ACS, which may have a protective role against ACS.
ISSN:0002-9173
1943-7722
DOI:10.1309/AJCP3CX3AUVRBHCF